Department of Medicine-Division of Cardiovascular Diseases, University of Alabama at Birmingham, Birmingham, Alabama 35294, USA.
Prehosp Emerg Care. 2010 Jan-Mar;14(1):62-70. doi: 10.3109/10903120903349838.
Since the initial development of the defibrillator, there has been concern that, while delivery of a large electric shock would stop fibrillation, it would also cause damage to the heart. This concern has been raised again with the development of the biphasic defibrillator.
To compare defibrillation efficacy, postshock cardiac function, and troponin I levels following 150-J and 360-J shocks.
Nineteen swine were anesthetized with isoflurane and instrumented with pressure catheters in the left ventricle, aorta, and right atrium. The animals were fibrillated for 6 minutes, followed by defibrillation with either low-energy (n = 8) or high-energy (n = 11) shocks. After defibrillation, chest compressions were initiated and continued until return of spontaneous circulation (ROSC). Epinephrine, 0.01 mg/kg every 3 minutes, was given for arterial blood pressure < 50 mmHg. Hemodynamic parameters were recorded for four hours. Transthoracic echocardiography was performed and troponin I levels were measured at baseline and four hours following ventricular fibrillation (VF).
Survival rates at four hours were not different between the two groups (low-energy, 5 of 8; high-energy, 7 of 11). Results for arterial blood pressure, positive dP/dt (first derivative of pressure measured over time, a measure of left ventricular contractility), and negative dP/dt at the time of lowest arterial blood pressure (ABP) following ROSC were not different between the two groups (p = not significant [NS]), but were lower than at baseline. All hemodynamic measures returned to baseline by four hours. Ejection fractions, stroke volumes, and cardiac outputs were not different between the two groups at four hours. Troponin I levels at four hours were not different between the two groups (12 +/- 11 ng/mL versus 21 +/- 26 ng/mL, p = NS) but were higher at four hours than at baseline (19 +/- 19 ng/mL versus 0.8 +/- 0.5 ng/mL, p < 0.05, groups combined).
Biphasic 360-J shocks do not cause more cardiac damage than biphasic 150-J shocks in this animal model of prolonged VF and resuscitation.
自除颤器最初开发以来,人们一直担心,尽管大电流电击可以终止纤维性颤动,但也会对心脏造成损害。随着双相除颤器的发展,这种担忧再次出现。
比较 150-J 和 360-J 电击后的除颤效果、电击后心功能和肌钙蛋白 I 水平。
19 头猪用异氟烷麻醉,并在左心室、主动脉和右心房内置入压力导管。动物被纤维性颤动 6 分钟,然后用低能量(n=8)或高能量(n=11)电击除颤。除颤后,立即开始胸外按压,直至自主循环(ROSC)恢复。当动脉血压<50mmHg 时,给予肾上腺素 0.01mg/kg,每 3 分钟一次。四小时内记录血流动力学参数。在心室颤动(VF)后基线和四小时进行经胸超声心动图检查,并测量肌钙蛋白 I 水平。
两组 4 小时生存率无差异(低能量组 5/8;高能量组 7/11)。两组动脉血压、正压力微分(压力随时间的变化率,左心室收缩力的衡量指标)和 ROSC 时最低动脉血压(ABP)时的负压力微分的结果无差异(p=不显著[NS]),但均低于基线。所有血流动力学指标在四小时内恢复到基线。两组 4 小时时射血分数、每搏量和心输出量无差异。两组 4 小时时肌钙蛋白 I 水平无差异(12±11ng/ml 与 21±26ng/ml,p=NS),但均高于基线(19±19ng/ml 与 0.8±0.5ng/ml,p<0.05,两组合并)。
在这种长时间 VF 和复苏的动物模型中,双相 360-J 电击不会比双相 150-J 电击引起更多的心脏损伤。