Hyperkalemia

Hyperkalemia (>5.5 mEq/L) may occur in various disease states, in response to drugs that diminish renal potassium excretion ( Table 46-9 ), or after sudden transcellular shifts of potassium from the intracellular to the ECF. A potentially lethal occurrence of hyperkalemia during anesthesia may happen with reperfusion of a large vascular bed after a period of ischemia (usually more than 4 hours). Ischemia results in significant acidosis in the affected area, which causes an outflow of intracellular potassium. When the area is reperfused, the body receives a large bolus of potassium that cannot be redistributed rapidly enough, resulting in potentially fatal hyperkalemia.

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Hyperkalemia can be separated into acute and chronic processes. Acute hyperkalemia can occur in a variety of circumstances and usually is more poorly tolerated than chronic hyperkalemia. The most common cause of chronic hyperkalemia occurring with anesthesia is renal failure. A patient undergoing anesthesia with even moderately elevated potassium concentration (>5.5 mEq/L) should have electrocardiographic evaluation to determine the severity of hyperkalemia.

Clinically, hyperkalemia can cause muscle weakness and even paralysis. Alterations in initiation and conduction of cardiac conduction increase automaticity and enhance repolarization. Mild elevations in potassium levels (6 to 7 mEq/L) may present with peaked T waves and can progress to a prolonged PR interval, widening of the QRS complex, ventricular fibrillation, or even asystole as levels approach 10 to 12 mEq/L.^[48]

Clinical treatment of hyperkalemia is determined by the setting and presence of electrocardiographic changes; it involves stabilization of the heart from effects of the potassium with intravenous calcium and redistribution of potassium from the plasma into cells. In addition to calcium, intravenous glucose, insulin, bicarbonate, and hyperventilation are the major therapies used in the operating room setting. Ten units of insulin, administered with dextrose,

TABLE 46-10 -- Major causes of hyperkalemia

Mechanism	Causes
Pseudohyperkalemia	Sample lysis, technical problems
Altered internal potassium balance	Acidosis, insulin deficiency, hypoaldosteronism, malignant hyperthermia, periodic paralysis, cell necrosis
	Drugs, including succinylcholine, digitalis, and nonselective β-blockers
Altered external potassium balance	Increased uptake by replacement therapy; transfusions; antibiotics containing potassium salts
	Decreased excretion by renal disease; hypoaldosteronism; drugs including heparin, amiloride, triamterene, spironolactone, nonsteroidal drugs, angiotensin-converting enzyme inhibitors, and angiotensin-receptor antagonists
Adapted from Solomon RJ, Katz JD: Disorders of potassium homeostasis. In Stoelting RK (ed): Advances in Anesthesia, Chicago, Year Book, 1986.

lowers serum potassium levels within 10 to 20 minutes, and the effects last 4 to 6 hours.^[49] Resin exchange, dialysis, diuretics, aldosterone agonists, and β-adrenergic agonists are well-established additional therapies ( Table 46-10 ).