DISEASE OF THE MONTH Metabolic Alkalosis

Metabolic alkalosis is common—half of all acid-base disorders as described in one study (1). This observation should not be surprising since vomiting, the use of chloruretic diuretics, and nasogastric suction are common among hospitalized patients. The mortality associated with severe metabolic alkalosis is substantial; a mortality rate of 45% in patients with an arterial blood pH of 7.55 and 80% when the pH was greater than 7.65 has been reported (2). Although this relationship is not necessarily causal, severe alkalosis should be viewed with concern, and correction by the appropriate intervention should be undertaken with dispatch when the arterial blood pH exceeds 7.55. Metabolic alkalosis occurs when a primary pathophysiologic process leads to the net accumulation of base within or the net loss of acid from the extracellular fluid (ECF); typically, the intracellular compartment becomes more acidic in potassiumdepletion alkalosis (3). Unopposed by other primary acid-base disorders, metabolic alkalosis is recognized by increases in both arterial blood pH—alkalemia—and plasma bicarbonate concentration. The increase in arterial blood pH promptly, normally, and predictably depresses ventilation resulting in increased PaCO2 and the buffering of the alkalemia. The PaCO2 increases about 0.5 to 0.7 mmHg for every 1.0 mM increase in plasma HCO3 concentration (4). Although a PaCO2 greater than 55 mmHg is uncommon, compensatory increases to 60 mmHg have been documented in severe metabolic alkalosis. Failure of an appropriate compensatory increase in PaCO2 should be interpreted as a mixed acid-base disturbance in which a stimulus to hyperventilation—primary respiratory alkalosis—accompanies primary metabolic alkalosis.