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Pathogenesis 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 is a relatively common disorder that is most often generated by diuretic therapy or the loss of gastric secretions due to vomiting (which may be surreptitious) or nasogastric suction. Metabolic alkalosis may also result from severe hypokalemia, alkali ingestion when renal function is markedly diminished, primary aldosteronism, or disorders that mimic primary aldosteronism.

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


The development of metabolic alkalosis and its subsequent maintenance generally have distinct and separate explanations [1-3]:

An elevation in the plasma bicarbonate concentration can develop due to excessive hydrogen ion loss in the urine or gastrointestinal tract, hydrogen ion movement into the cells, the administration of bicarbonate salts (or other alkalinizing salts such as sodium acetate or lactate), or volume contraction around a relatively constant amount of extracellular bicarbonate (called a contraction alkalosis). (See "Causes of metabolic alkalosis".)

An elevated bicarbonate concentration is maintained by conditions that reduce bicarbonate filtration, enhance bicarbonate reabsorption, or impair bicarbonate secretion, and thereby prevent rapid excretion of the excess bicarbonate in the urine. Rapid bicarbonate excretion would otherwise correct the alkalosis [1,4].


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Literature review current through: Sep 2016. | This topic last updated: Mar 28, 2016.
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