Effects of ethanol on systemic hemodynamics in a porcine model of accidental hypothermia

Abstract

ObjectivesAccidental hypothermia is frequently associated with ethanol intoxication. Each has independent effects on systemic hemodynamics, but their combined effects are poorly understood. We aimed to describe the hemodynamic effects of ethanol intoxication in a model of severe hypothermia and rewarming. MethodsAnesthetized pigs was assigned to control (n = 8) or ethanol groups (ETOH) (n = 7, 3 mg/kg of ethanol via an orogastric tube). Subjects were cooled to 25°C using ice packs and then warmed to baseline core temperature with passive external and active core rewarming. ResultsIn the ETOH group, peak serum ethanol concentration was 202 mg/dL at 25°C. Ethanol had no effect on time of cooling or rewarming. In both the control and ETOH, there were similar maximal decreases in mean arterial pressure (from 94 ± 24 to 50 ± 15 mm Hg and 100 ± 27 to 31 ± 12 mm Hg, respectively), ventricular contractility (rate of maximal left ventricular pressure rise from 5731 ± 1462 to 2610 ± 596 mm Hg/s and 6832 ± 1384 to 1937 ± 437 mm Hg/s, respectively), and cardiac output (from 2.14 ± 0.8 to 0.53 ± 0.3 L/min and 2.93 ± 0.9, to 0.44 ± 0.2 L/min, respectively; all P < .001). After rewarming, only in the ETOH group were persistent decreases in mean arterial pressure (59 ± 14 mm Hg), contractility (3982 ± 1573 mm Hg/s), and cardiac output (1.6 ± 0.9 L/min, all P < .03) observed. ConclusionsHypothermia caused significant adverse effects on cardiac function and systemic hemodynamics, which returned to baseline with rewarming. Ethanol intoxication had no additional effects on systemic hemodynamics during cooling; however, it caused more prolonged depression of cardiac function and adverse effects on systemic hemodynamics during rewarming. These data may have implications for resuscitation of ethanol-intoxicated victims of accidental hypothermia.