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 Figure 27.2 • • • 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 • • • 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 Major Cations in body fluids Sodium (Na+) Potassium (K+) Calcium (Ca++) Magnesium (Mg++) Implies Treat an underlying disease process the electrolyte change, but seek the cause Clinical manifestations usually not specific to a particular electrolyte change, e.g., seizures, arrhythmias Clinical manifestations determine urgency of treatment, not laboratory values Speed and magnitude of correction dependent on clinical circumstances Frequent reassessment of electrolytes required 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 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. 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 Neurologic • Seizure • Coma • Agitation Gastrointestinal • Anorexia • Nausea/vomiting Muscular • Cramps • weakness • • • Headache Cerebral edema Confusion 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!!! 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 hours 5% saline is almost never needed Calculate the Na deficit Na mEq = ([Na desired] - [Na measured]) X TBW TBW = .5 or .6 X weight in KG 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 Tremulousness Irritability Ataxia Mental Coma confusion d/t cerebral water loss Renal 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!!! 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 Treatment Calculate the water deficit H2O 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 Major electrolyte and principle cation in the extracellular fluid Regulates metabolic activities Required for glycogen deposits in the liver and skeletal muscle Required for transmission of nerve impulses, normal cardiac conduction and normal smooth and skeletal muscle contraction Regulated by dietary intake and renal excretion Potassium balance Major intracellular cation Balance: ingestion = excretion (via kidneys) Aldosterone primarily controls potassium It exchanges potassium for sodium Insulin also regulates potassium It 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- hyperkalemia Alkalosis: 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 27-30 Causes • • • • • • Gastrointestinal losses Systemic alkalosis Diabetic ketoacidosis Diuretic therapy Sympathetic nervous system stimulation Administration of beta-adrenergic receptor agonists Spurious hypokalemia Marked leukocytosis A dose of insulin right before the blood draw Redistribution hypokalemia Alkalosis (K decreases .3 for every .1 increase in pH) Increased Beta2 adrenergic activity Theophylline toxicity Familial Extrarenal depletion diarrhea laxative abuse sweat losses fasting or inadequate intake Renal potassium depletion urine potassium > 20 mEq/24 hrs spot urine with > 20 mEq K/gram creatinine classified whether they occur with a metabolic alkalosis vomiting/NG suction diuretic tx Mineralocorticoid excess syndromes Renal metabolic acidosis losses RTA Type I and II DKA Carbonic anhydrase inhibitor therapy Ureterosigmoidostomy No acid-base disorder Mg deficiency Drugs Autonomic neuropathy Skeletal muscle weakness Increased sensitivity to Digoxin Cardiac • Decreased myocardial contractility • Electrical conduction abnormalities • Arrhythmias • Tachycardia • Ventricular fibrillation Copyright 2008 by Pearson Education, Inc. • Prolonged PR interval • Prolonged T interval • Widening of QRS • Flattened T wave 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 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) 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 Areflexia Weakness Paralysis Paresthesia Cardiac conduction abnormalities • 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 Etiology – renal failure, transcellular shifts, cell death, drugs, pseudohyperkalemia Manifestations – cardiac, neuromuscular 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 Treatment Stop potassium! Get and ECG Hyperkalemia with ECG changes is a medical emergency 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 Treatment Therapy directed at actual removal of potassium from the body sodium polystyrene sulfonate (Kayexalate) dialysis Determine and correct the underlying cause 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 Regulated within narrow range Elevated extracellular levels prevent membrane depolarization Decreased levels lead to spontaneous action potential generation Terms Hypocalcemia Hypercalcemia PTH increases Ca2+ extracellular levels and decreases extracellular phosphate levels Vitamin D stimulates Ca2+ uptake in intestines Calcitonin decreases extracellular Ca2+ levels 27-50 27-51 Causes: • • • • • • Decreased serum albumin concentration Chelation of calcium by citrate Rhabdomyolysis Hypoparathyroidism Pancreatitis Renal failure Neuromuscular • • • irritability Tetany Laryngospasm Hyperactive deep tendon reflexes Weakness Vasodilation Myocardial dysfunction Bradycardia Heart block Calcium replacement Intraoperative – hyperventilation and respiratory alkalosis Causes: • Calcium mobilization from bone due to immobility • Tumors • Hyperparathyroidism Anorexia Nausea Constipation Cognitive depression EKG changes • • • Prolonged PR interval Shortened QT interval PVC’s 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. Chloride ions Predominant anions in ECF Magnesium ions Capacity of kidney to reabsorb is limited Excess lost in urine Decreased extracellular magnesium results in greater degree of reabsorption 27-59 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 27-61 Serum magnesium less than 1.5mEq/L Causes: • • • • • • • • Inadequate intake of magnesium TPN Gastrointestinal losses Pancreatitis Parathyroid hormone disorders Hyperaldosteronism Ketoacidosis Chronic alcoholism CNS irritability • Seizures • Hyperreflexia • Skeletal muscle spasm IV administration of magnesium sulfate Serum magnesium level greater than 2.5 mEq/L Causes: • Iatrogenic administration • • • Preeclampsia Antacids/laxatives Renal failure CNS depression Skeletal stupor muscle weakness coma respiratory failure Decreased peripheral vascular tone Decreased myocardial contractility Tocolysis Prolonged Widened PQ interval QRS Supportive Fluid care loading Diuresis Acute hypermagnesemia –IV calcium to counter the elevated magnesium levels • • • 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 27-70 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 Involved in acid–base buffering system, ATP production, and cellular uptake of glucose Maintenance Essential function requires adequate renal functioning to muscle, RBCs, and nervous system High serum PO43 caused by Acute or chronic renal failure Chemotherapy Excessive ingestion of phosphate or vitamin D Manifestations Calcified deposition: joints, arteries, skin, kidneys, and corneas Neuromuscular irritability and tetany Management Identify and treat underlying cause Restrict foods and fluids containing PO43 Adequate hydration and correction of hypocalcemic conditions Low serum PO43 caused by Malnourishment/malabsorption Alcohol withdrawal Use of phosphate-binding antacids During parenteral nutrition with inadequate replacement Manifestations CNS depression Confusion Muscle weakness and pain Dysrhythmias Cardiomyopathy Management Oral supplementation Ingestion of foods high in PO43 IV administration of sodium or potassium phosphate Saya akan perlakukan teman sejawat saya seperti saudara kandung Saya akan memperlakukan teman sejawat saya sebagaimana saya ingin diperlakukan.