Abstract
AimsTreatment of arrhythmias evoked by hypothermia/rewarming remains challenging, and the underlying mechanisms are unclear. This in vitro experimental study assessed cardiac electrophysiology in isolated rabbit hearts at temperatures occurring in therapeutic and accidental hypothermia.Methods and resultsDetailed ECG, surface electrogram, and panoramic optical mapping were performed in isolated rabbit hearts cooled to moderate (31°C) and severe (17°C) hypothermia. Ventricular activation was unchanged at 31°C while action potential duration (APD) was significantly prolonged (176.9 ± 4.2 ms vs. 241.0 ± 2.9 ms, P < 0.05), as was ventricular repolarization. At 17°C, there were proportionally similar delays in both activation and repolarization. These changes were reflected in the QRS and QT intervals of ECG recordings. Ventricular fibrillation threshold was significantly reduced at 31°C (16.3 ± 3.1 vs. 35 ± 3.5 mA, P < 0.05) but increased at 17°C (64.2 ± 9.9, P < 0.05). At 31°C, transverse conduction was relatively unchanged by cooling compared to longitudinal conduction, but at 17°C both transverse and longitudinal conduction were proportionately reduced to a similar extent. The gap junction uncoupler heptanol had a larger relative effect on transverse than longitudinal conduction and was able to restore the transverse/longitudinal conduction ratio, returning ventricular fibrillation threshold to baseline values (16.3 ± 3.1 vs. 36.3 ± 4.3 mA, P < 0.05) at 31°C. Rewarming to 37°C restored the majority of the electrophysiological parameters.ConclusionsModerate hypothermia does not significantly change ventricular conduction time but prolongs repolarization and is pro-arrhythmic. Further cooling to severe hypothermia causes parallel changes in ventricular activation and repolarization, changes which are anti-arrhythmic. Therefore, relative changes in QRS and QT intervals (QR/QTc) emerge as an ECG-biomarker of pro-arrhythmic activity. Risk for ventricular fibrillation appears to be linked to the relatively low temperature sensitivity of ventricular transmural conduction, a conclusion supported by the anti-arrhythmic effect of heptanol at 31°C.
Highlights
Ventricular arrhythmias and cardiac arrest contribute to the high mortality rates observed in accidental hypothermia patients, reported between 29%1 and 80%.2 several case reports demonstrate successful resuscitation after hours of cardiac arrest and core temperatures below 20C.3 This neuroprotective effect of hypothermia is utilized during aortic arch surgery, using temperatures down to 15C.4 Hypothermia has been applied therapeutically in comatose survivors of cardiac arrest, where temperatures above 30C are considered safe.[5]
Risk for ventricular fibrillation appears to be linked to the relatively low temperature sensitivity of ventricular transmural conduction, a conclusion supported by the antiarrhythmic effect of heptanol at 31C
Further cooling to severe hypothermia levels (17C) causes parallel changes in transmural conduction and repolarization which appears anti-arrhythmic. These non-uniform changes in conduction and APD are reflected in QR and QT-intervals of the ECG and suggests QR/ QTc as a potential biomarker for pro-arrhythmic state during hypothermia; where a relative prolongation of the corrected QT-interval compared to QR-interval, as observed in moderate hypothermia (31C), indicates increased risk for ventricular arrhythmia
Summary
Ventricular arrhythmias and cardiac arrest contribute to the high mortality rates observed in accidental hypothermia patients, reported between 29%1 and 80%.2 several case reports demonstrate successful resuscitation after hours of cardiac arrest and core temperatures below 20C.3 This neuroprotective effect of hypothermia is utilized during aortic arch surgery, using temperatures down to 15C.4 Hypothermia has been applied therapeutically in comatose survivors of cardiac arrest, where temperatures above 30C are considered safe.[5]. Ventricular arrhythmias and cardiac arrest contribute to the high mortality rates observed in accidental hypothermia patients, reported between 29%1 and 80%.2. Several case reports demonstrate successful resuscitation after hours of cardiac arrest and core temperatures below 20C.3. This neuroprotective effect of hypothermia is utilized during aortic arch surgery, using temperatures down to 15C.4. Hypothermia has been applied therapeutically in comatose survivors of cardiac arrest, where temperatures above 30C are considered safe.[5] survival is possible after extreme accidental exposure, treatment of arrhythmias during rewarming is still challenging. Current guidelines provide only general suggestions for pharmacologic treatment,[6] which is based solely on pre-clinical studies.[7] In order to develop targeted anti-arrhythmic strategies in this specific situation, we need to understand the basis for proarrhythmia during cooling and rewarming
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