Abstract

Aims: Rewarming from accidental hypothermia and therapeutic temperature management could be complicated by cardiac dysfunction. Although pharmacologic support is often applied when rewarming these patients, updated treatment recommendations are lacking. There is an underlying deficiency of clinical and experimental data to support such interventions and this prevents the development of clinical guidelines. Accordingly, we explored the clinical effects of epinephrine during hypothermic conditions.Materials and methods: Anesthetized pigs were immersion cooled to 32°C. Predetermined variables were compared at temperature/time-point baseline, after receiving 30 ng/kg/min and 90 ng/kg/min epinephrine infusions: (1) before and during hypothermia at 32°C, and after rewarming to 38°C (n = 7) and (2) a time-matched (5 h) normothermic control group (n = 5).Results: At 32°C, both stroke volume and cardiac output were elevated after 30 ng/kg/min administration, while systemic vascular resistance was reduced after 90 ng/kg/min. Epinephrine infusion did not alter blood flow in observed organs, except small intestine flow, and global O2 extraction rate was significantly reduced in response to 90 ng/kg/min infusion. Electrocardiographic measurements were unaffected by epinephrine infusion.Conclusion: Administration of both 30 ng/kg/min and 90 ng/kg/min at 32°C had a positive inotropic effect and reduced afterload. We found no evidence of increased pro-arrhythmic activity after epinephrine infusion in hypothermic pigs. Our experiment therefore suggests that β₁-receptor stimulation with epinephrine could be a favorable strategy for providing cardiovascular support in hypothermic patients, at core temperatures >32°C.

Highlights

  • Guidelines for targeted temperature management (TTM) and therapeutic hypothermia recommend reducing core temperatures to 36–32°C for neuroprotection in comatose patients after resuscitation from sudden cardiac arrest (Nolan et al, 2015)

  • We found that low dose (0.125 μg/min) Epi compared to high dose (1.25 μg/min) gave positive inotropic effect during hypothermia (28°C; Tveita and Sieck, 2011)

  • Hemodynamics Compared to baseline values, hemodynamic responses were identical in the two groups (Figures 2–4)

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Summary

Introduction

Guidelines for targeted temperature management (TTM) and therapeutic hypothermia recommend reducing core temperatures to 36–32°C for neuroprotection in comatose patients after resuscitation from sudden cardiac arrest (Nolan et al, 2015). After return of spontaneous circulation, these patients often suffer acute heart failure and need inotropic drugs to support inadequate circulatory function (Bernard et al, 2002; Safar and Kochanek, 2002). Temperatures similar to those used in TTM are regularly observed in victims of accidental hypothermia. These patients often display hypothermia-induced cardiac dysfunction (HCD), associated with reduced cardiac output (CO) during rewarming. Despite its frequent use as an inotropic agent, little is known about the clinical effects of epinephrine (Epi) in TTM patients and victims of accidental hypothermia. It is vital to acquire more translational data to understand the pharmacological properties of Epi at low core temperatures

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