Epinephrine-mediated changes in carbon dioxide tension during reperfusion of ventricular fibrillation in a canine model.

Abstract

Previous studies suggest that epinephrine may alter the correlation of perfusion with measures of PCO2 during cardiopulmonary resuscitation. This study investigated the effects of epinephrine on PaCO2 and mixed venous PCO2 in a high-flow reperfusion model of cardiac arrest. Prospective, block randomized, blinded, placebo-controlled, laboratory study. Thirty mixed breed canines. After a 12-min ventricular fibrillation cardiac arrest, 30 mixed breed canines were reperfused with standardized (3200 revolutions/min) cardiopulmonary bypass and were given placebo (n = 10), standard dose epinephrine (0.02 mg/kg; n = 10), or high-dose epinephrine (0.2 mg/kg; n = 10). Arterial and mixed venous blood gases, coronary perfusion pressure, pump flow and peripheral vascular resistance were compared between groups during the early reperfusion period using analysis of variance with a post hoc Tukey's multiple comparison test. Baseline variables were similar between groups. With reperfusion, the high-dose epinephrine group had higher coronary perfusion pressures (p < .002), lower systemic pump flow (p < .01), and higher peripheral vascular resistance (p < .001). In the high-dose epinephrine group, both PaCO2 (high-dose epinephrine, 40 +/- 6 torr [5.3 +/- 0.8 kPa]; standard dose epinephrine, 45 +/- 7 torr [6.0 +/- 0.9 kPa]; placebo, 54 +/- 4 torr [7.2 +/- 0.5 kPa]; p < .01) and mixed venous PCO2 (high-dose epinephrine, 55 +/- 10 torr [7.3 +/- 1.3 kPa]; standard dose epinephrine, 57 +/- 9 torr [7.6 +/- 1.2 kPa]; placebo, 67 +/- 4 torr [8.9 +/- 0.5 kPa]; p < .05) were significantly decreased, and arterial pH, PaO2, and mixed venous PO2 were significantly increased compared with the placebo group. In this model, when ventilation and CO2 production are constant, the decrease in PaCO2 with epinephrine is due to decreased pulmonary blood flow (flow to membrane oxygenator) and peripheral shunting.