Janata Andreas, Bayegan Keywan, Weihs Wolfgang, Schratter Alexandra, Holzer Michael, Frossard Martin, Sipos Wolfgang, Springler Gregor, Schmidt Peter, Sterz Fritz, Losert Udo M, Laggner Anton N, Kochanek Patrick M, Behringer Wilhelm
Department of Emergency Medicine, Medical University of Vienna, Austria.
Crit Care Med. 2007 Dec;35(12):2785-91. doi: 10.1097/01.CCM.0000288103.86029.66.
Outcome after prolonged normovolemic cardiac arrest is poor, and new resuscitation strategies have to be found. We hypothesized that the induction of deep hypothermia for emergency preservation and resuscitation (EPR) during prolonged cardiac arrest, before the start of reperfusion, will mitigate the deleterious cascades leading to neuronal death and will thus improve outcome.
Prospective experimental study.
University research laboratory.
Thirteen pigs, Large White breed (27-37 kg).
After 15 mins of ventricular fibrillation, pigs were subjected to 1) EPR (n = 6), 20 mins of hypothermic stasis induced with a cold saline aortic flush; or 2) 20 mins of conventional resuscitation (n = 7). Then cardiopulmonary bypass was initiated in both groups, followed by defibrillation. Controlled ventilation and mild hypothermia were continued for 20 hrs; survival was for 9 days. For neurologic evaluation, neurologic deficit score (100% = brain dead, 0-10% = normal), overall performance category (1 = normal, 5 = dead or brain dead), and brain histologic damage score were used.
In the EPR group, brain temperature decreased from 38.5 degrees C +/- 0.2 degrees C to 16.7 degrees C +/- 2.5 degrees C within 235 +/- 27 secs. Five animals achieved restoration of spontaneous circulation and survived to 9 days: two pigs with overall performance category 2 and three pigs with overall performance category 3. Their neurologic deficit score was 45% (interquartile range 35, 50) and histologic damage score was 142 (interquartile range 109, 159). In the control group, four pigs achieved restoration of spontaneous circulation: one survived to 9 days with overall performance category 3, neurologic deficit score 45%, and histologic damage score 226 (restoration of spontaneous circulation, p = .6; survival, p = .03; overall performance category, p = .02).
EPR is feasible in an experimental pig model and improves survival after prolonged cardiac arrest in pigs. Further experimental studies are needed before this concept can be brought into clinical practice.
长时间正常血容量性心脏骤停后的预后较差,必须找到新的复苏策略。我们假设在长时间心脏骤停期间、再灌注开始前,诱导深度低温用于紧急保存和复苏(EPR),将减轻导致神经元死亡的有害级联反应,从而改善预后。
前瞻性实验研究。
大学研究实验室。
13头大白猪(体重27 - 37千克)。
心室颤动15分钟后,猪被分为两组:1)EPR组(n = 6),用冷盐水主动脉冲洗诱导20分钟低温停滞;2)传统复苏组(n = 7),进行20分钟传统复苏。然后两组均开始体外循环,随后进行除颤。持续控制通气和轻度低温20小时;观察9天的生存情况。神经功能评估采用神经功能缺损评分(100% = 脑死亡,0 - 10% = 正常)、总体表现分类(1 = 正常,5 = 死亡或脑死亡)和脑组织学损伤评分。
在EPR组,脑温在235±27秒内从38.5℃±0.2℃降至16.7℃±2.5℃。5只动物实现自主循环恢复并存活9天:2只总体表现分类为2级的猪和3只总体表现分类为3级的猪。它们的神经功能缺损评分为45%(四分位间距35, 50),组织学损伤评分为142(四分位间距109, 159)。在对照组,4只猪实现自主循环恢复:1只存活9天,总体表现分类为3级,神经功能缺损评分为45%,组织学损伤评分为226(自主循环恢复,p = 0.6;生存,p = 0.03;总体表现分类,p = 0.02)。
EPR在实验猪模型中是可行的,可提高猪长时间心脏骤停后的生存率。在将这一概念应用于临床实践之前,还需要进一步的实验研究。