D N Thrush1, J B Downs, R A Smith. 1. Department of Anesthesiology, University of South Florida College of Medicine, Tampa 33612, USA.
Abstract
BACKGROUND: Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear. METHODS AND RESULTS: Forty-four anesthetized swine received an infusion of six inert gases. Animals underwent ventricular fibrillation with CPR and intravenous administration of saline (control), epinephrine (15 microg/kg), or methoxamine (150 microg/kg). Cardiac output, aortic blood pressure, pH, and arterial oxygen saturation were recorded. Distributions of VA and Q were determined by the multiple inert gas elimination technique. Ventricular fibrillation and CPR caused significant decreases in cardiac output, aortic blood pressure, and arterial pH. With epinephrine (versus saline), diastolic blood pressure was significantly higher (23+/-7 versus 8+/-4 mm Hg), but the increase in shunt (from 7+/-4% to 29+/-17%) and the reduction in SaO2 (from 99.7% to 76.8%) were significantly larger. Also, the increase in dead space was greater and elimination of CO2 less. There were no differences between animals given methoxamine or saline, except for increased diastolic blood pressure. CONCLUSIONS: During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt approximately 300% more than saline or methoxamine and significantly reduced arterial oxygen saturation. We suspect that the beta-adrenergic receptor activity of epinephrine attenuated hypoxic pulmonary vasoconstriction. Methoxamine is as effective a pressor as epinephrine for CPR and devoid of beta-adrenergic activity. We recommend that such an agent be considered, instead of epinephrine, for CPR.
BACKGROUND: Why pulmonary gas exchange deteriorates after administration of epinephrine during cardiopulmonary resuscitation (CPR) is unclear. METHODS AND RESULTS: Forty-four anesthetized swine received an infusion of six inert gases. Animals underwent ventricular fibrillation with CPR and intravenous administration of saline (control), epinephrine (15 microg/kg), or methoxamine (150 microg/kg). Cardiac output, aortic blood pressure, pH, and arterial oxygen saturation were recorded. Distributions of VA and Q were determined by the multiple inert gas elimination technique. Ventricular fibrillation and CPR caused significant decreases in cardiac output, aortic blood pressure, and arterial pH. With epinephrine (versus saline), diastolic blood pressure was significantly higher (23+/-7 versus 8+/-4 mm Hg), but the increase in shunt (from 7+/-4% to 29+/-17%) and the reduction in SaO2 (from 99.7% to 76.8%) were significantly larger. Also, the increase in dead space was greater and elimination of CO2 less. There were no differences between animals given methoxamine or saline, except for increased diastolic blood pressure. CONCLUSIONS: During experimental ventricular fibrillation and CPR, epinephrine increased intrapulmonary shunt approximately 300% more than saline or methoxamine and significantly reduced arterial oxygen saturation. We suspect that the beta-adrenergic receptor activity of epinephrine attenuated hypoxic pulmonary vasoconstriction. Methoxamine is as effective a pressor as epinephrine for CPR and devoid of beta-adrenergic activity. We recommend that such an agent be considered, instead of epinephrine, for CPR.