The pathophysiology, symptomatology, and treatment of metabolic alkalosis are reviewed, with emphasis on treatment with intravenous hydrochloric acid. Three buffering systems are used by the body to correct an arterial pH above 7.45--tissue, respiratory, and renal systems. The kidneys have the primary responsibility for correcting a severe metabolic alkalosis, but several conditions (e.g., severe volume contraction) can interfere with the renal mechanisms. No unique symptoms are associated with metabolic alkalosis. Conventional conservative treatment of metabolic alkalosis involves meeting the patient's fluid and electrolyte needs and allowing the body to correct the alkalosis through its own mechanisms. However, when more rapid resolution of the alkalosis is needed or the patient cannot tolerate fluid and electrolyte therapy, mineral acids may be administered. Ammonium chloride and arginine monohydrochloride infusions may both be used; since both require hepatic conversion for full activity, patients with hepatic dysfunction may require alternative therapy. Dilute hydrochloric acid (0.1-0.2 N) may be given intravenously to these patients through a central-venous catheter. Dosage guidelines and formulation procedures are described in the paper, as are other possible therapeutic alternatives (dialysis, acetazolamide, cimetidine). Most cases of metabolic alkalosis can be managed with fluid and electrolyte therapy. When metabolic alkalosis needs to be resolved quickly or when conventional therapy cannot be tolerated, mineral acid administration should be instituted. The primary drug of choice for these patients is intravenous ammonium chloride; patients with hepatic or severe renal dysfunction should receive dilute hydrochloric acid via a central-venous catheter.