Changes in Ventricular Fibrillation Threshold During Acute Hypothermia. A Model for Future Studies

Abstract

Hypothermia and rewarming are associated with an increased incidence of lethal arrhythmias in man. The relationship between reduction in body temperature and ventricular fibrillation threshold was studied in 7 pentobarbital anaesthetized dogs using programmable electrical stimulation while cooling and rewarming between 37 degrees C and 25 degrees C in steps of 3 degrees C. Fibrillation threshold was defined as the number of extrastimuli required to evoke ventricular fibrillation. QRS-durations and corrected QT-intervals (QTc) were measured from surface electrocardiograms. Monophasic action potential durations were recorded from the base and apex of the heart. Fibrillation threshold decreased with decreasing temperatures; e.g., at 37 degrees C ventricular fibrillation was not inducible after 5 extrastimuli, while at 25 degrees C only 2 extrastimuli were required. From 37 degrees C to 25 degrees C QRS-width, monophasic action potential durations and QTc increased while conduction velocity decreased. The differential effects on conduction and monophasic action potential duration provide a basis for induction of ventricular fibrillation during acute hypothermia. This model of hypothermia-induced ventricular fibrillation should prove useful for future studies aimed at understanding the mechanisms responsible for hypothermia-related deaths.

Moderate hypothermia increases the chance of spiral wave collision in favor of self-termination of ventricular tachycardia/fibrillation

“…Most previous studies in humans and animals have shown that hypothermia is associated with increased susceptibility for ventricular arrhythmias and VF (18,23), and this effect has been related to the slowing of conduction, a heterogeneous increase in ventricular repolarization and the dispersion of refractoriness (21). However, there is experimental evidence suggesting the antiarrhythmic therapeutic potential of hypothermia (7,10).…”

Pentobarbital versus medetomidine-ketamine-fentanyl anaesthesia: effects on haemodynamics and the incidence of ischaemia-induced ventricular fibrillation in swine

“…However, in the present study, swine anaesthetized with medetomidineketamine-fentanyl showed a substantially higher incidence of ischaemia-induced ventricular brillation than swine anaesthetized with pentobarbital. This nding cannot be ascribed to differences in known determinants of ischaemia-induced ventricular brillation such as pre-ischaemic heart rate (Wainwright & Parratt 1993), body temperature (Mouritzen & Andersen 1966, Mortensen et al 1993, size of ischaemic area (Verdouw & Hartog 1986), collateral blood ow (Yoshida & Downey 1986, von Mutius et al 1988, and arterial pH (Dong et al 1967). A positive correlation between pre-ischaemic heart rate and occurrence of VF during ischaemia has been shown in swine (Wainwright & Parratt 1993).…”

Effects of acute reduction of temperature on ventricular fibrillation activation patterns

“…maximum rate of phase 0 of the action potential, the conduction velocity, the peak potentials reached during depolarization (19,27,28,31), and the delayed rectifier and inwardly rectifying potassium currents (10,15,27). Hypothermia is associated with an increased susceptibility for ventricular arrhythmias and ventricular fibrillation (VF) (2,19,20,30,31), and this effect has been related to slowing of conduction, a heterogeneous increase in ventricular repolarization, and the dispersion of refractoriness (25,29).…”

“…Hypothermia is associated with an increased susceptibility for ventricular arrhythmias and ventricular fibrillation (VF) (2,19,20,30,31), and this effect has been related to slowing of conduction, a heterogeneous increase in ventricular repolarization, and the dispersion of refractoriness (25,29). On the other hand, myocardial cooling has also been used to modify different cardiac rhythm disturbances.…”

“…The activation patterns during VF depend on the electrophysiological properties of myocardial cells (4,5,14,16,18,23,33,36), and these properties are temperature dependent (1,2,10,15,19,(27)(28)(29)31). Thus hypothermia can influence the mechanisms that intervene in the sustaining of VF, and we hypothesized that a rapid and profound reduction of myocardial temperature impedes the maintenance of VF, leading to termination of the arrhythmia.…”