dr. andi sulistyo haribowo, sp.pd. spesialis penyakit dalam program studi pendidikan dokter...
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GANGGUAN PADA KESEIMBANGAN
ELEKTROLIT dr. Andi Sulistyo Haribowo,
Sp.PD.
SPESIALIS PENYAKIT DALAM
Program Studi Pendidikan Dokter
UNIVERSITAS ISLAM MALANG
2012
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FLUIDS and ELECTROLYTES
ELECTROLYTES
Functions of Electrolytes
Contribute most of the osmotically active particles in body fluids
Provide buffer systems for pH regulation
Provide the proper ionic environment for normal neuromuscular irritability & tissue function
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DISTRIBUTION OF ELECTROLYTES
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CATIONS AND ANIONS IN BODY FLUIDS
Figure 27.2
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DISTRIBUTION OF MAJOR ELECTROLYTES• Na+ and CL- predominate in extracellular
fluids (interstitial fluid and plasma) but are very low in the intracellular fluid (cytoplasm)
• K+ and HPO42- predominate in intracellular
fluid (cytoplasm) but are in very low concentration in the extracellular fluids (interstitial fluid and plasma)
• At body fluid pH, proteins [P-] act as anions; total protein concentration [P-] is relatively high, the second most important “anion,” in the cytoplasm, [P-] is intermediate in blood plasma, but [P-] is very low in the interstitial fluid
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DISTRIBUTION OF MINOR ELECTROLYTES• HCO3
- is in intermediate concentrations in all fluids, a bit lower in the intracellular fluid (cytoplasm); it is an important pH buffer in the extracellular comparments
• Ca++ is in low concentration in all fluid compartments, but it must be tightly regulated, as small shifts in Ca++ concentration in any compartment have serious effects
• Mg++ is in low concentration in all fluid compartments, but Mg++ is a bit higher in the intracellular fluid (cytoplasm), where it is a component of many cellular enzymes
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REGULATION OF ELECTROLYTES Major Cations in body fluids
Sodium (Na+)Potassium (K+)Calcium (Ca++)Magnesium (Mg++)
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PRINCIPLES OF ELECTROLYTE DISTURBANCESPRINCIPLES OF ELECTROLYTE DISTURBANCES
Implies an underlying disease process Treat the electrolyte change, but seek
the cause Clinical manifestations usually not
specific to a particular electrolyte change, e.g., seizures, arrhythmias
Implies an underlying disease process Treat the electrolyte change, but seek
the cause Clinical manifestations usually not
specific to a particular electrolyte change, e.g., seizures, arrhythmias
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PRINCIPLES OF ELECTROLYTE DISTURBANCESPRINCIPLES OF ELECTROLYTE DISTURBANCES
Clinical manifestations determine urgency of treatment, not laboratory values
Speed and magnitude of correction dependent on clinical circumstances
Frequent reassessment of electrolytes required
Clinical manifestations determine urgency of treatment, not laboratory values
Speed and magnitude of correction dependent on clinical circumstances
Frequent reassessment of electrolytes required
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ELECTROLYTES & THEIR IMBALANCES
SODIUM (NA+) Sodium balance
Sodium = major cation in extracellular fluid (ECF) Sodium = most common problem with electrolyte
balance
Key to balance: ingestion via G-I tract = excretion via kidney Aldosterone controls sodium levels via the kidney
Remember aldosterone’s antagonist = ANP Sodium contributes to resting membrane potential
Sodium rushing into cell via open channels causes depolarization of nerves and muscles
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DISORDERS OF SODIUM BALANCE Na+ is the most abundant electrolyte in
the ECF.
Na+ and accompanying anion Cl- are responsible for normal osmotic activity of the ECF.
All gain/loss of Na+ is accompanied by gain/loss of water.
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HYPONATREMIA Hypovolemic hyponatremia
• Vomiting • Diarrhea• Diuretics • Adrenal insufficiency
Normovolemic hyponatremia• Syndrome of inappropriate secretion of antidiuretic
hormone• Renal failure• Water intoxication
Hypervolemic hyponatremia• CHF• Liver failure• Nephrotic syndrome
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CLINICAL MANIFESTATIONS OF HYPONATREMIA Neurologic
• Seizure• Coma• Agitation
Gastrointestinal• Anorexia • Nausea/vomiting
Muscular• Cramps• weakness
• Headache• Cerebral edema• Confusion
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TREATMENT OF HYPONATREMIA Fluid restriction
Administration of hypertonic saline and an osmotic or loop diuretic
!!!Correction of serum sodium levels too rapidly can result in neurologic damage and central pontine myelinolysis!!!
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HYPONATREMIA Acute, symptomatic hyponatremia
Correct no faster than 1 mEq/L per hour for the first 6-8 mEq/L
No more than 10-12 mEq/L in first 24 hours5% saline is almost never neededCalculate the Na deficit
Na mEq = ([Na desired] - [Na measured]) X TBW TBW = .5 or .6 X weight in KG
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CAUSES OF HYPERNATREMIA Most common cause is water deficiency d/t:
• Excessive loss• Inadequate intake
Also may be caused by:• Exogenous Na+ load• Primary hyperaldosteronism• Diabetes insipidus• Renal dysfunction
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CLINICAL MANIFESTATIONS OF HYPERNATREMIA Tremulousness
Irritability
Ataxia
Mental confusion
Coma d/t cerebral water loss
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TREATMENT OF HYPERNATREMIARenal tubular diuretics
Hemodialysis
Treat central diabetes insipidus with vasopressin
!!!Correction of serum sodium level too rapidly can result in neurologic damage secondary to cerebral edema!!!
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HYPERNATREMIA Treatment
Severe ECFV depletion is the priority and should be corrected with NS first. Subsequent fluid replacement can be hypotonic
Major complication of overly rapid correction is cerebral edema
Safe rate is no more than .5- 1 mEq/L per hour
Should take 36-72 to hours to completely correct
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HYPERNATREMIA Treatment
Calculate the water deficitH2O deficit = TBW X ([Na meas]- [Na
des])/[Na des] Important to take into account ongoing
losses insensible losses .5 - 1 liter/24 hours with fever, these losses increase by 60-80ml/24
hrs for each degree Farenheit
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POTASSIUM REGULATION Major electrolyte and principle cation in the
extracellular fluidRegulates metabolic activitiesRequired for glycogen deposits in the liver and
skeletal muscleRequired for transmission of nerve impulses,
normal cardiac conduction and normal smooth and skeletal muscle contraction
Regulated by dietary intake and renal excretion
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ELECTROLYTES & THEIR IMBALANCES
POTASSIUM (K+) Potassium balance
Major intracellular cation Balance: ingestion = excretion (via kidneys)
Aldosterone primarily controls potassiumIt exchanges potassium for sodium
Insulin also regulates potassiumIt drives it into cells (with sugar) & thus produces
hypokalemia pH also affects potassium secretion
Acidosis: more H+ in blood which finds its way into cell & pushes K+ into blood Also get kidney to exchange H+ for K+
Acidosis -gives- hyperkalemiaAlkalosis: less H+ in blood
Kidneys exchange K+ for H+; thus get hypokalemia
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The relation between potassium and hydrogen ions in the plasma
Saladin’s Anatomy & Physiology fourth edition McGraw Hill
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Potassium balance in the body
Costanzo Physiology second edition Saunders
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POTASSIUM ION REGULATION IN ECF
27-30
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HYPOKALEMIA Causes
• Gastrointestinal losses• Systemic alkalosis• Diabetic ketoacidosis• Diuretic therapy• Sympathetic nervous system stimulation• Administration of beta-adrenergic receptor
agonists
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HYPOKALEMIA Spurious hypokalemia
Marked leukocytosisA dose of insulin right before the blood draw
Redistribution hypokalemiaAlkalosis (K decreases .3 for every .1
increase in pH) Increased Beta2 adrenergic activityTheophylline toxicityFamilial
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HYPOKALEMIA Extrarenal depletion
diarrhea laxative abusesweat losses fasting or inadequate intake
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HYPOKALEMIA Renal potassium depletion
urine potassium > 20 mEq/24 hrsspot urine with > 20 mEq K/gram creatinineclassified whether they occur with a
metabolic alkalosis vomiting/NG suction diuretic tx Mineralocorticoid excess syndromes
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HYPOKALEMIA Renal losses
metabolic acidosis RTA Type I and II DKA Carbonic anhydrase inhibitor therapy Ureterosigmoidostomy
No acid-base disorder Mg deficiency Drugs
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CLINICAL MANIFESTATIONS OF HYPOKALEMIA Autonomic neuropathy
Skeletal muscle weakness
Increased sensitivity to Digoxin
Cardiac• Decreased myocardial contractility• Electrical conduction abnormalities
• Arrhythmias• Tachycardia• Ventricular fibrillation
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POTASSIUM
Copyright 2008 by Pearson Education, Inc.
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HYPOKALEMIA AND THE EKG• Prolonged PR
interval
• Prolonged T interval
• Widening of QRS
• Flattened T wave
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TREATMENT OF HYPOKALEMIA Slow IV potassium supplements
Anesthesia related concerns:• Increased risk of myocardial irritability K+
<2.6• Avoid hyperventilation of the lungs• Avoid glucose containing IV solutions • Avoid rapid infusion of IV K+ supplements
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HYPERKALEMIA Severe hyperkalemia is a medical
emergency Neuromuscular signs (weakness,
ascending paralysis, respiratory failure) Progressive ECG changes (peaked T
waves, flattened P waves, prolonged PR interval, idioventricular rhythm and widened QRS complex, “sine wave” pattern, V fib)
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HYPERKALEMIA Causes
• Increased total body potassium• Renal failure• Potassium-sparing diuretics• Excessive IV K+ supplements• Excessive use of salt substitutes
• Altered distribution of potassium• Metabolic or respiratory acidosis• Digitalis intoxication• Insulin deficiency• Hemolysis• Tissue and muscle damage after burns• Administration on succinylcholine
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CLINICAL MANIFESTATIONS OF HYPERKALEMIAAreflexia
Weakness
Paralysis
Paresthesia
Cardiac conduction abnormalities
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HYPERKALEMIA AND THE EKG• Narrowing and peaking of T
waves
• 1st degree AV block
• QRS widening
• ST segment depression
• Progression to merging of QRS an T waves to a sine wave
• Tachycardia
• Ventricular fibrillation
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HYPERKALEMIAHYPERKALEMIA
Etiology – renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia
Manifestations – cardiac, neuromuscular
Etiology – renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia
Manifestations – cardiac, neuromuscular
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TREATMENT OF HYPERKALEMIA
Primary goal Avoid adverse cardiac effects Insulin and glucose to shift K+ into cells IV calcium to antagonize cardiac effects of
hyperkalemia
Anesthesia related concerns: A serum K+ of 5.5mEq/L is upper limit for
elective procedures
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HYPERKALEMIA Treatment
Stop potassium!Get and ECGHyperkalemia with ECG changes is a
medical emergency
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HYPERKALEMIA Treatment
First phase is emergency treatment to counteract the effects of hyperkalemia IV Calcium
Temporizing treatment to drive the potassium into the cells glucose plus insulin Beta2 agonist NaHCO3
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HYPERKALEMIA Treatment
Therapy directed at actual removal of potassium from the body sodium polystyrene sulfonate (Kayexalate) dialysis
Determine and correct the underlying cause
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ELECTROLYTES & THEIR IMBALANCES
CALCIUM (CA++) Calcium balance
Calcium is most abundant mineral in body Calcium is important as an extracellular cation Calcium & phosphorus have a reciprocal relationship Calcium balance is dependent on:
Parathyroid hormone (PTH) Calcitriol (active vitamin D) Calcitonin (from thyroid)
98% of calcium reabsorbed at the kidneys Calcium functions
Structural strength for bones & teeth Maintains stability of nerve membrane Required for muscle cell contraction Necessary for blood clotting
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REGULATION OF CALCIUM IONS Regulated within
narrow rangeElevated
extracellular levels prevent membrane depolarization
Decreased levels lead to spontaneous action potential generation
TermsHypocalcemiaHypercalcemia
PTH increases Ca2+ extracellular levels and decreases extracellular phosphate levels
Vitamin D stimulates Ca2+ uptake in intestines
Calcitonin decreases extracellular Ca2+ levels
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REGULATION OF CALCIUM IONS
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HYPOCALCEMIA Causes:
• Decreased serum albumin concentration• Chelation of calcium by citrate• Rhabdomyolysis• Hypoparathyroidism• Pancreatitis• Renal failure
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CLINICAL MANIFESTATIONS OF HYPOCALCEMIANeuromuscular irritability
• Tetany• Laryngospasm• Hyperactive deep tendon reflexes
WeaknessVasodilationMyocardial dysfunctionBradycardiaHeart block
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TREATMENT OF HYPOCALCEMIA Calcium replacement
Intraoperative – hyperventilation and respiratory alkalosis
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HYPERCALCEMIA Causes:
• Calcium mobilization from bone due to immobility
• Tumors
• Hyperparathyroidism
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CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Anorexia Nausea Constipation Cognitive depression EKG changes
• Prolonged PR interval • Shortened QT interval• PVC’s
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TREATMENT OF HYPERCALCEMIA Treatment of underlying cause Volume expansion Intraoperative hypercalcemia should be
managed with administration of adequate fluids and maintenance of urine output.
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Copyright 2008 by Pearson Education, Inc.
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REGULATION OF CHLORIDE & MAGNESIUM IONS Chloride ions
Predominant anions in ECF Magnesium ions
Capacity of kidney to reabsorb is limitedExcess lost in urineDecreased extracellular magnesium
results in greater degree of reabsorption
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MAGNESIUM REGULATION Essential for enzyme activities Neurochemical activities Cardiac and skeletal muscle excitability Regulation
Dietary Renal mechanisms Parathyroid hormone action
50 – 60% of magnesium contained in bones 1% in ECF Minimal amount in cell
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REGULATION OF BLOOD MAGNESIUM
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HYPOMAGNESEMIA Serum magnesium less than 1.5mEq/L Causes:
• Inadequate intake of magnesium• TPN• Gastrointestinal losses• Pancreatitis• Parathyroid hormone disorders• Hyperaldosteronism• Ketoacidosis• Chronic alcoholism
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CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA CNS irritability
• Seizures
• Hyperreflexia
• Skeletal muscle spasm
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TREATMENT OF HYPOMAGNESEMIA
IV administration of magnesium sulfate
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HYPERMAGNESEMIA Serum magnesium level greater than
2.5 mEq/L Causes:
• Iatrogenic administration• Preeclampsia• Antacids/laxatives
• Renal failure
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CLINICAL MANIFESTATIONS OF HYPERMAGNESEMIA
CNS depression stupor coma
Skeletal muscle weakness respiratory failure
Decreased peripheral vascular tone
Decreased myocardial contractility
Tocolysis
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HYPERMAGNESEMIA AND THE EKG Prolonged PQ interval
Widened QRS
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TREATMENT OF HYPERMAGNESEMIA Supportive care
Fluid loading
Diuresis
Acute hypermagnesemia –IV calcium to counter the elevated magnesium levels
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ANIONS CONT’D.• Phosphate (PO4---)
▫ Buffer ion found in ICF▫ Assists in acid-base regulation▫ Helps to develop and maintain bones and teeth▫ Calcium and phosphate are inversely proportional▫ Promotes normal neuromuscular action and participates in
carbohydrate metabolism▫ Absorbed through GI tract▫ Regulated by diet, renal excretion, intestinal absorption and
PTH• Under normal conditions, reabsorption of phosphate occurs at
maximum rate in the nephron• An increase in plasma phosphate increases amount of phosphate
in nephron beyond that which can be reabsorbed; excess is lost in urine
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REGULATION OF BLOOD PHOSPHATE
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OTHER ELECTROLYTE DEFICITSCA, PO4, MG OTHER ELECTROLYTE DEFICITSCA, PO4, MG
May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects
All are primarily intracellular ions, so deficits difficult to estimate
Titrate replacement against clinical findings
May produce serious but nonspecific cardiac, neuromuscular, respiratory, and other effects
All are primarily intracellular ions, so deficits difficult to estimate
Titrate replacement against clinical findings
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PHOSPHATE
Involved in acid–base buffering system, ATP production, and cellular uptake of glucose
Maintenance requires adequate renal functioning
Essential to muscle, RBCs, and nervous system function
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HYPERPHOSPHATEMIA
High serum PO43 caused by
Acute or chronic renal failureChemotherapyExcessive ingestion of phosphate or vitamin D
Manifestations Calcified deposition: joints, arteries, skin,
kidneys, and corneasNeuromuscular irritability and tetany
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HYPERPHOSPHATEMIA
Management Identify and treat underlying causeRestrict foods and fluids containing PO4
3
Adequate hydration and correction of hypocalcemic conditions
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HYPOPHOSPHATEMIA
Low serum PO43 caused by
Malnourishment/malabsorptionAlcohol withdrawalUse of phosphate-binding antacidsDuring parenteral nutrition with inadequate
replacement
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HYPOPHOSPHATEMIA
ManifestationsCNS depressionConfusion Muscle weakness and painDysrhythmias Cardiomyopathy
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HYPOPHOSPHATEMIA
ManagementOral supplementation Ingestion of foods high in PO4
3
IV administration of sodium or potassium phosphate
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1995
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Saya akan perlakukan teman sejawat saya seperti saudara kandung
Saya akan memperlakukan teman sejawat saya sebagaimana saya ingin diperlakukan.
2010