Metabolic Alkalosis

A condition characterized by a primary increase in extracellular fluid bicarbonate; pH and carbon dioxide content are increased.

Metabolic alkalosis results from net acid loss or alkali gain in the extracellular fluid. Acid loss can result from vomiting, prolonged gastric suctioning, and diuretic use. The concomitant chloride deficiency requires that the high bicarbonate be reabsorbed with sodium and will not correct until adequate chloride ion is available (ie, treated with sodium chloride, potassium chloride, or hydrochloride). The chloride-resistant forms of metabolic alkalosis common in the elderly include an excessive mineralocorticoid effect of chronic prednisone administration, renin-angiotensin-aldosterone stimulation due to renal atherosclerosis, Cushing's disease, primary aldosteronism, and ectopic corticotropin (ACTH) production due to malignancy. In these cases, the mineralocorticoid excess dictates excessive renal generation of bicarbonate because of stimulated sodium/hydrogen exchange. Treatment is directed toward mineralocorticoid antagonism.

Lethargy and stupor may occur from adverse effects on the cerebral circulation. Arrhythmias, especially due to digitalis toxicity, are common. Therapy depends on whether the metabolic alkalosis is sensitive or resistant to chloride. The chloride-sensitive forms respond to administration of chloride, such as in normal saline. Gastric acid and chloride losses can be reduced by giving a histamine-2 blocker or a proton pump inhibitor. Bicarbonate diuresis can also be accomplished using carbonic anhydrase inhibition; acetazolamide 250 mg IV can be given bid or qid in severe cases or when patients are unable to take drugs orally. Chloride-resistant forms require treatment of the underlying disorder or mineralocorticoid antagonism with spironolactone. A dose of 50 to 100 mg/day po in divided doses may help patients with chronic alkalosis.