dr. andi sulistyo haribowo, sp.pd. spesialis penyakit dalam program studi pendidikan dokter...

GANGGUAN PADA KESEIMBANGAN

ELEKTROLIT dr. Andi Sulistyo Haribowo,

Sp.PD.

SPESIALIS PENYAKIT DALAM

Program Studi Pendidikan Dokter

UNIVERSITAS ISLAM MALANG

2012

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

DISTRIBUTION OF ELECTROLYTES

CATIONS AND ANIONS IN BODY FLUIDS

Figure 27.2

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

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

REGULATION OF ELECTROLYTES Major Cations in body fluids

Sodium (Na+)Potassium (K+)Calcium (Ca++)Magnesium (Mg++)

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

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

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

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.

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

CLINICAL MANIFESTATIONS OF HYPONATREMIA Neurologic

• Seizure• Coma• Agitation

Gastrointestinal• Anorexia • Nausea/vomiting

Muscular• Cramps• weakness

• Headache• Cerebral edema• Confusion

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!!!

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

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

CLINICAL MANIFESTATIONS OF HYPERNATREMIA Tremulousness

Irritability

Ataxia

Mental confusion

Coma d/t cerebral water loss

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!!!

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

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

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

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

The relation between potassium and hydrogen ions in the plasma

Saladin’s Anatomy & Physiology fourth edition McGraw Hill

Potassium balance in the body

Costanzo Physiology second edition Saunders

POTASSIUM ION REGULATION IN ECF

27-30

HYPOKALEMIA Causes

• Gastrointestinal losses• Systemic alkalosis• Diabetic ketoacidosis• Diuretic therapy• Sympathetic nervous system stimulation• Administration of beta-adrenergic receptor

agonists

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

HYPOKALEMIA Extrarenal depletion

diarrhea laxative abusesweat losses fasting or inadequate intake

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

HYPOKALEMIA Renal losses

metabolic acidosis RTA Type I and II DKA Carbonic anhydrase inhibitor therapy Ureterosigmoidostomy

No acid-base disorder Mg deficiency Drugs

CLINICAL MANIFESTATIONS OF HYPOKALEMIA Autonomic neuropathy

Skeletal muscle weakness

Increased sensitivity to Digoxin

Cardiac• Decreased myocardial contractility• Electrical conduction abnormalities

• Arrhythmias• Tachycardia• Ventricular fibrillation

POTASSIUM

Copyright 2008 by Pearson Education, Inc.

HYPOKALEMIA AND THE EKG• Prolonged PR

interval

• Prolonged T interval

• Widening of QRS

• Flattened T wave

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

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)

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

CLINICAL MANIFESTATIONS OF HYPERKALEMIAAreflexia

Weakness

Paralysis

Paresthesia

Cardiac conduction abnormalities

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

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

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

HYPERKALEMIA Treatment

Stop potassium!Get and ECGHyperkalemia with ECG changes is a

medical emergency

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

HYPERKALEMIA Treatment

Therapy directed at actual removal of potassium from the body sodium polystyrene sulfonate (Kayexalate) dialysis

Determine and correct the underlying cause

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

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

27-50

REGULATION OF CALCIUM IONS

27-51

HYPOCALCEMIA Causes:

• Decreased serum albumin concentration• Chelation of calcium by citrate• Rhabdomyolysis• Hypoparathyroidism• Pancreatitis• Renal failure

CLINICAL MANIFESTATIONS OF HYPOCALCEMIANeuromuscular irritability

• Tetany• Laryngospasm• Hyperactive deep tendon reflexes

WeaknessVasodilationMyocardial dysfunctionBradycardiaHeart block

TREATMENT OF HYPOCALCEMIA Calcium replacement

Intraoperative – hyperventilation and respiratory alkalosis

HYPERCALCEMIA Causes:

• Calcium mobilization from bone due to immobility

• Tumors

• Hyperparathyroidism

CLINICAL MANIFESTATIONS OF HYPERCALCEMIA Anorexia Nausea Constipation Cognitive depression EKG changes

• Prolonged PR interval • Shortened QT interval• PVC’s

TREATMENT OF HYPERCALCEMIA Treatment of underlying cause Volume expansion Intraoperative hypercalcemia should be

managed with administration of adequate fluids and maintenance of urine output.

Copyright 2008 by Pearson Education, Inc.

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

27-59

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

REGULATION OF BLOOD MAGNESIUM

27-61

HYPOMAGNESEMIA Serum magnesium less than 1.5mEq/L Causes:

• Inadequate intake of magnesium• TPN• Gastrointestinal losses• Pancreatitis• Parathyroid hormone disorders• Hyperaldosteronism• Ketoacidosis• Chronic alcoholism

CLINICAL MANIFESTATIONS OF HYPOMAGNESEMIA CNS irritability

• Seizures

• Hyperreflexia

• Skeletal muscle spasm

TREATMENT OF HYPOMAGNESEMIA

IV administration of magnesium sulfate

HYPERMAGNESEMIA Serum magnesium level greater than

2.5 mEq/L Causes:

• Iatrogenic administration• Preeclampsia• Antacids/laxatives

• Renal failure

CLINICAL MANIFESTATIONS OF HYPERMAGNESEMIA

CNS depression stupor coma

Skeletal muscle weakness respiratory failure

Decreased peripheral vascular tone

Decreased myocardial contractility

Tocolysis

HYPERMAGNESEMIA AND THE EKG Prolonged PQ interval

Widened QRS

TREATMENT OF HYPERMAGNESEMIA Supportive care

Fluid loading

Diuresis

Acute hypermagnesemia –IV calcium to counter the elevated magnesium levels

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

REGULATION OF BLOOD PHOSPHATE

27-70

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

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

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

HYPERPHOSPHATEMIA

Management Identify and treat underlying causeRestrict foods and fluids containing PO4

3

Adequate hydration and correction of hypocalcemic conditions

HYPOPHOSPHATEMIA

Low serum PO43 caused by

Malnourishment/malabsorptionAlcohol withdrawalUse of phosphate-binding antacidsDuring parenteral nutrition with inadequate

replacement

HYPOPHOSPHATEMIA

ManifestationsCNS depressionConfusion Muscle weakness and painDysrhythmias Cardiomyopathy

HYPOPHOSPHATEMIA

ManagementOral supplementation Ingestion of foods high in PO4

3

IV administration of sodium or potassium phosphate

1995

Saya akan perlakukan teman sejawat saya seperti saudara kandung

Saya akan memperlakukan teman sejawat saya sebagaimana saya ingin diperlakukan.

2010