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
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 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
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
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
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 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
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
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
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
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
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
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
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
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
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
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
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 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 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 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 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 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 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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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 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
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
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
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
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
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
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 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
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
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
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
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
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
- 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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
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
Message for Today
ICF
Interstitial
Pla
sma
5 Dex
bull Do not reccussitate sick patients with any Dextrose solution