AIMS: Therapeutic hypothermia (TH) is used in neuroprotection following cardiac arrest due to ventricular tachycardia (VT) and ventricular fibrillation (VF). Accidental hypothermia is itself known to cause prolongation of the corrected QT interval (QTc). QTc prolongation can cause polymorphic VT and VF. If this also occurs in TH, it may induce refibrillation. We investigated the effect of TH on the QTc interval. METHODS AND RESULTS: Prospective case series of all patients undergoing TH following cardiac arrest following VT/VF at our hospital between July 2008 and January 2009. We studied the effect of temperature on QTc. All electrocardiograms (ECGs) undertaken during TH were studied and compared with the ECG prior to this. Four patients underwent TH. A total of 10 ECGs were undertaken during TH. The QTc was normal prior to TH. It became prolonged (>460 ms) in all cases during TH and normalized after cessation of TH, apart from Patient 4 who did not have an ECG post-TH since she died from cardiogenic shock. There was a negative correlation between temperature and QTc (Pearson's correlation coefficient, r= -0.71). CONCLUSION: Our series illustrates QTc prolongation during TH. This carries potential for refibrillation. Guidelines on ECG monitoring during TH are needed, especially since hypothermic myocardium is intrinsically prone to arrhythmias and commonly used antiarrythmic drugs such as amiodarone can prolong the QTc.
AIMS: Therapeutic hypothermia (TH) is used in neuroprotection following cardiac arrest due to ventricular tachycardia (VT) and ventricular fibrillation (VF). Accidental hypothermia is itself known to cause prolongation of the corrected QT interval (QTc). QTc prolongation can cause polymorphic VT and VF. If this also occurs in TH, it may induce refibrillation. We investigated the effect of TH on the QTc interval. METHODS AND RESULTS: Prospective case series of all patients undergoing TH following cardiac arrest following VT/VF at our hospital between July 2008 and January 2009. We studied the effect of temperature on QTc. All electrocardiograms (ECGs) undertaken during TH were studied and compared with the ECG prior to this. Four patients underwent TH. A total of 10 ECGs were undertaken during TH. The QTc was normal prior to TH. It became prolonged (>460 ms) in all cases during TH and normalized after cessation of TH, apart from Patient 4 who did not have an ECG post-TH since she died from cardiogenic shock. There was a negative correlation between temperature and QTc (Pearson's correlation coefficient, r= -0.71). CONCLUSION: Our series illustrates QTc prolongation during TH. This carries potential for refibrillation. Guidelines on ECG monitoring during TH are needed, especially since hypothermic myocardium is intrinsically prone to arrhythmias and commonly used antiarrythmic drugs such as amiodarone can prolong the QTc.
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