Disorders of Potassium Balance Potassium is the major

Disorders of Potassium Balance

�Potassium is the major intracellular cation �Steep concentration gradient for potassium across the cell membrane of excitable cells plays an important part in generating the resting membrane potential and allowing the propagation of the action potential

�Potassium is driven into the cells from the plasma by extracellular alkalosis and by a number of hormones, including insulin, catecholamines (through the β 2 receptor) and aldosterone �In the steady state, the kidneys excrete 90% of the daily intake of potassium, typically 80 – 100 mmol/day through late distal/cortical collecting duct tubule

�↑Plasma [K+] stimulates Aldosterone secretion from Adrenal cortex which acts on kidney to excrete excess potassium �Rate of sodium delivery and fluid flow through the late distal/cortical collecting ducts influence the rate of potassium secretion

�Since the plasma aldosterone concentration is the net effect of two different stimuli, factors reducing angiotensin II levels may indirectly impair potassium balance by blunting the rise in aldosterone which would otherwise be provoked by hyperkalaemia

Hypokalaemia �Hypokalemia, is defined as a plasma K+ concentration <3. 6 m. M �Occurs in up to 20% of hospitalized patients �Associated with a tenfold increase in inhospital mortality rates due to adverse effects on cardiac rhythm, blood pressure, and cardiovascular morbidity rate

�Mechanistically, hypokalemia can be caused by redistribution of K+ between tissues and the ECF or by renal and nonrenal loss of K+

Causes �Decreased intake: Starvation � Redistribution into cells � Metabolic alkalosis �Insulin � Beta 2 -Adrenergic agonists: bronchodilators

Increased loss Nonrenal � Gastrointestinal loss (diarrhea) � Integumentary loss (sweat)

Renal � Diuretics �Osmotic diuresis �Salt-wasting nephropathies Mineralocorticoid excess �Primary hyperaldosteronism �Secondary hyperaldosteronism �Proximal renal tubular acidosis

Magnesium deficiency �Magnesium depletion reduces influx of K+ into muscle cells and causes secondary kaliuresis � In addition, magnesium depletion causes exaggerated K+ secretion by the distal nephron

Clinical Features �Hypokalemia has prominent effects on cardiac, skeletal, and intestinal muscle cells �It is a major risk factor for both ventricular and atrial arrhythmias �Predisposes to digoxin toxicity

�Electrocardiographic changes in hypokalemia include broad flat T waves, ST depression, and QT prolongation �These are most marked when serum K+ is <2. 7 mmol/L �Muscular weakness and even paralysis �Intestinal paralytic ileus

�The functional effects of hypokalemia on the kidney include Na+-Cl– and HCO 3– retention, generating metabolic alkalosis, polyuria

Evaluation �Redistribution of potassium into cells should be considered, since correction of the factors involved may be sufficient to correct the plasma concentration �Hypokalaemia usually is abnormal potassium loss from the body, through either the kidney or the gastrointestinal tract

�When there is no obvious clinical clue, measurement of urinary potassium may be helpful if the kidney is the route of potassium loss, the urine potassium is relatively high (> 30 mmol/day) �The renal causes can be divided into those with or without hypertension

�Hypertensive disorders with hypokalaemia may be due to excess mineralocorticoid activity �If blood pressure is normal or low, renal potassium loss can be classified according to the associated acid– base change �If hypokalaemia is associated with alkalosis diuretic use should be excluded

�If hypokalaemia is associated with a normal blood pressure but with metabolic acidosis, renal tubular acidosis (proximal) should be suspected �When hypokalaemia is due to potassium wasting through the gastrointestinal tract, the cause is usually obvious clinically

Treatment �The goals of therapy are, � To prevent life-threatening and/or chronic consequences �To replace the associated K+ deficit �To correct the underlying cause and/or mitigate future hypokalemia

�The urgency of therapy depends on �Severity of hypokalemia �Associated clinical factors (cardiac disease, digoxin therapy, etc. ) �Rate of decline in serum K+ �Urgent K+replacement should be considered in patients with severe hypokalemia (plasma K+ concentration <2. 5 m. M)

�Oral replacement with K+-Cl– is the mainstay of therapy for hypokalemia �The use of intravenous administration should be limited to patients unable to utilize the enteral route or in the setting of severe complications

�Intravenous K+-Cl– should always be administered in saline solutions rather than dextrose since the dextrose-induced increase in insulin can acutely exacerbate hypokalemia �The peripheral intravenous dose is usually 20– 40 mmol of K+-Cl– per liter

Hyperkalaemia �Hyperkalemia is defined as a plasma potassium level of 5. 5 m. M. �It occurs in up to 10% of hospitalized patients �Severe hyperkalemia (>6. 0 m. M) occurs in approximately 1%, with a significantly increased risk of mortality

�Although redistribution and reduced tissue uptake can acutely cause hyperkalemia, a decrease in renal K+ excretion is the most common underlying cause �Excessive intake of K+ is a rare cause because of the adaptive capacity to increase renal secretion except chronic in kidney disease

Causes of Hyperkalemia �Pseudo" hyperkalemia Cellular efflux: thrombocytosis, erythrocytosis, leukocytosis, in vitro hemolysis

�Intra- to extracellular shift Acidosis Hyperkalemic periodic paralysis Rapid tumor lysis

�Inadequate excretion � Inhibition of the renin-angiotensinaldosterone axis Angiotensin-converting enzyme (ACE) inhibitors ARBs

�Blockade of the mineralocorticoid receptor: spironolactone � Blockade of ENa. C: amiloride, triamterene �Advanced renal insufficiency Chronic kidney disease End-stage renal disease Acute oliguric kidney injury

�Primary adrenal insufficiency Autoimmune: Addison's disease Infectious: HIV, tuberculosis

Clinical Features �Hyperkalemia is a medical emergency because of its effects on the heart �Sinus bradycardia, sinus arrest, slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole

�Electrocardiographic manifestations in hyperkalemia progress from tall peaked T waves (5. 5– 6. 5 m. M), to a loss of P waves (6. 5– 7. 5 m. M), to a widened QRS complex (7 – 8 m. M), and ultimately to a sine wave pattern (8 m. M)

�Hyperkalemia can also present with ascending paralysis �Within the kidney, hyperkalemia inhibits excretion of an acid load, and so per se can contribute to metabolic acidosis �Restoration of normokalemia can in many instances correct hyperkalemic metabolic acidosis

Evaluation �The first priority in the management is to assess the need for emergency treatment, followed by a comprehensive workup to determine the cause

�History and physical examination should focus on medications, diet and dietary supplements, risk factors for kidney failure, reduction in urine output, blood pressure, and volume status

Treatment �ECG manifestations of hyperkalemia should be considered a medical emergency and treated urgently �Pts with significant hyperkalemia (plasma K+ concentration 6. 5– 7 m. M) in the absence of ECG changes should be aggressively managed because of the limitations of ECG changes as a predictor of cardiac toxicity

�Urgent management of hyperkalemia includes, �Admission to the hospital �Continuous cardiac monitoring �Immediate treatment

� The treatment is divided into three stages: �Immediate antagonism of the cardiac effects of hyperkalemia �Rapid reduction in plasma K+ concentration by redistribution into cells � Use of Beta 2 -agonists

�Intravenous bicarbonate has no role in the routine treatment of hyperkalemia �Removal of potassium. This typically is accomplished by using cation exchange resins, diuretics, and/or dialysis

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