A total body deficit of about 350 meq occurs for each 1 meq/L decrement in serum potassium concentration below a level of 4 meq/L. However, changes in blood pH and hormones (insulin, b-adrenergic agonists, and aldosterone) independently affect serum potassium levels. Elevated serum epinephrine may contribute to the hypokalemia commonly seen in trauma patients; this normalizes within 24 hours after injury without significant potassium replacement.

A. Symptoms and Signs: Muscular weakness, fatigue, and muscle cramps are frequent complaints in mild to moderate hypokalemia. Smooth muscle involvement may result in constipation or ileus. Flaccid paralysis, hyporeflexia, hypercapnia, tetany, and rhabdomyolysis may be seen with severe hypokalemia (< 2.5 meq/L).

B. Laboratory Findings: The ECG shows decreased amplitude and broadening of T waves, prominent U waves, depressed ST segments, and, in more severe deficits, atrioventricular block and finally cardiac arrest. Hypokalemia also increases the likelihood of digitalis toxicity.

Hypokalemia can occur as a result of shift of potassium from outside to inside the cell, extrarenal potassium loss (or insufficient potassium intake), or renal potassium loss. Potassium uptake by the cell is stimulated by insulin in the presence of glucose. It is also facilitated by adrenergic beta-stimulation, whereas adrenergic alpha-stimulation blocks it. All of these effects are transient. Urinary potassium concentration is low (< 20 meq/L) as a result of extrarenal fluid loss (eg, diarrhea, vomiting) and inappropriately high (> 40 meq/L) with renal fluid loss (eg, mineralocorticoid excess, Bartter's syndrome, Liddle's syndrome). Genetic mutation of Na-K-2Cl cotransporter in the thick ascending limb in the loop of Henle has been shown in some patients with Bartter's syndrome.

The safest way to treat mild to moderate deficiency is with oral potassium, which is rapidly absorbed. Liquid potassium chloride has an unpleasant taste and may be better tolerated if added to fruit juice. Rarely, enteric-coated or slow-release tablets or capsules of potassium chloride can cause peptic ulceration.

Intravenous potassium replacement is indicated for patients with severe hypokalemia and in those who cannot take oral supplementation. If the serum potassium level is greater than 2.5 meq/L and there are no electrocardiographic abnormalities characteristic of hypokalemia, potassium can be given at a rate of 10 meq/L/h by peripheral intravenous line in concentrations that should never exceed 40 meq/L. For severe deficiency, potassium may be given through a peripheral intravenous line at rates up to 40 meq/L/h. Continuous electrocardiographic monitoring is indicated, and the serum potassium level should be checked every 3–6 hours.

Occasionally, hypokalemia may be refractory to potassium replacement. Magnesium deficiency may make potassium correction more difficult. Concomitant magnesium repletion avoids this problem.