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Causes of metabolic alkalosis

Michael Emmett, MD
Harold Szerlip, MD, FACP, FCCP, FASN, FNKF
Section Editor
Richard H Sterns, MD
Deputy Editor
John P Forman, MD, MSc


Metabolic alkalosis, a disorder that elevates the serum bicarbonate, can result from several mechanisms: intracellular shift of hydrogen ions; gastrointestinal loss of hydrogen ions; excessive renal hydrogen ion loss; administration and retention of bicarbonate ions; or volume contraction around a constant amount of extracellular bicarbonate (contraction alkalosis) (table 1) [1-4].

Hydrogen ions are derived from the dissociation of water into hydrogen and hydroxyl ions; therefore, when hydrogen ions are removed from the extracellular fluid, the remaining hydroxyl ion combines with carbon dioxide to form bicarbonate. Gastrointestinal and renal hydrogen loss is usually accompanied by the loss of chloride and potassium, resulting in hypochloremia and hypokalemia.

Patients with preserved renal function will most often rapidly excrete excess bicarbonate in the urine. Thus, metabolic alkalosis can only persist if the ability to excrete excess bicarbonate in the urine is impaired due to one of the following causes: hypovolemia; reduced effective arterial blood volume (due, for example, to heart failure or cirrhosis); chloride depletion; hypokalemia; reduced glomerular filtration rate; hyperaldosteronism; or combinations of these factors [3,5,6].

The causes of metabolic alkalosis will be reviewed here. The pathogenesis, evaluation, and treatment of this disorder are discussed separately. (See "Pathogenesis of metabolic alkalosis" and "Clinical manifestations and evaluation of metabolic alkalosis" and "Treatment of metabolic alkalosis".)


Metabolic alkalosis can be generated by a shift of hydrogen ions into the cells. This most often occurs in patients with potassium deficits and hypokalemia. This may be an important pathophysiologic mechanism in patients with metabolic alkalosis due to vomiting or nasogastric suction [7]. (See "Potassium balance in acid-base disorders".)


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Literature review current through: Oct 2015. | This topic last updated: Oct 9, 2015.
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