Hypokalemia is defined as a serum [K+] of less than 3.5 meq/L. The most frequent causes of hypokalemia are intracellular shifts and increased losses ( T.§bIe 2.3.-7). K+ tends to shift into cells as the pH of the ECF rises in exchange for hydrogen ions. A rise in the pH of 0.10 generally causes a 0.5 ± 0.2-meq/L decrease in serum [K +] levels. This relationship applies to metabolic acid-base derangements. Although the reasons are unclear, respirator alkalosis and acidosis have minimum effect on K + shift. K+ losses usually involve either the gastrointestinal tract or the kidneys. It is important to note that the hypokalemia associated with vomiting has very little to do with the actual K+ lost in the vomitus and much more to do with the metabolic alkalosis that follows. The hypovolemia from volume loss leads to increases in aldosterone secretion, which acts on the kidney to preserve Na+ and bicarbonate in exchange for K+. The resultant alkalosis also causes K+ to shift into cells in exchange for H+.

TABLE 23-7 Etiology of Hypokalemia

The clinical manifestations of hypokalemia usually start when serum concentrations reach 2.5 meq/L, although they may appear sooner with rapid decreases in concentration. The symptoms result from abnormalities in membrane polarization and affect almost every system. Manifestation by system includes

Neuromuscular: Generalized malaise, weakness, fatigue, hyporeflexia, cramps, and paresthesias all begin as early signs. Paralysis (even of the respiratory muscles) and rhabdomyolysis are seen at levels below 1.5 meq/L.

Gastrointestinal: The gastrointestinal tract demonstrates an increased tendency to intestinal ileus.

Renal: Hypokalemia increases renal tubular production of ammonia, which may aggravate hepatic encephalopathy. Its direct effect on the kidney results in urinary-concentrating defects and decreased glomerular filtration and tends to cause a metabolic alkalemia with increased acid excretion in the urine (paradoxical aciduria). Severe hypokalemia can lead to nephrogenic DI with volume loss.

Endocrine: Hypokalemia leads to glucose intolerance.

Cardiovascular: Perhaps the most important effects are those on the cardiovascular system. These include worsening hypertension, orthostatic hypotension, potentiation of digitalis, and dysrhythmias. The classic electrocardiographic (ECG) abnormalities associated with hypokalemia include T-wave flattening, prominent U waves, and ST-segment depression. Tachyarrhythmias predominate.

TREATMENT The treatment of hypokalemia is quite simple: replacement of K+. This can be done orally in stable patients who are able to tolerate oral intake. Either foods rich in K+, salt substitutes, or K+ supplements will work. Intravenous replacement is appropriate for patients with severe hypokalemia. It can also be given as 10 to 20 meq/L in 100 mL of 0.9% saline. The ECG should be continually monitored for any patient receiving intravenous K +. As a rule, no more than 40 meq of K+ should be in a single liter of intravenous fluid and no more than 40 meq should be given in 1 h. Concentrations greater than 20 meq/L should be infused through a central line. A 20-meq infusion will raise serum [K+] by approximately 0.25 meq/L.5

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