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Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital
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Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Dec 21, 2015

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Page 1: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid and Electrolyte Management of the

Surgical Patient

Dr Abdollahi

Afshar Hospital

Fluid therapy is often poorly taught poorly understood and

poorly done

lsquolsquoFluid therapy should be directed not only to Fluid therapy should be directed not only to effective volume expansion of a leaky effective volume expansion of a leaky circulation but also to micro vascular circulation but also to micro vascular protectionrsquoprotectionrsquo

Fluid and electrolyte management are paramount to the care of the surgical patient Changes in both fluid volume and electrolyte composition occur preoperatively intraoperatively and post operatively as well as in response to trauma and sepsis

Total Body Water

Who is having higher proportion of body weight as water And Why

1048699Males or Females

1048699Lean or Obese

1048699Young or elderly

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 2: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid therapy is often poorly taught poorly understood and

poorly done

lsquolsquoFluid therapy should be directed not only to Fluid therapy should be directed not only to effective volume expansion of a leaky effective volume expansion of a leaky circulation but also to micro vascular circulation but also to micro vascular protectionrsquoprotectionrsquo

Fluid and electrolyte management are paramount to the care of the surgical patient Changes in both fluid volume and electrolyte composition occur preoperatively intraoperatively and post operatively as well as in response to trauma and sepsis

Total Body Water

Who is having higher proportion of body weight as water And Why

1048699Males or Females

1048699Lean or Obese

1048699Young or elderly

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 3: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

lsquolsquoFluid therapy should be directed not only to Fluid therapy should be directed not only to effective volume expansion of a leaky effective volume expansion of a leaky circulation but also to micro vascular circulation but also to micro vascular protectionrsquoprotectionrsquo

Fluid and electrolyte management are paramount to the care of the surgical patient Changes in both fluid volume and electrolyte composition occur preoperatively intraoperatively and post operatively as well as in response to trauma and sepsis

Total Body Water

Who is having higher proportion of body weight as water And Why

1048699Males or Females

1048699Lean or Obese

1048699Young or elderly

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 4: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid and electrolyte management are paramount to the care of the surgical patient Changes in both fluid volume and electrolyte composition occur preoperatively intraoperatively and post operatively as well as in response to trauma and sepsis

Total Body Water

Who is having higher proportion of body weight as water And Why

1048699Males or Females

1048699Lean or Obese

1048699Young or elderly

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 5: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Total Body Water

Who is having higher proportion of body weight as water And Why

1048699Males or Females

1048699Lean or Obese

1048699Young or elderly

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 6: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Body Fluid CompartmentsBody Fluid Compartments

ICFICF55~7555~75

IntravascularIntravascularplasmaplasma

X 50~70 X 50~70 lean body weightlean body weight

ExtravascularExtravascularInterstitial Interstitial

fluidfluid

TBWTBW

ECFECF

34

14

bull Male (55) gt female (45)bull Most concentrated in skeletal musclebull TBW=06xBWbull ICF=04xBWbull ECF=02xBW

23

13

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 7: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Total body water (TBW)

bull TBW varies with age gender and body habitus

bull In adult males= 55 of body weight

bull In adult female=45 of body weight

bull In infant = 80 of body weight

bull Obese patients have less TBW per Kg than lean body

adult

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 8: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

1= Intracellular fluid (ICF)=55 TBW or 30-40 BW

2= Extracellular fluid (ECF) =45TBW or 20 BW

Interstitial fluid =15 of body weight

Intravascular fluid or plasma volume

= 5 of body weight

Body compartment fluid

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 9: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Example men with 70kg TBW= 5570 =385 L

ICF = 55 385 =212L

ECF = 45 385=173L

1 ISF = 15 70 = 105L

2 PV = 5 70 =35L

Your User Name

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 10: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 11: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 12: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 13: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 14: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 15: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid compartments

ICF

ECF

Interstitial

Pla

sma

Capillary Membrane Cell Membrane

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 16: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 17: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 18: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

H2O

H2O

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 19: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid osmotic pressure

ECF

Interstitial

Pla

sma

Capillary Membrane

Capillary membrane freely permeable to water and electrolytes but not to large molecules such as proteins (albumin)

The albumin on the plasma side gives rise to a colloid osmotic pressure gradient favouring movement of water into the plasma

This is balanced out by the hydrostatic pressure difference

H2O

H2O12080

H2O

H2O

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 20: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 21: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Na+

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 22: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 23: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 24: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 25: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cell Membrane

ICF

Cell Membrane

Na-

K+

Interstitial

H2O

H2O

Cell membrane is freely permeable to H20 but Na and K are pumped across this membrane to maintain a gradient

[K+] =4 [K+] =150

Na+= 144Na+= 10

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 26: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Composition of Fluid Compartments

CATIONS ANIONS

Na+ 142 Cl - 103

HC03- 27

504mdash

3 PO4

---

K+ 4 organicCa++ 5 Acid 5

Mg++ 3 Protein 16

CATIONS ANIONS

Na+ 144 Cl - 114

HC03- 30

504mdash

K+ 4 3 PO4

---

organic

Ca++ 3 Acid 5

Mg++ 2 Protein 1

CATIONS ANIONS

K+ 150 HPO4

150 504

mdash

HCO3- 10

Mg++ 40 Protein 40

Na+ 10

154 mEqL 153 mEqL 153 mEqL154 mEqL

PLASMA INTERSTITAL FLID

200 mEqL 200 mEqL

INTRACELLULAR FLID

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 27: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Composition of Body FluidsComposition of Body Fluids

Ca 2+

Mg 2+

K+

Na+

Cl-

PO43-

Organic anion

HCO3-

Protein

0

50

50

100

150

100

150

Cations Anions

EC

FICF

Osmolarity = solute(solute+solvent)Osmolarity = solute(solute+solvent) Osmolality = solutesolvent (290~310mOsmL)Osmolality = solutesolvent (290~310mOsmL) Tonicity = effective osmolalityTonicity = effective osmolality Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28)Plasma osmolility = 2 x (Na) + (Glucose18) + (Urea28) Plasma tonicity = 2 x (Na) + (Glucose18)Plasma tonicity = 2 x (Na) + (Glucose18)

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 28: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

والکترولیت آب تغییرات روی موثر عوامل

1 ndash - آب ) تبخیر خونریزی میزان جراحی عمل نوعسوم ( فضای حجم

عمل 2 از قبل والکترولیت آب وضعیت

اندوکرینوپاتی )3 همراه )بیماریهای

4 - - پروپوفل ) نسدونال بیهوشی داروهای -MRاثرRA)

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 29: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Reasons for fluid therapyReasons for fluid therapy

Preserve oxygen delivery to tissuesPreserve oxygen delivery to tissues

bull Correct hypovolaemiaCorrect hypovolaemia

bull Maintain cardiac outputMaintain cardiac output

bull Optimise gas exchangeOptimise gas exchange

bull Replace electrolytes amp waterReplace electrolytes amp water

bull Maintain urine outputMaintain urine output

Colloids + RBCs

Crystalloids

Identify what is the goal

Choose fluid which best achieves the goal

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 30: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

عروقی داخل مایع حجم ارزیابی

بیمار bull حال شرحخوابیده ) ndash (bull ایستاده خون فشاربیمار bull قلب ضربانادراری bull ده برونهماتوکریتbullخون bull نیتروژنها bull الکترولیتbullABGbullCVP

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 31: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

وریدی محلولهای

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 32: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluids bull Crystalloids

bull Colloids

bull blood

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 33: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Which of the following solutions is isotonic

A D5W

B 045 saline

C 09 saline

D D5 in 09 saline

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 34: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

SolutionsSolutions VolumesVolumes NaNa++ KK++ CaCa2+2+ MgMg2+2+ ClCl-- HCOHCO33-- DextroseDextrose mOsmLmOsmL

ECFECF 142 4 5 103 27 280-310

Lactated Lactated RingerrsquosRingerrsquos

130 4 3 109 28 273

09 NaCl09 NaCl 154 154 308

045 045 NaClNaCl

77 77 154

D5WD5W

D5045 D5045 NaClNaCl

77 77 50 406

3 NaCl3 NaCl 513 513 1026

6 6 HetastarchHetastarch

500 154 154 310

5 5 AlbuminAlbumin

250500130-160

lt25130-160

330

25 25 AlbuminAlbumin

2050100130-160

lt25130-160

330

Common parenteral fluid therapyCommon parenteral fluid therapy

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 35: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

CrystalloidsCrystalloids

bull Isotonic crystalloids - Lactated Ringerrsquos 09 NaCl - only 25 remain intravascularly bull Hypertonic saline solutions - 3 NaClbull Hypotonic solutions - D5W 045 NaCl - less than 10 remain intra- vascularly inadequate for fluid resuscitation

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 36: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid SolutionsColloid Solutions

bull Contain high molecular weight substancesdo not readily migrate across capillary wallsbull Preparations - Albumin 5 25 - Dextran - Gelifundol

- Haes-steril 10

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 37: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

الکتات رینگردست bull از جایگزینی جهت ایزوتونیک نمکی مایع

کاهش GIدادنهای در ECFو عمده اشکاالت بدون است الکتات رینگر اجزا و ترکیبات

ایزوتونیک bullbullNa=130meql CL=109meql lactat=28meql

osm=273

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 38: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

09Nacl

bull Na=154

bull CL= 154

کاهش bull جبران جهت مایع حضور ECFاین درال ایده متابولیک آلکالوز و وهیپوکلرمی هیپوناترمی

PH=56است

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 39: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Postoperative (maintenance)

045Nacl +5 dextrose +KCL

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 40: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Perioperative management of fluid balance include

1 Preoperative evaluation

2 Intraoperative maintenance

3 Replacement of fluid losses

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 41: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Preexisting fluid deficits

bull NPO time and abnormal fluid losses (vomiting-dirreha- asites- infected tissue-fever ndashsweating- hyperventilation)

bull Hypotonic fluid (05 saline ) or isotonic crystalloids

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 42: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Maintenance requirements

bull Up to 10 kg = 4cckghr

bull 11-20kg = add 2cckghr

bull 21kg and above = add 1cckghr

bull Insensible losses = 2cckghr

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 43: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Surgical fluid losses

Blood loss (measurement)

1 Suction container

2 Surgical sponge

3 Hct and tachycardia not specific

4 ABG and UO if hypoperfusion occur

5 Blood loss=31 with crystalloid

Other losses (third space loss)

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 44: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Third space loss

1 Minimal (herniorrapy) =2-4cckghr

2 Moderate (cholecystectomy)=4-6cckghr

3 Severe (bowel resection) = 6-8cckghr

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 45: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Crystalloid solution

1 The main solutions is either glucose or saline

2 Hypotonic or isotonic or hypertonic

3 Safe nontoxic reaction free inexpensive

4 Complication is edema if large volumes are needed

5 During surgery isotonic solution favored (normal saline - lactate ringer and plasma lyte)

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 46: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloids

1 Albumin

2 Hydroxyethyl starch

3 Dextran

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 47: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Complications 1 Hypersensitivity reactions (anaphylaxis )2 Pruritis (hetastarch)3 Couglopathy (dextran 70 and hetastarch) gt 1 litter bull Dextran ( platelet aggregation adhesive)bull Hetastarch (reduction in factor vlll and VOB

factor )These colloid is best avoided in patients with

coagulopaty

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 48: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

The Influence of Colloid amp Crystalloid The Influence of Colloid amp Crystalloid on Blood Volumeon Blood Volume

1000cc

500cc

500cc

500cc

200

600

1000

Lactated Ringers

5 Albumin

6 Hetastarch

Whole blood

Blood volumeInfusion volume

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 49: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Colloid versus crystalloid solutions

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 50: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Transfusion consideration

bull HB lt7 mg dl increase CO

bull Ideal Hb is 7-8 mgdl

bull In IHD patients or pulmonary disease gt 10 mgdl

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 51: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

بدن مایعات حجم در اختالل

1 Fluid volume deficit

2 Fluid volume excess

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 52: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid volume deficit(FVD)

) مایعات در که نسبتی به بدن والکترولیتهای آب کاهشنسبت ) که صورتی به دارد وجود بدن طبیعی

کاهش بماند باقی یکنواخت آب به بدن الکترولیتهایمایع آمد FVDحجم خواهد وجود کاهش( به

ایزوتونیک)در سرم الکترولیتهای میماند FVDمیزان باقی نرمال

باشد آن با همراه دیگری اختالل مگر

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 53: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

DEHYDRATION

سدیم bull افزایش با همراه آب کاهش دهیدریشن در دارد وجود سرمی

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 54: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

سلولی خارج حجم کاهش علل

1ndash استفراغ بدن آب طبیعی غیر دادن دست ازNGTتعریق--اسهال-

2 ناتوانی یا تهوع بدن آب دریافت میزان کاهشمایعات به دسترسی

کاردیواسکوالر (3 سیستم از مایعات thirdخروجspace loss ndash (جراحی ترومای سوختگی مثل

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 55: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Signs of HypovolemiaSigns of Hypovolemia

bull Diminished skin turgorbull Dry oral mucus membranebull Oliguria - lt500mlday - normal 05~1mlkghbull Tachycardiabull Hypotensionbull Hypoperfusioncyanosisbull Altered mental status

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 56: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical Diagnosis of Clinical Diagnosis of HypovolemiaHypovolemia

bull Thorough history taking poor intake GI bleedinghellipetcbull BUN Creatinine gt 20 1 - BUNuarr hyperalimentation glucocorticoid therapy UGI bleedingbull Increased specific gravitybull Increased hematocritbull Electrolytes imbalancebull Acid-base disorder

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 57: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Signs of HypervolemiaSigns of Hypervolemia

bull Hypertensionbull Polyuriabull Peripheral edemabull Wet lungbull Jugular vein engorgement

Especially when hypo-albuminemia

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 58: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Management of Management of HypervolemiaHypervolemia

bull Prevention is the best waybull Guide fluid therapy with CVP level or pulmonary wedge pressurebull Diureticsbull Increase oncotic pressure FFP or albumin infusion (may followed by diuretics)bull Dialysis

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 59: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Fluid ManagementFluid Management

bull GoalGoal - to maintain urine output of 05~10mgkghbull RuleRule bull Electrolytes requireElectrolytes require - Na+ 1-2mmolkgday - K+ 05~10mmolkgdaybull Avoid fluid overload especially in malnutrition heart failure and renal insufficiency patient

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 60: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Electrolyte physiology

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 61: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Sodium physiology

Na is the most abundant positive ion of ECF compartment and is critical in determining the ECF and ICF osmolality

Normal amount 135-145 meql

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 62: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Osmotic Pressure

Calculated serum osmolality =

2 sodium+ glucose18 + BUN 28

Osmolality = 290 mosm

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 63: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Concentration

1Serum sodium concentration2Serum osmolarity

bull Hypovolemichypernatremic (burn fever)bull Hypovolemichyponatremic (vomiting diarrhea or fistula

drainage)bull Normovolemichyponatremic (decrease kidney reserve )bull Hypervolemichyponatremic (excessive water intakeTURP

DW5)

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 64: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hypernatremia

Serum Nagt145mEqL

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 65: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

- Hypernatremia

Loss of Free Water

Gain of sodium in excess of water

Hypernatremia

-Hypernatremia Hypo volemic

Hyper volemic

Normo volemic

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 66: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hypernatremia

Volume Status

Normal

Nonrenal water loss

Skin

Gastrointestinal

Renal water loss

Renal disease

Diuretics

Diabetes insipidus

High

Iatrogenic sodium administration

Mineralocorticoid excess

Aldosteronism

Cushingrsquos disease

Congenital adrenal

hyperplasia

Low

Nonrenal water loss

Skin

Gastrointestinal losses

Renal water losses

Renal (tubular) Diuretics

Osmotic diuretics

Diabetes insipidus

Adrenal failure

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 67: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Asymptomatic

Hypernatremia Symptomatic (Nagt160 meqL)

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 68: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical Manifestations of Abnormalities in Serum Sodium

Central nervous system Restlessness lethargy ataxia irritability tonic spasms delirium seizures coma Musculoskeletal weaknessCardiovascular Tachycardia hypotension syncopeTissue Dry sticky mucous membranes red swollen tongue decreased saliva and tearsRenal Oliguria Metabolic Fever

Body system hypernatremia

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 69: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

Normal saline in hypovolemic patients

Hypotonic fluid (Dw 5 DW 5 in frac14 or frac12 normal

saline or entral water)

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 70: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Water deficit (L)= times TBW

The formula used to estimate the amount of water required to correct hypernatremia

Estimate TBW as 55 of lean body mass in men and 45 in women

Serum sodium-140

140

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 71: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

The rate of fluid administration

1 Acute hypernatremia a decrease in serum sodium of no more than 1meqh and 12meqd

2 Chronic hypernatremia a decrease in serum sodium of no more than 07meqLh

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 72: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hyponatremia Nalt135mEqL

Causes

1 Sodium depletion

2 Sodium dilution

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 73: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

bull Incidence = 45

bull After surgery=1

bull Mortality = 2 times normal

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 74: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Sodium depletion1 Decrease intake 1048699Low Na diet 1048699Enteral feeds2 Increase loss Gastrointestinal Losses 1048699Vomiting 1048699Prolonged NGT suctioning 1048699Diarrhea Renal Losses 1048699Diuretics 1048699Primary renal disease3 Depletional hyponatreamia is often accompanied by extracellulr

volume deficit

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 75: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Sodium dilution1 Due to excess extracellular water 1048699Intentional excessive oral intake 1048699Iatrogenic Intravenous2 Drugs 1048699Antipsychotics 1048699Tricyclic antidepressants 1048699Angiotensin-converting enzyme inhibitors3 Hyperosmolar 1048699Mannitol 1048699Hyperglycemia4Pseudohyponatremia 1048699Plasma lipids 1048699Plasma proteins

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 76: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Sign and symptoms

bull CNS symptom when Nalt123 meql

bull Cardiac symptom when Nalt100 meql

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 77: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

For every 100 mgdL increment in plasma glucose above normal the plasma sodium should decrease by 16 mEqL

Body System Hyponatremia

central nervous system Headache confusion hyper-or hypoactive deep tendon

reflexes seizures coma increased intracranial pressure

Musculoskeletal Weakness fatigue muscle crampstwitching

Gastrointestinal Anorexia nausea vomiting watery diarrhea

Cardiovascular Hypertension and bradycardia if significant increases in

intracranial pressure

Tissue Lacrimation salivation

Renal Oliguria

Clinical Manifestations of Abnormalities in Serum Sodium

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 78: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

1=Depend on ECF

2=CNS sign

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 79: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

1 Asymptomatic increase the sodium level by no more than

05-1 meqLh to a maximum increase of 12 meqL per day

2 Symptomatic (Nalt120 meqL) Increase the sodium level by no

more than 1meqL per hour until the serum Na level reaches 130

meqL or neurologic symptoms are improved

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 80: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Rapid correction of hyponatremia

Pontine myelinolysis

Seizures weaknessparesis akinetic

movements unresponsiveness

Permanent brain damage

Death

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 81: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Dose

Na deficit meq =(140- Na meql) TBW

باید به h 05-1 meqlاصالح سدیم تا و 125meqlباشد برسد

شود اصالح آهسته سپس

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 82: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Potassium abnormalities

bull The average dietary intake of potassium 50-100meqd

bull The average renal excretion of potassium 10-700 meqd

- 2 of the total body potassium in ECF (45meqL)

- Factors that influence serum potassium

1 Surgical stress

2 Injury

3 Acidosis

4 Tissue catabolism

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 83: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hyperkalemia

The normal range of serum potassium 35-5 meqL

Etiology of Hyperkalemia

Increased intake Potassium supplementation

Blood transfusions

Endogenous loaddestruction

hemolysis rhabdomyolysis

cruch injury gastrointestinal hemorrhage

Increased release Acidosis

Rapid rise of extracellure osmolality (hyperglycemia or mannitol)Impaired excretion of potassium

Renal insufficiencyfailure

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 84: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical manifestation of hyperkalemia

System hyperkalemia

Gastrointestinal Nauseavomiting colic diarrhea

Neuromuscular weakness paralysis respiratory failure

Cardiovascular Arrhythmia arrest

ECG changes Peaked T waves (early change)

Flattened P wave

Prolonged PR interval (first-degree block)

Widened QRS complex

Sine wave formation

Ventricular fibrillation

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 85: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

Treatment of symptomatic hyperkalemia

Potassium removal Kayexalate

Oral administration is 15-30 g in 50-100 mLof 20 sorbitol

Rectal administration is 50 g in 200 mL 20 sorbitol

Dialysis

Shift potassium Glucose 1 vial of D50 and regular insulin 5-10 units intravenous

Bicarbonate 1 vial intravenous

Counteract cardiac effects Calcium gluconate 5-10 mL of 10 solution

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 86: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

HypokalemiaEtiology

inadequate intake

Dietary potassium-free intravenous fluids potassium-deficient

total parenteral nutrition

Excessive potassium excretion

Hyperaldosteronism

Medications

Gastrointestinal losses

Direct loss of potassium from gastrointestinal fluid (diarrhea)

Renal loss of potassium (gastric fluid either as vomiting or high

nasogastric output)

Intracellular-shift (metabolic alkalosis or insulin therapy)

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 87: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Potassium changes associated with alkalosis

Potassium decrease by 03 meqL for every 01

increase in PH above normal

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 88: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Magnesium Depletion

(drug induced amphotericin amioglycosides cisplatin)

Renal potassium wastage

Hypokalemia

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 89: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical Manifestation of Abnormalities in potassium

System hypokalemia

Gastrointestinal Ileus constipation

Neuromuscular Decreased reflexes fatigue weakness

paralysis

Cardiovascular Arrest

ECG changes U-waves

T-wave flattening

ST-segment changes

Arrhythmias

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 90: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

Potassium

Serum potassium level lt40 mEqL

Asymptomatic tolerating enteral nutrition KC1 40 mEq per entral access

times 1 doses

Asymptomatic not tolerating entral nutrition KC1 20 mEq IV q2h times 2 doses

Symptomatic KC1 20 mEq IV q1h times 4 doses

Recheck potassium level 2 hours after end of infusion if lt35 mEqL and

asymptomatic replace as per above protocol

Electrolyte Replacement Therapy Protocol

bull Oral repletion for mild and asymptomatic hypokalemia

bull IV repletion for severe and symptomatic hypokalemia

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 91: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Calcium از bull است 99بيش اسكلتي سيستم در بدن كلسيم از

( دندانها( ndash استخوانbull كلسيم نقش

عصبي 1 ايمپالسهاي )NMJ(انتقال

صاف 2 عضالت انقباض

هاي 3 واكنش برای الزم آنزيمهاي آزادسازي مسببشيميائي

انعقاد 4

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 92: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

یونیزه Calt45 meql هيپوكلسمي

عللbullپاراتيروئيد 1 كاري كمپانكراتيت2ویتامین ( 3 تبدیل شدن مختل و فسفر احتباس كليه به Dنارسائي

( کلیه در فعالش فرم4 ( کلسیم ( شدن باند افزایش باعث تنفسي آلكالوز هيپرونتيالسيون

میشود آلبومین باماسيو 5 ترانسفيو زن6( پاراتورمون ( ترشح مهار منیزیوم تخلیهتزریق ( 7 بیکربنات با مستقبم طور به کلسیم بیکربنات انفوزیون

( شود می پیوند شده

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 93: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

هیپوکلسمی عالئم

رفلکسی bull هیپرتشنجbullتتانیbullbullChevostek) 25( دارد وجود نرمال افرادbullTrousseau )30در ( ندارد وجود هیپوکلسمی مواردهیپوتانسیونbullقلبی bull ده برون کاهشآریتمیbull

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 94: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

سایرعالئم

قلب bull انقباضي قدرت كاهشمركزي bull هاي وريد فشار افزايشخون bull فشار كاهشحنجره bull اسپاسماسكلتي bull عضالت اسپاسم

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 95: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

درمان

ای bull زمینه علت کردن طرف بروریدی bull کلسیم

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 96: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Cagt55meql هيپركلسمي

هيپرپاراتيروئيديسمbullاستخواني bull متاستاز با كانسرهامدت bull طوالنی حرکتی بیدیورتیک ( ndash )bull لیتیوم داروها

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 97: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

عالئم

bullGI

bullCardiovascular bullRenal (polyuria)

bullCNS

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 98: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

قلبی عالئم

bull Cagt7 meqlفاصله ( افزايش قلبي هدايت شدن P-Rاختالالت پهن

QRS شدن )Q-Tوكوتاه

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 99: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

درمان

ایزوتونیک 1 نمکی محلول انفوزیون

الزیکس2

تونین 3 کلسی

کورتون4

دیالیز5

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 100: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Magnesium Abnormalities

Normal dietary intake 20meq (240mg)

Excretion in both the feces and urine

Normal serum level 19-25 mgdL

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 101: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

منیزیومbull است سلولی داخل فراوان کاتیون دومینهای bull واکنش در کمکی فاکتور عنوان به آن نقش

تون و قلب انقباضی قدرت حفظ در و آنزیمی دارد محیطی عروق

bull55 ( و ( فعال یونیزه شکل پروتئین 45به بانداست

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 102: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hypermagnesemia

Etiology

1 Impaired renal function

2 Excess intake (in the from of TPN or magnesium-containing laxatives and antacids)

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 103: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical manifestation hypermanesemia

System hypermanesemia

Gastrointestinal Nauseavomiting

Neuromuscular weakness lethargy Decreased

reflexes

Cardiovascular Hypotension arrest

ECG changes Increased PR interval

Widened QRS complex

Elevated T waves

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 104: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

1 Withhold exogenous sources of magnesium

2 Correct volume deficit

3 Correct acidosis if present

4 Calcium chloride (5-10 ml) to manage acute symptoms (cardiovascular effects)

5 Dialysis (if elevated levels or symptoms persist)

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 105: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

عالئم

bull Patellar reflexes lost 8-10 meqLbull Respiratory depression 10-15

meqLbull Respiratory paralysis 12-15 meqLbull Cardiac arrest 25-30

meqL

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 106: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Hypomagnesemia

Calcium magnesium receptors on renal tubular cells is primarily responsible for mg

homeostasis

Etiology

1 Poor intake (starvation alcoholism prolonged use of IV fluids and TPN with

inadequate supplementation of magnesium)

2 Increased renal excretion (alcohol most diuretics and amphotericin B)

3 GI losses (diarrhea)

4 Malabsorption

5 Acute pancreatitis

6 Diabetic ketoacidosis

7 Primary aldosteronism

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 107: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Clinical manifestation of hypomagnesemia(similar to hypocalcemia)

1 Hyper active reflexes muscle tremors tetany with chevostekrsquos sign

2 Delirium and seizures in severe deficiency

3 ECG changes Prolonged QT and PR interval

ST-segment depression

Flattening or inversion of P waves

Torsades de pointes

Arrhythmia

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 108: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Treatment

1 For asymptomatic and mild hypomagnesemia administer oral mg

2 For severe deficit (lt1meqL) or symptomatic patient administer 1 to 2 g of mg-sulfate IV over 2 minute (simultaneous with ca-gluconate)

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 109: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.

Message for Today

ICF

Interstitial

Pla

sma

5 Dex

bull Do not reccussitate sick patients with any Dextrose solution

  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116
Page 110: Fluid and Electrolyte Management of the Surgical Patient Dr Abdollahi Afshar Hospital.
  • Fluid and Electrolyte Management of the Surgical Patient
  • Slide 2
  • Slide 3
  • Slide 4
  • Total Body Water
  • Body Fluid Compartments
  • Total body water (TBW)
  • Body compartment fluid
  • Example men with 70kg
  • Fluid compartments
  • Slide 11
  • Slide 12
  • Slide 13
  • Slide 14
  • Slide 15
  • Colloid osmotic pressure
  • Slide 17
  • Slide 18
  • Slide 19
  • Cell Membrane
  • Slide 21
  • Slide 22
  • Slide 23
  • Slide 24
  • Slide 25
  • Composition of Fluid Compartments
  • Composition of Body Fluids
  • عوامل موثر روی تغییرات آب والکترولیت
  • Reasons for fluid therapy
  • ارزیابی حجم مایع داخل عروقی
  • محلولهای وریدی
  • Fluids
  • Slide 33
  • Slide 34
  • Slide 35
  • Crystalloids
  • Colloid Solutions
  • رینگر لاکتات
  • 09Nacl
  • Postoperative (maintenance)
  • Slide 41
  • Preexisting fluid deficits
  • Maintenance requirements
  • Surgical fluid losses
  • Third space loss
  • Crystalloid solution
  • Colloids
  • Complications
  • The Influence of Colloid amp Crystalloid on Blood Volume
  • Colloid versus crystalloid solutions
  • Transfusion consideration
  • اختلال در حجم مایعات بدن
  • Fluid volume deficit (FVD)
  • DEHYDRATION
  • علل کاهش حجم خارج سلولی
  • Signs of Hypovolemia
  • Clinical Diagnosis of Hypovolemia
  • Signs of Hypervolemia
  • Management of Hypervolemia
  • Fluid Management
  • Electrolyte physiology
  • Sodium physiology
  • Osmotic Pressure
  • Concentration
  • Hypernatremia
  • - Hypernatremia
  • Slide 67
  • Slide 68
  • Clinical Manifestations of Abnormalities in Serum Sodium
  • Treatment
  • Water deficit (L)= times TBW
  • The rate of fluid administration
  • Hyponatremia Nalt135mEqL
  • Slide 74
  • Sodium depletion
  • Sodium dilution
  • Sign and symptoms
  • Slide 78
  • Treatment
  • Slide 80
  • Slide 81
  • Dose
  • Potassium abnormalities
  • Hyperkalemia
  • Clinical manifestation of hyperkalemia
  • Slide 86
  • Slide 87
  • Hypokalemia
  • Potassium changes associated with alkalosis
  • Slide 90
  • Clinical Manifestation of Abnormalities in potassium
  • Slide 92
  • Calcium
  • هيپوكلسمي یونیزه Calt45 meql
  • علائم هیپوکلسمی
  • Slide 96
  • Slide 97
  • Slide 98
  • Slide 99
  • سایرعلائم
  • درمان
  • هيپركلسمي Cagt55meql
  • علائم
  • علائم قلبی
  • Slide 105
  • Magnesium Abnormalities
  • منیزیوم
  • Hypermagnesemia
  • Clinical manifestation hypermanesemia
  • Slide 110
  • Slide 111
  • Hypomagnesemia
  • Clinical manifestation of hypomagnesemia (similar to hypocalcemia)
  • Slide 114
  • Message for Today
  • Slide 116