Metabolic alkalosis, which produces an elevation of the serum bicarbonate, is a relatively frequent clinical problem that is most commonly due to the loss of hydrogen ions from the gastrointestinal tract or in the urine. These lost hydrogen ions are derived from the dissociation of water into hydrogen and hydroxyl ions. When the hydrogen ion is removed, 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 as well as the development of hypochloremia and hypokalemia.
The plasma bicarbonate concentration may also be increased by hydrogen movement into the cells, alkali administration, or volume contraction around a relatively constant amount of extracellular bicarbonate (called a contraction alkalosis) (table 1) [1-4].
Patients with preserved renal function will most often rapidly excrete excess bicarbonate in the urine. Thus, for metabolic alkalosis to persist, there must be a reduction in the ability to excrete the excess bicarbonate in the urine. This is usually due to hypovolemia, reduced effective arterial blood volume (including heart failure and cirrhosis), chloride depletion, hypokalemia, renal impairment, 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".)
GASTROINTESTINAL HYDROGEN LOSS
Gastrointestinal hydrogen loss can result from the removal of gastric secretions (vomiting or nasogastric suction) or loss of intestinal secretions (some unusual causes of diarrhea).