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

Abstract

☆ Sources of fundings: This study was supported by Haa Sinai Medical Center (Cleveland, OH) (GL) and a Depar Foundation Grant from the MetroHealth Medical Center ( ☆☆ The authors have no conflicts of interest related to th an investigator-directed research grant from Gilead Scienc to this work. ⁎ Corresponding author at: Heart and Vascular Researc Case Western Reserve University, 2500, MetroHealth D Tel.: +1 216 778 5293; fax: +1 216 778 7342. E-mail address: lwilson@metrohealth.org (L.D. Wilson http://dx.doi.org/10.1016/j.ajem.2015.07.012 0735-6757/© 2015 Elsevier Inc. All rights reserved. Article history: Received 18 May 2015 Received in revised form 14 July 2015 Accepted 14 July 2015 Objectives: Accidental 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. Methods:Anesthetized pigswas assigned to control (n=8) or ethanol groups (ETOH) (n=7, 3mg/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. Results: In 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 b .001). After rewarming, only in the ETOH group were persistent decreases in mean arterial pressure (59 ± 14 mmHg), contractility (3982 ± 1573 mmHg/s), and cardiac output (1.6 ± 0.9 L/min, all P b .03) observed. Conclusions:Hypothermia 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. © 2015 Elsevier Inc. All rights reserved.