Resistance to ventricular fibrillation predicted by the QRS/QTc - Ratio in an intact rat model of hypothermia/rewarming

Erik Sveberg Dietrichs,Anders Lund Selli,Timofei Kondratiev,Karen Mcglynn,Godfrey Smith,Torkjel Tveita

doi:10.1016/j.cryobiol.2021.01.003

Abstract

Accidental hypothermia is associated with increased risk for arrhythmias. QRS/QTc is proposed as an ECG-marker, where decreasing values predict hypothermia-induced ventricular arrhythmias. If reliable it should also predict nonappearance of arrhythmias, observed in species like rat that regularly tolerate prolonged hypothermia.A rat model designed for studying cardiovascular function during cooling, hypothermia and subsequent rewarming was chosen due to species-dependent resistance to ventricular arrhythmias. ECG was recorded throughout the protocol.No ventricular arrhythmias occurred during experiments. QRS/QTc increased throughout the cooling period and remained above normothermic baseline until rewarmed.Different from the high incidence of hypothermia-induced ventricular arrhythmias in accidental hypothermia patients, where QRS/QTc ratio is decreased in moderate hypothermia; hypothermia and rewarming of rats is not associated with increased risk for ventricular fibrillation. This resistance to lethal hypothermia-induced arrhythmias was predicted by QRS/QTc.

Highlights

Hypothermia is defined as a reduction of core-temperature to below 35 ◦C [17]
Different from the high incidence of hypothermia-induced ventricular arrhythmias in accidental hypothermia patients, where QRS/QTc ratio is decreased in moderate hypothermia; hypothermia and rewarming of rats is not associated with increased risk for ventricular fibrillation
In a series of recent preclinical experiments, we have investigated the pathophysiology of hypothermia-induced ven tricular fibrillation (VF) and cardiac arrest (HCA) [6,7,8]

Summary

Introduction

The neuroprotective effect of hypothermia is undisputed, but it is questioned whether therapeutic hypothermia, with core tempera ture reduction below 35 ◦C, should be initiated in comatose survivors of cardiac arrest [3]. Similar neuroprotection is obvious in victims of accidental hypothermia, where survival after several hours of cardiac arrest is reported after core-temperature reduction down to 13.7 ◦C [10]. Neuroprotective effects of hypothermia are present at temperatures where increased risk for arrhythmias and cardiac arrest occur, a wellknown complication of hypothermia [8]. The underlying mechanisms causing pro-arrhythmic activity in hypothermia, are not well known. This lack of evidence-based knowledge is reflected by guidelines for treating victims of accidental hypothermia, where recommendations for prevention and treatment of hypothermia-induced arrhythmias are missing [23]

Methods

Results

Discussion

Conclusion