• N H Mark, J M Leung, A I Arieff, and D T Mangano.
• Department of Anesthesia, Department of Veterans Affairs Medical Center, San Francisco, CA 94121.
• Crit. Care Med. 1993 May 1;21(5):659-65.

ObjectivesRecent recommendations suggest that sodium bicarbonate may not be useful for the treatment of metabolic acidosis. However, these recommendations are based primarily on both clinical studies and animal models of metabolic acidosis with arterial hypoxemia (PaO2 of < 80 torr [< 10.7 kPa]). This study was designed to determine the safety and physiologic effects of low-dose sodium bicarbonate in humans who developed intraoperative metabolic acidosis in the absence of hypoxemia.DesignProspective, double-blind, randomized trial.SettingVeterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco).PatientsWe prospectively studied 40 patients with coronary artery disease who underwent major surgery and developed mild intraoperative metabolic acidosis (decrease of plasma bicarbonate by > 3 mM).InterventionsPatients were randomly assigned to receive either sodium bicarbonate (n = 20) or sodium chloride (n = 20) by intravenous bolus, up to a maximum dose of 88 mmol of sodium.Measurements And Main ResultsBicarbonate treatment significantly increased the mean arterial pH from 7.36 to 7.39; the mean serum bicarbonate concentration from 21 to 25 mmol/L; and PCO2 from 41 to 44 torr (5.5 to 5.9 kPa). Total body oxygen consumption and lactate production did not change. Similarly, no adverse changes occurred in systemic or pulmonary arterial pressures or in cardiac ejection fraction. After bicarbonate administration, both the cardiac output and systemic oxygen consumption decreased by 8% to 11%, while both variables increased by 13% after sodium chloride administration; but, none of the changes was significant. One patient in the bicarbonate group developed myocardial ischemia, compared with three patients in the saline group.ConclusionsAdministration of sodium bicarbonate to well-oxygenated patients with mild metabolic acidosis resulted in a correction of the acidosis, without significant changes in cardiac output, total body oxygen use, or PaO2 (oxygen tension). These effects remain to be validated in patients with hypoxemia, more severe acidosis, or less stable circulation.

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