Abstract
IntroductionMild therapeutic hypothermia (MTH) is being used after cardiac arrest for its expected improvement in neurological outcome. Safety of MTH concerning inducibility of malignant arrhythmias has not been satisfactorily demonstrated. This study compares inducibility of ventricular fibrillation (VF) before and after induction of MTH in a whole body swine model and evaluates possible interaction with changing potassium plasma levels.MethodsThe extracorporeal cooling was introduced in fully anesthetized swine (n = 6) to provide MTH. Inducibility of VF was studied by programmed ventricular stimulation three times in each animal under the following: during normothermia (NT), after reaching the core temperature of 32°C (HT) and after another 60 minutes of stable hypothermia (HT60). Inducibility of VF, effective refractory period of the ventricles (ERP), QTc interval and potassium plasma levels were measured.ResultsStarting at normothermia of 38.7 (IQR 38.2; 39.8)°C, HT was achieved within 54 (39; 59) minutes and the core temperature was further maintained constant. Overall, the inducibility of VF was 100% (18/18 attempts) at NT, 83% (15/18) after reaching HT (P = 0.23) and 39% (7/18) at HT60 (P = 0.0001) using the same protocol. Similarly, ERP prolonged from 140 (130; 150) ms at NT to 206 (190; 220) ms when reaching HT (P < 0.001) and remained 206 (193; 220) ms at HT60. QTc interval was inversely proportional to the core temperature and extended from 376 (362; 395) at NT to 570 (545; 599) ms at HT. Potassium plasma level changed spontaneously: decreased during cooling from 4.1 (3.9; 4.8) to 3.7 (3.4; 4.1) mmol/L at HT (P < 0.01), then began to increase and returned to baseline level at HT60 (4.6 (4.4; 5.0) mmol/L, P = NS).ConclusionsAccording to our swine model, MTH does not increase the risk of VF induction by ventricular pacing in healthy hearts. Moreover, when combined with normokalemia, MTH exerts an antiarrhythmic effect despite prolonged QTc interval.
Highlights
Mild therapeutic hypothermia (MTH) is being used after cardiac arrest for its expected improvement in neurological outcome
We hypothesized that MTH related hypokalemia together with prolongation of the QT interval might predispose the heart to greater electrical instability and lower ventricular fibrillation (VF) threshold
In our experimental study we have proven that MTH is safe in terms of inducibility of malignant ventricular tachyarrhythmias in healthy pig hearts
Summary
Mild therapeutic hypothermia (MTH) is being used after cardiac arrest for its expected improvement in neurological outcome. The occurrence of malignant ventricular tachyarrhythmias during MTH still remains a major cause of death considering predisposing factors such as myocardial ischemia/reperfusion damage, often reported hypokalemia during the cooling phase [23,24,25], slowing of the heart rate and QT interval prolongation [25,26,27,28,29] The aim of this experimental study was to assess the safety of MTH in terms of inducibility of malignant ventricular tachyarrhythmias in relation to spontaneous changes of potassium plasma level and QT interval in a whole body pig model. We hypothesized that MTH related hypokalemia together with prolongation of the QT interval might predispose the heart to greater electrical instability and lower VF threshold
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