kuliolektrolit Dan Keseimbangan Asam Basa
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Keseimbangan cairan, asam danbasa dan elektrolit
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Fungsi Air dalam Fisiologi
Manusia1. Media semua reaksi kimia tubuh
2. Berperan dalam pengaturan distribusi kimia &biolistrik dalam sel
3. Alat transport hormon & nutrien4. Membawa O2 dari paru-paru ke sel tubuh
5. Membawa CO2 dari sel ke paru-paru
6. Mengencerkan zat toksik dan waste productsertamembawanya ke ginjal dan hati
7. Distribusi panas ke seluruh tubuh
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Distribusi Cairan Tubuh
Volume cairan tubuh- wanita (17-39 th) : 50% BB- pria (17-39 th): 60% BB
Distribusi cairan tubuh- cairan intrasel (CIS) = 2/3 cairan tubuh- cairan ekstrasel (CES) = 1/3 cairan tubuh
* intravaskular (plasma) = 25% CES* intersisial = 75% CES
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Komposisi Ion pd Cairan Tubuh
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Perpindahan Cairan &
Elektrolit1. Difusiperpindahan molekul dari tekanan/konsentrasi tinggi ketekanan/konsentrasi rendah
2. Osmosis
perpindahan air dari konsentrasi zat terlarut rendah kekonsentrasi zat terlarut tinggiosmolaritas: ukuran konsentrasi suatu larutan- isotonus konsentrasi larutan = plasma darah
3. Transport aktifperpindahan molekul dari tekanan/konsentrasi rendah kekonsntrasi tinggi dgn menggunakan energi
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Tekanan Cairan
1. Tekanan osmotik & onkotikTekanan osmotik: tekanan untuk mencegah aliranosmotik cairan
Tekanan onkotik: gaya tarik s/ koloid agar air tetapberada dalam plasma darah di intravaskular
2. Tekanan hidrostatik (filtration force)tekanan yang digunakan oleh air dalam sistemtertutup
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Perpindahan cairan di
kapiler
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Selektivitas Permeabilitas
Membran Membran sel
lipid bilayer
Permeabilitas membran sel bersifat selektifterhadap: ion (kanal ion), air (aquaporin)
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PENGATURAN VOLUME CAIRAN
EKSTRASEL
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Peranan ginjal
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Filtrasi, Reabsorpsi, Sekresi &
Ekskresi di Nefron
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Respons thd Peningkatan Tekanan Darah
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Respons thd Penurunan Tekanan Darah
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Peranan Atriopeptin
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Peranan Renin-Angiotensin-Aldosteron
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Respons thd Asupan Garam
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PENGATURAN OSMOLARITAS CAIRANEKSTRASEL
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Perubahan osmolaritas di
Nefron
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Peranan Vasopresin
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Mekanisme Kerja Vasopresin/ADH
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Perubahan Volume & Osmolaritas Cairan
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Faktor-faktor yang mempengaruhi
Keseimbangan Cairan &
Elektrolit
Umur
Suhu lingkungan Diet
Stres
Penyakit
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Keseimbangan Asam & Basa
Keseimbangan asam-basa pengaturankonsentrasi ion H+ dalam cairan tubuh
Ion H
+
sbg hasil dari metabolisme:C6H12O6 + O2CO2 + H2OH2CO3H+ + HCO3-
[H+] dlm plasma pH plasma darah = 7,4
Sistem dapar (buffer) menghambatperubahan pH yang besar jika adapenambahan asam atau basa
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Sistem Dapar
1. Asam karbonat:Bikarbonat
sistem dapar di CES untuk asam non-karbonat
2. Protein
sistem dapar di CIS & CES
3. Hemoglobin
sistem dapar di eritrosit untuk asam karbonat
4. Phosphat
sistem dapar di ginjal dan CIS
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Keseimbangan ion H+
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Mekanisme Regulasi Keseimbangan
Asam-Basa
Sistem dapar hanya mengatasi ketidakseimbanganasam-basa sementara
Ginjal: meregulasi keseimbangan ion H+
denganmenghilangkan ketidakseimbangan kadar H+ secaralambat; terdapat sistem dapar fosfat & amonia
Paru-paru: berespons scr cepat thd perubahan kadarH+ dalam darah & mempertahankan kadarnya
sampai ginjal menhilangkan ketidakseimbangantersebut
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Regulasi Pernapasan dlm
Keseimbangan Asam-Basa
Kadar CO2 meningkat pH menurun
Kadar CO2 menurun pH meningkat
Kadar CO2 & pH merangsang kemoreseptoryg kemudian akan mempengaruhi pusatpernapasan hipoventilasi meningkatkan kadar CO2
dlm darah hiperventilasi menurunkan kadar CO2dlm darah
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Regulasi Pernapasan dlm
Keseimbangan Asam-Basa
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Regulasi Ginjal dlm
Keseimbangan Asam-Basa
Sekresi H+ ke dalam filtrat & reabsorpsiHCO3- ke CES menyebabkan pH ekstraselmeningkat
HCO3- di dlm filtrat diabsorbsi
Laju sekresi H+ meningkat akibat penurunanpH cairan tubuh atau peningkatan kadar
aldosteron
Sekresi H+ dihambat jika pH urin < 4,5
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Gangguan Keseimbangan
Asam-Basa1. Asidosis respiratori
hipoventilasi retensi CO2H2CO3H+
2. Alkalosis respiratori
hiperventilasiCO2 banyak yg hilangH2CO3H+
3. Asidosis metabolik
Diare, DMHCO3-PCO2H
+
4. Alkalosis metabolik
muntahH+HCO3-PCO2
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Kompensasi Sistem Pernafasan
terhadap Asidosis Metabolik
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Kompensasi Ginjal terhadap
Asidosis Respiratorik
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Nomogram Davenport
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INTERPRETASI AGD
Lihat pH darah
pH < 7,35 pH > 7,45
ASIDOSISALKALOSIS
Lihat pCO2 Lihat HCO3-
< 40mmHg > 40 mmHg < 24 mM > 24 mM
METABOLIKRESPIRATORIKRESPIRATORIKMETABOLIK
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TERKOMPENSASI atau TIDAK?
Lihat pH kembali- jika mendekati kadar normal (7,35-7,45) terkompensasi
- jika belum mendekati normal tidak terkompensasi atau terkompensasi
sebagian
Jika asidosis respiratorik dgn HCO3-
< 24 mM
terkompensasi sebagian
Jika asidosis metabolik dgn pCO2 < 40 mmHg
terkompensasi sebagian
Jika alkalosis respiratorik dgn HCO3- > 24 mM
terkompensasi sebagian Jika alkalosis metabolik dgn pCO2 > 40 mmHg
terkompensasi sebagian
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GANGGUAN ELEKTROLIT
Dr. SUHAEMI, SpPD, Finasim
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Electrolyte and protein anion concentrations in plasma,
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Electrolyte and protein anion concentrations in plasma,
interstitial fluid, & intercellular fluid
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Electrolytes
sodium (Na+
) potassium (K+)
chloride (Cl-)
calcium (Ca2+)
magnesium (Mg2+)
bicarbonate (HCO3-
) phosphate (PO4
2-)
sulfate (SO42-)
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Korey Stringer
1974 - 2001
Korey Stringer was a professional football player forthe Minnesota Vikings. He collapsed during practicefrom excessive heat and died the following day.
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Electrolytes
Charged particles in solution
Cations (+)
Anions (-)
Integral part of metabolic and cellularprocesses
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Positive or Negative?
Cations (+)
Sodium Potassium
Calcium
Magnesium
Anions (-)
Chloride Bicarbonate
Phosphate
Sulfate
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Major Cations
EXTRACELLULAR
SODIUM (Na+)
INTRACELLULAR
POTASSIUM (K+)
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Electrolyte Imbalances
Hyponatremia/
hypernatremia
Hypokalemia/
Hyperkalemia
Hypomagnesemia/
Hypermagnesemia
Hypocalcemia/
Hypercalcemia Hypophosphatemia/
Hyperphosphatemia
Hypochloremia/
Hyperchloremia
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Sodium
Major extracellular cation
Attracts fluid and helps preserve fluid volume
Combines with chloride and bicarbonate to help
regulate acid-base balance
Normal range of serum sodium 135 - 145 mEq/L
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Sodium and Water
If sodium intake suddenly increases,extracellular fluid concentration also rises
Increased serum Na+ increases thirst and therelease of ADH, which triggers kidneys toretain water
Aldosterone also has a function in water andsodium conservation when serum Na+ levelsare low
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Sodium-Potassium Pump
Sodium (abundantoutside cells) tries to
get into cells
Potassium (abundant
inside cells) tries to get
out of cells
Sodium-potassiumpump maintains
normal concentrations
Pump uses ATP,magnesium and anenzyme to maintain
sodium-potassiumconcentrations
Pump prevents cellswelling and creates
an electrical chargeallowingneuromuscularimpulse transmission
k l i
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Hypokalemia
Usually secondary to: GI loss (vomiting, diarrhea) Urinary losses (diuretics, RTA)
Also think about : co-existing electrolyte abnormality
(hypomagnesemia), hyperaldosteronism, insulin therapy,albuterol, alkalosis)
Indications for replacement: Evidence of potassium loss
Significant deficit in body potassium
Acute therapy in redistributive disorders (periodicparalysis, thyrotoxicosis)
k l i
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Hypokalemia
Symptoms: usually manifest when serum K
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Therapy
Calculate potassium deficit (if normal distribution is present-
do NOT use in DKA or HONK)
Acute: .27meq/L decrease in serum K+ for every 100meq reduction in totalpotassium stores
Chronic: 1meq/L decrease in serum K+ for every 200-400meq reduction in
total potassium stores
Simplified:
Goal K Serum K x 100 = total meq K required
serum Cr
10meq of KCL will raise the serum K by ~.1meq/L
Formulations
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Formulations
Potassium Chloride : PREFERRED AGENT
Most patients with hypokalemia and acidosis are also chloridedepleted
Raises serum potassium at a faster rate
Available as salt substitute, liquid, slow release tablet or capsule, andIV
Oral: 40meq tid-qid; IV: Peripheral line 10meq/hr
Central line 20meq/hr
Potassium Bicarbonate/Citrate/Acetate: can be used in patients with hypokalemia and metabolic acidosis
Potassium Phosphate: Rarely used (Fanconi syndrome with phosphate wasting)
Example
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Example 72 year old female admitted for weakness and dehydration
due to acute gastroenteritis. She is having up to 6 BM/day.
Her serum K on admission is 2.5 meq and serum Cr is 2.0. EKGreveals u-waves.
1. How much potassium do you order?4-2.5 x 100 = 75meq
2
2. What formulation do you choose?
KCL; if bicarb is low then consider potassium bicarb or acetate
3. What route should the potassium be administered? 40meq(initial) oral and 40meq IV; (re-assess 2-4 hours later and give more
orally if needed and tolerating po)4. Serum potassium remains low, what else could be
contributing?
Low magnesium, ongoing diarrhea
H i
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Hypomagnesemia
Average daily intake: 360mg
Presence of low magnesium (nearly 12% of hospitalizedpatients) suspected in following cases: Chronic diarrhea
Hypocalcemia
Refractory hypokalemia
Ventricular arrhythmias
Symptoms/Signs : Tetany (seizures in children/neonates)
Hypokalemia
Hypoparathyroidism hypocalcemia (
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What Do You See?
CNS
Altered LOC
Confusion
Hallucinations
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What Do You See?
Neuromuscular
Muscle weakness
Leg/foot cramps
Hyper DTRs
Tetany
Chvosteks & Trousseaus signs
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What Do You See?
Cardiovascular
Tachycardia
Hypertension
EKG changes
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What Do You See?
Gastrointestinal
Dysphagia
Anorexia
Nausea/vomiting
Therapy
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Therapy IV if symptomatic (magnesium sulfate)
1.5-1.9mg/dL 2g magnesium sulfate IV
1.2-1.4mg/dL4g .8-1.1mg/dL 6g
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Therapy
Goal of therapy: maintain plasma magnesium concentration over 1.0mg/dL acutely in
symptomatic patients
In cardiac patients, maintain Mg >1.7 (usually goal 2.0mg/dL) to avoidarrhythmias
Serum levels are poor reflection of actual body stores (mostlyintracellular) so aim for high-normal serum level
Adverse effects: Abrupt elevation of plasma Mg can remove the stimulus for Mg
retention and lead to increased excretion
Diarrhea
Drug interactions
Magnesium intoxication, Aluminum intoxication
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Mag Sulfate Infusion
Use infusion pump - no faster than 150mg/min
Monitor vital signs for hypotension and
respiratory distress
Monitor serum Mg++ level q6h
Cardiac monitoring
Calcium gluconate as an antidote foroverdosage
Hypocalcemia
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Hypocalcemia
Clinical Manifestations: Acute: serum Ca
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Therapy Correct for albumin
Ca lower by .8mg/dL for every 1g/dL reduction in serum albumin
or check ionized calcium Level can be altered by acid/base disturbance
Symptomatic or acute serum Ca 7.5mg/dL or chronic: Oral therapy: calcium carbonate or citrate 1-2g/day (500mg bid-
qid)
Add Vitamin D in following cases: Hypoparathyroidism: Vitamin D (Calcitriol .25-.5mcg bid)
Vitamin D deficiency: 50,000IU/week for 6-8 weeks then 800-1000IUdaily
Erogcalciferol (D3)
Cholecalciferol (D2)
Therapy
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Therapy
Goals of therapy:
Treat and prevent manifestations of hypocalcemia In hypoparathyroidism: to raise serum Ca to low-normal range (8.0-
8.5mg/dL)
Adverse Effects: Rapid infusion- bradycardia, hypotension
Extravasation- tissue necrosis
Hypercalcemia
Hypercalciuria Constipation
Hypophosphatemia
Milk-alkali syndrome
Example
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Example
35 y/o male with hypoparathyroidism secondary to DiGeorges
presents with serum Ca of 6.2, albumin of 3.8, ionized Ca .77. Hassome mild muscle cramps, otherwise asymptomatic.
1. How do you initially treat his hypocalcemia?
- IV Calcium Gluconate 1g IV over 10-20min2. Repeat serum Ca is 6.6, how do you proceed with treatment?
-start Calcium gluconate 1mg/mL in D5W 50mL/hr infusion
2. After initial treatment, what maintenance regimen should you
initiate?-Calcitriol (.5mcg bid, titrated up in this patient)
-Calcium carbonate (1950mg po tid in this patient)
Preferred Route PreferredFormulation
Dosage Response
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Formulation
Potassium Oral PotassiumChloride
10meq tabs .1 increaseserum K for
10meq given
Magnesium Oral
IV- arrhythmia
MagnesiumOxide
Magnesium
Sulfate
2-4 tabs/day(420mg; 20meq/tab)
2g IVP or slow
infusion
.5 increase for2g (50meq) IV
Calcium IV- acute
Oral- maintenance
CalciumGluconate
CalciumCarbonate
1-2amp (rapid)
1mg/mL in D5W,50mL/hr Infusion
1-2g/day
.5mg/dLincrease serumCa for 1g given
Phosphate Oral SodiumPhosphate(neutra-phos)
1-2 packet tid-qid1packet=250mg or
8mmol
(weight based)
1.2mg/dLincrease serumPO4
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Electrolyte Imbalances
Electrolyte Normal range
(mmol / L)
Excess Defiency
Sodium
Na+
135 - 145 Hypernatremia(increased urine excretion;
excess water loss)
Hyponatremia
(dehydration; diabetes-
related low blood pH;
vomiting, diarrhea)
Potassium
K+3.5 5.0 Hyperkalemia
(renal failure, low blood pH)
Hypokalemia
(gastointestinal conditions)
Hydrogen carbonate
HCO3-
24 - 30 Hypercapina(high blood pH;
hypoventilation)
Hypocapnia
(low blood pH; hyper-
ventilation; dehydration)
Chloride
Cl-100 - 106 Hyperchloremia
(anemia, heart conditions,
dehydration)
Hypochloremia
(acute infections; burns;
hypoventilation)
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Regulation of Sodium
Renal tubule reabsorption affected byhormones:
Aldosterone
Renin/angiotensin
Atrial Natriuretic Peptide (ANP)
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Electrolyte imbalances:
Sodium
Hypernatremia (high levels of sodium)
Plasma Na+ > 145 mEq / L
Due to Na + or water Water moves from ICF ECF
Cells dehydrate
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Hypernatremia Due to:
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Hypernatremia Due to:
Hypertonic IV soln.
Oversecretion of aldosterone Loss of pure water
Long term sweating with chronic fever
Respiratory infection water vapor loss
Diabetes polyuria
Insufficient intake of water (hypodipsia)
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Clinical manifestations
of Hypernatremia
Thirst
Lethargy
Neurological dysfunction due to dehydrationof brain cells
Decreased vascular volume
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Treatment of Hypernatremia
Lower serum Na+
Isotonic salt-free IV fluid
Oral solutions preferable
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Hyponatremia
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Overall decrease in Na+ in ECF
Two types: depletional and dilutional Depletional Hyponatremia
Na+ loss:
diuretics, chronic vomiting Chronic diarrhea
Decreased aldosterone
Decreased Na+ intake
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Dilutional Hyponatremia:
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Dilutional Hyponatremia:
Renal dysfunction with intake of hypotonic fluids
Excessive sweating increased thirst intake ofexcessive amounts of pure water
Syndrome of Inappropriate ADH (SIADH) or oliguricrenal failure, severe congestive heart failure, cirrhosis
all lead to: Impaired renal excretion of water
Hyperglycemia attracts water
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Cli i l if t ti f
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Clinical manifestations of
Hyponatremia Neurological symptoms
Lethargy, headache, confusion, apprehension, depressedreflexes, seizures and coma
Muscle symptoms Cramps, weakness, fatigue
Gastrointestinal symptoms
Nausea, vomiting, abdominal cramps, and diarrhea
Tx limit water intake or discontinue meds
83
h ?
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What Do You See?
Think S-A-L-T
Skin flushed
Agitation
Low grade fever
Thirst
Neurological symptoms
Signs of hypovolemia
Wh t D W D ?
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What Do We Do?
Correct underlyingdisorder
Gradual fluidreplacement
Monitor for s/s ofcerebral edema
Monitor serum Na+level
Seizure precautions
H k l i
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Hypokalemia
Serum K+ < 3.5 mEq /L
Beware if diabetic
Insulin gets K+
into cell Ketoacidosis H+ replaces K+, which is
lost in urine
adrenergic drugs or epinephrine
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C f H k l i
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Causes of Hypokalemia
Decreased intake of K+
Increased K+ loss
Chronic diuretics Acid/base imbalance
Trauma and stress
Increased aldosterone Redistribution between ICF and ECF
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Clinical manifestations of
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Hypokalemia
Neuromuscular disorders Weakness, flaccid paralysis, respiratory
arrest, constipation
Dysrhythmias, appearance of U wave
Postural hypotension
Cardiac arrest
Others table 6-5
Treatment- Increase K+ intake, but slowly, preferably by foods
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Wh t D Y S ?
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What Do You See?
Think S-U-C-T-I-O-N
Skeletal muscle weakness
U wave (EKG changes) Constipation, ileus
Toxicity of digitalis glycosides
Irregular, weak pulse
Orthostatic hypotension
Numbness (paresthesias)
Wh t D W D ?
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What Do We Do?
Increase dietary K+
Oral KCl supplements
IV K+ replacement
Change to K+-sparing diuretic
Monitor EKG changes
IV K R l t
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IV K+ Replacement
Mix well whenadding to an IVsolution bag
Concentrationsshould not exceed40-60 mEq/L
Rates usually 10-20mEq/hr
NEVER GIVE IV PUSHPOTASSIUM
Hypocalcemia
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Hyperactive neuromuscular reflexes and tetanydifferentiate it from hypercalcemia
Convulsions in severe cases
Caused by:
Renal failure
Lack of vitamin D
Suppression of parathyroid function
Hypersecretion of calcitonin
Malabsorption states Abnormal intestinal acidity and acid/ base bal.
Widespread infection or peritoneal inflammation
92
Hypocalcemia
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Hypocalcemia
Diagnosis:
Chvosteks sign
Trousseaus sign
Treatment
IV calcium for acute Oral calcium and vitamin D for chronic
93
Hyperkalemia
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Hyperkalemia
Serum K+ > 5 mEq/L
Less common than
hypokalemia
Caused by altered
kidney function,
increased intake (salt
substitutes), blood
transfusions, meds (K+-
sparing diuretics), cell
death (trauma)
What Do You See?
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What Do You See?
Irritability
Paresthesia
Muscle weakness (especially legs)
EKG changes (tented T wave)
Irregular pulse
Hypotension Nausea, abdominal cramps, diarrhea
What Do We Do?
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What Do We Do?
Mild
Loop diuretics (Lasix)
Dietary restriction
Moderate
Kayexalate
Emergency
10% calcium gluconate
for cardiac effects Sodium bicarbonate for
acidosis
Electrolytes
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Electrolytes
water, sucrose syrup, glucose-fructose syrup, citric acid, naturaland artificial flavors, salt, sodiumcitrate, monopotassium phosphate,ester gum, sucrose acetateisobutyrate, red 40, blue 1
Per 8 fl oz
Total fat 0gSodium 110mgPotassium 30mgTotal carbs 14g
water, dextrose, potassium citrate,sodium chloride and sodium
citrate. Nonmedicinal ingredients:FD&C Blue #1 and Red #40 (grapeflavor) and FD&C Red #40(bubblegum flavor).
Per 8 fl oz
Sodium 10.6 mgPotassium 4.7mgChloride 8.3 mgDextrose 5.9g
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