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ESSENTIALS OF DIAGNOSIS

  • Serum potassium level less than 3.5 mEq/L (3.5 mmol/L).

  • Severe hypokalemia may induce arrhythmias and rhabdomyolysis.

  • Transtubular potassium concentration gradient (TTKG) can distinguish renal from nonrenal loss of potassium.

GENERAL CONSIDERATIONS

Hypokalemia can result from insufficient dietary potassium intake, intracellular shifting of potassium from the extracellular space, extrarenal potassium loss, or renal potassium loss (Table 21–4). Cellular uptake of potassium is increased by insulin and beta-adrenergic stimulation and blocked by alpha-adrenergic stimulation. Aldosterone is an important regulator of total body potassium, increasing potassium secretion in the distal renal tubule. The most common cause of hypokalemia, especially in developing countries, is gastrointestinal loss from infectious diarrhea. The potassium concentration in intestinal secretion is ten times higher (80 mEq/L) than in gastric secretions. Hypokalemia in the presence of acidosis suggests profound potassium depletion and requires urgent treatment. Self-limited hypokalemia occurs in 50–60% of trauma patients, perhaps related to enhanced release of epinephrine.

Table 21–4.Causes of hypokalemia.

Hypokalemia induced by beta-2-adrenergic agonists and diuretics may substantially increase the risk of arrhythmias. Hypokalemia increases the likelihood of digitalis toxicity. Numerous genetic mutations affect fluid and electrolyte metabolism, including disorders of potassium metabolism (Table 21–5).

Table 21–5.Genetic disorders associated with electrolyte metabolism disturbances.

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