Wisløff-Aase Kristin, Kerans Viesturs, Haugaa Kristina, Halvorsen Per Steinar, Skulstad Helge, Espinoza Andreas
Department of Anaesthesiology, Oslo University Hospital - Rikshospitalet, Nydalen, PO Box 4950, 0424, Oslo, Norway.
Institute of Clinical Medicine, Faculty of Medicine, University of Oslo, Oslo, Norway.
Intensive Care Med Exp. 2020 Dec 14;8(1):76. doi: 10.1186/s40635-020-00363-7.
Targeted hypothermia, as used after cardiac arrest, increases electrical and mechanical systolic duration. Differences in duration of electrical and mechanical systole are correlated to ventricular arrhythmias. The electromechanical window (EMW) becomes negative when the electrical systole outlasts the mechanical systole. Prolonged electrical systole corresponds to prolonged QT interval, and is associated with increased dispersion of repolarization and mechanical dispersion. These three factors predispose for arrhythmias. The electromechanical relations during targeted hypothermia are unknown. We wanted to explore the electromechanical relations during hypothermia at 33 °C. We hypothesized that targeted hypothermia would increase electrical and mechanical systolic duration without more profound EMW negativity, nor an increase in dispersion of repolarization and mechanical dispersion.
In a porcine model (n = 14), we registered electrocardiogram (ECG) and echocardiographic recordings during 38 °C and 33 °C, at spontaneous and atrial paced heart rate 100 beats/min. EMW was calculated by subtracting electrical systole; QT interval, from the corresponding mechanical systole; QRS onset to aortic valve closure. Dispersion of repolarization was measured as time from peak to end of the ECG T wave. Mechanical dispersion was calculated by strain echocardiography as standard deviation of time to peak strain.
Electrical systole increased during hypothermia at spontaneous heart rate (p < 0.001) and heart rate 100 beats/min (p = 0.005). Mechanical systolic duration was prolonged and outlasted electrical systole independently of heart rate (p < 0.001). EMW changed from negative to positive value (- 20 ± 19 to 27 ± 34 ms, p = 0.001). The positivity was even more pronounced at heart rate 100 beats/min (- 25 ± 26 to 41 ± 18 ms, p < 0.001). Dispersion of repolarization decreased (p = 0.027 and p = 0.003), while mechanical dispersion did not differ (p = 0.078 and p = 0.297).
Targeted hypothermia increased electrical and mechanical systolic duration, the electromechanical window became positive, dispersion of repolarization was slightly reduced and mechanical dispersion was unchanged. These alterations may have clinical importance. Further clinical studies are required to clarify whether corresponding electromechanical alterations are accommodating in humans.
心脏骤停后采用的目标性低温治疗可增加电收缩期和机械收缩期的时长。电收缩期和机械收缩期时长的差异与室性心律失常相关。当电收缩期长于机械收缩期时，机电延迟（EMW）变为负值。电收缩期延长对应QT间期延长，并与复极离散度和机械离散度增加相关。这三个因素易引发心律失常。目标性低温治疗期间的机电关系尚不清楚。我们想要探究33℃低温治疗期间的机电关系。我们假设目标性低温治疗会增加电收缩期和机械收缩期的时长，但不会使EMW更显著地变为负值，也不会增加复极离散度和机械离散度。
在猪模型（n = 14）中，我们记录了38℃和33℃时、自发心率和心房起搏心率为100次/分钟时的心电图（ECG）和超声心动图记录。EMW通过从相应的机械收缩期（QRS波起始至主动脉瓣关闭）中减去电收缩期（QT间期）来计算。复极离散度通过从ECG T波峰值到结束的时间来测量。机械离散度通过应变超声心动图计算为达到峰值应变时间的标准差。
在自发心率（p < 0.001）和心率为100次/分钟（p = 0.005）的低温治疗期间，电收缩期增加。机械收缩期时长延长，且独立于心率长于电收缩期（p < 0.001）。EMW从负值变为正值（-20±19至27±34毫秒，p = 0.001）。在心率为100次/分钟时，正值更为明显（-25±26至41±18毫秒，p < 0.001）。复极离散度降低（p = 0.027和p = 0.003），而机械离散度无差异（p = 0.078和p = 0.297）。
目标性低温治疗增加了电收缩期和机械收缩期的时长，机电延迟变为正值，复极离散度略有降低，机械离散度未改变。这些改变可能具有临床意义。需要进一步的临床研究来阐明人类是否也存在相应的适应性机电改变。
