Cardiovascular performance and oxyhemoglobin dissociation after acetazolamide in metabolic alkalosis.

In patients with metabolic alkalosis, compensatory alveolar hypoventilation may induce hypercapnia and hypoxemia. In edematous or normally-hydrated patients without electrolyte deficiencies, acetazolamide--a carbonic anhydrase inhibitor--has been advocated to correct the primary acid-base disturbance, thereby preventing hypoxemia. The hemodynamic consequences and the effect on oxyhemoglobin dissociation of acetazolamide, were studied. Twelve critically ill patients with metabolic alkalosis were given 15 mg/kg body wt. acetazolamide intravenously. Cardiovascular performance was completely unchanged. The P50 was 26.6 mm Hg at the beginning and the end of the study, indicating that hemoglobin-oxygen affinity is unaffected by acetazolamide. In six patients, investigated after open-heart surgery, the arterial oxygen tension increased by 10-45%. This was probably related to the combined effects of slight reductions in total body oxygen consumption or shunting of venous blood through the lungs. Eight of the 12 patients were on controlled ventilation. After acetazolamide there was a mean increase in mixed venous carbon dioxide tension (PvCO2) of 4.5 mm Hg, with no increase in arterial carbon dioxide tension (PaCO2), indicating only a limited interference with carbon dioxide uptake and release of the carbonic anhydrase inhibition. No other adverse reactions were observed.