Metabolic alkalosis results from the loss of acid or the increase of base.

Causes of acid loss include vomiting, nasogastric (NG) tube drainage or lavage without adequate electrolyte replacement, fistulas, and the use of steroids and certain diuretics (furosemide, thiazides, and ethacrynic acid). Hyperadrenocorticism is another cause of severe acid loss. Cushing’s disease, primary hyperaldosteronism, and Bartter’s syndrome, for example, all lead to retention of sodium and chloride and urinary loss of potassium and hydrogen.

Excessive retention of base can result from excessive intake of bicarbonate of soda or other antacids (usually for treatment of gastritis or peptic ulcer), excessive intake of absorbable alkali (as in milk-alkali syndrome, commonly seen in patients with peptic ulcers), administration of excessive amounts of I.V. fluids with high concentrations of bicarbonate or lactate, massive blood transfusions, or respiratory insufficiency.

Untreated metabolic alkalosis may result in coma, atrioventricular (AV) arrhythmias, and death.

The patient’s history (obtained from a family member, if necessary) may disclose such risk factors as excessive ingestion of alkali antacids. The history may include extracellular fluid (ECF) volume depletion, which is commonly associated with conditions leading to metabolic alkalosis (for example, vomiting or NG tube suctioning). The patient or a family member may report irritability, belligerence, and paresthesia.

Inspection may reveal the presence of tetany if serum calcium levels are borderline or low. The rate and depth of the patient’s respirations may be decreased as a compensatory mechanism; however, this mechanism is limited because of the development of hypoxemia, which stimulates ventilation.