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Hypokalemia is a common clinical problem. Potassium enters the body via oral intake or intravenous infusion, is then largely stored in the cells, and then excreted in the urine. Thus, decreased intake, increased translocation into the cells, or, most often, increased losses in the urine (or gastrointestinal tract or sweat) all can lead to potassium depletion and a reduction in the plasma potassium concentration (table 1).
This topic will review the major causes of hypokalemia. The diagnosis and treatment of hypokalemia are discussed separately. (See "Diagnosis of hypokalemia" and "Clinical manifestations and treatment of hypokalemia".)
The normal range of potassium intake is 40 to 120 meq per day, most of which is then excreted in the urine. The kidney is able to lower potassium excretion to a minimum of 5 to 25 meq per day in the presence of potassium depletion [1]. Thus, decreased intake alone will cause hypokalemia only in rare cases. However, it can contribute to the severity of potassium depletion when another problem is superimposed, such as diuretic therapy or the use of hypocaloric, liquid protein diets for rapid weight loss [2,3].
The normal distribution of potassium between the cells (which contains approximately 98 percent of exchangeable potassium) and the extracellular fluid is maintained by the Na-K-ATPase pump in the cell membrane [4]. In some cases, however, there is increased potassium entry into cells, resulting in transient hypokalemia.
An elevation in extracellular pH — Either metabolic or respiratory alkalosis can promote potassium entry into cells. In these settings, hydrogen ions leave the cells to minimize the change in extracellular pH; the necessity to maintain electroneutrality then requires the entry of some potassium (and sodium) into the cells. In general, this direct effect is relatively small, as the plasma potassium concentration falls less then 0.4 meq/L for every 0.1-unit rise in pH [5]. A similar change can be induced by the administration of sodium bicarbonate to treat metabolic acidosis; in this setting, however, a direct effect of bicarbonate may also contribute, independent of the elevation in pH [6].
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