SAFETY AND EFFICACY OF INTRAVENOUS CARBICARB(R) IN PATIENTS UNDERGOING SURGERY - COMPARISON WITH SODIUM-BICARBONATE IN THE TREATMENT OF MILD METABOLIC-ACIDOSIS

Objectives: To compare the safety and efficacy of intravenous Carbicar b(R) with intravenous sodium bicarbonate in well-oxygenated patients w ho developed metabolic acidosis while undergoing major surgery. Carbic arb is an equimolar solution of sodium bicarbonate and sodium carbonat e (Na2CO3). It does not undergo significant breakdown to CO2 and H2O, nor does it increase CO2 concentrations to the same extent as does pur e sodium bicarbonate. Because of these characteristics, Carbicarb may be a more suitable agent than bicarbonate in the treatment of metaboli c acidosis. Design: Prospective, double-blind, randomized, multicenter trial. Setting: Veterans Affairs Medical Center (a teaching hospital of the University of California, San Francisco), and the University of Massachusetts Medical Center, Worcester, MA. Patients: We prospective ly studied 36 patients who underwent either cardiac surgery or major n oncardiac surgery and developed intraoperative metabolic acidosis (pH <7.35 and whose serum bicarbonate concentration decreased by >3 mmol). Interventions: Patients were randomly assigned to receive either sodiu m bicarbonate (1 mEq sodium/mL, n = 18) or 1 mol Carbicarb (1 mEq sodi um/mL, n = 18) administered by intravenous bolus over a 30-sec period. Measurements and Main Results: For Carbicarb-treated patients, the me an arterial pH increased from 7.31 +/- 0.008 (baseline) to 7.36 +/- 0. 009 10 mins after treatment; for the sodium bicarbonate-treated patien ts, the mean pH increased from 7.31 +/- 0.006 to 7.37 +/- 0.01. The in creases in pH were statistically significant for both groups (p = .000 1). There was no statistically significant difference between treatmen t groups in the number of repetitions of initial dose that was require d to correct acidosis. Hemodynamic variables remained unchanged in bot h treatment groups during the study period, with the exception of the mean cardiac output which increased from 6.1 +/- 0.4 (baseline) to 6.9 +/- 1.4 L/min (60 mins after treatment) in a subset of Carbicarb-trea ted patients and decreased from 6.7 +/- 1.3 to 6.0 +/- 1.2 L/min in a subset of sodium bicarbonate-treated patients, p = .048 (between group s); and the mean pulmonary artery occlusion pressure decreased from 19 +/- 2 mm Hg (baseline) to 8 +/- 3 mm Hg (45 mins after treatment) in the Carbicarb-treated patients, and decreased from 18 +/- 2 to 13 +/- 4 mm Hg in the sodium bicarbonate-treated patients, p = .012 (between groups). Systemic utilization of lactate increased from 0.3 +/- 1.0 mm ol/min (baseline) to 5.6 +/- 4.3 mmol/min (45 mins after treatment) in Carbicarb-treated patients, and increased from 1.0 +/- 0.6 mmol/min ( baseline) to 1.5 +/- 1.3 mmol/min in the sodium bicarbonate-treated pa tients, p = .033 (between groups). The administration of Carbicarb was safe. No patients were discontinued from the study because of adverse events. Conclusions: Carbicarb corrects metabolic acidosis as well as sodium bicarbonate. However, the potential therapeutic advantage of C arbicarb remains to be determined, especially in patients with more se vere metabolic acidosis.