Key result
Mild therapeutic hypothermia cuts VF inducibility by ~61% versus normothermia in a healthy swine model.
Why the study?
Safety of mild therapeutic hypothermia concerning inducibility of malignant arrhythmias has not been satisfactorily demonstrated.
Does mild therapeutic hypothermia reduce the inducibility of ventricular fibrillation in a swine model?
Does mild therapeutic hypothermia reduce the inducibility of ventricular fibrillation in a swine model?
Absolute Event Rate: 39% vs 100%
p-value: p=0.0001
Mild therapeutic hypothermia does not increase the risk of VF induction in healthy swine hearts and may exert an antiarrhythmic effect when combined with normokalemia.
Should not change clinical VF management; hypothesis-generating for mild hypothermia's antiarrhythmic effects in translational models.
INTRODUCTION: Mild 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. METHODS: The 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. RESULTS: Starting 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). CONCLUSIONS: According 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.
No takes yet. Share an insight, caveat, or question.
Kudlička et al. (2015) studied Healthy swine model (n=6). Mild therapeutic hypothermia vs. Normothermia (38.7°C) was evaluated on Inducibility of ventricular fibrillation (p=0.0001). Mild therapeutic hypothermia maintained for 60 minutes significantly reduced the inducibility of ventricular fibrillation from 100% at normothermia to 39% in a healthy swine model.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: