The added tubular dysfunction is suggested by concomitant hyperkalemia. Initial treatment aims to correct the underlying disease process. Acute complete correction of arterial pH is not a goal of therapy, and caution must be used to avoid volume and sodium overload. 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.
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.