Spinelli Elena, Davis Ryan P, Ren Xiaodan, Sheth Parth S, Tooley Trevor R, Iyengar Amit, Sowell Brandon, Owens Gabe E, Bocks Martin L, Jacobs Teresa L, Yang Lynda J, Stacey William C, Bartlett Robert H, Rojas-Peña Alvaro, Neumar Robert W
1Extracorporeal Life Support Laboratory, Department of Surgery, University of Michigan, Ann Arbor, MI. 2Department of Anesthesia, Critical Care, and Pain Medicine, University of Milano, Milano, Italy. 3Department of Emergency Medicine, University of Michigan, Ann Arbor, MI. 4Michigan Center for Integrative Research in Critical Care (MCIRCC), University of Michigan, Ann Arbor, MI. 5Department of Pediatric Cardiology, University of Michigan, Ann Arbor, MI. 6Department of Neurology, University of Michigan, Ann Arbor, MI. 7Department of Neurosurgery, University of Michigan, Ann Arbor, MI. 8Department of Biomedical Engineering, University of Michigan, Ann Arbor, MI. 9Department of Surgery, Section of Transplantation, University of Michigan, Ann Arbor, MI.
Crit Care Med. 2016 Feb;44(2):e58-69. doi: 10.1097/CCM.0000000000001305.
To investigate the effects of the combination of extracorporeal cardiopulmonary resuscitation and thrombolytic therapy on the recovery of vital organ function after prolonged cardiac arrest.
Laboratory investigation.
University laboratory.
Pigs.
Animals underwent 30-minute untreated ventricular fibrillation cardiac arrest followed by extracorporeal cardiopulmonary resuscitation for 6 hours. Animals were allocated into two experimental groups: t-extracorporeal cardiopulmonary resuscitation (t-ECPR) group, which received streptokinase 1 million units, and control extracorporeal cardiopulmonary resuscitation (c-ECPR), which did not receive streptokinase. In both groups, the resuscitation protocol included the following physiologic targets: mean arterial pressure greater than 70 mm Hg, cerebral perfusion pressure greater than 50 mm Hg, PaO2 150 ± 50 torr (20 ± 7 kPa), PaCO2 40 ± 5 torr (5 ± 1 kPa), and core temperature 33°C ± 1°C. Defibrillation was attempted after 30 minutes of extracorporeal cardiopulmonary resuscitation.
A cardiac resuscitability score was assessed on the basis of success of defibrillation, return of spontaneous heart beat, weanability from extracorporeal cardiopulmonary resuscitation, and left ventricular systolic function after weaning. The addition of thrombolytic to extracorporeal cardiopulmonary resuscitation significantly improved cardiac resuscitability (3.7 ± 1.6 in t-ECPR vs 1.0 ± 1.5 in c-ECPR). Arterial lactate clearance was higher in t-ECPR than in c-ECPR (40% ± 15% vs 18% ± 21%). At the end of the experiment, the intracranial pressure was significantly higher in c-ECPR than in t-ECPR. Recovery of brain electrical activity, as assessed by quantitative analysis of electroencephalogram signal, and ischemic neuronal injury on histopathologic examination did not differ between groups. Animals in t-ECPR group did not have increased bleeding complications, including intracerebral hemorrhages.
In a porcine model of prolonged cardiac arrest, t-ECPR improved cardiac resuscitability and reduced brain edema, without increasing bleeding complications. However, early electroencephalogram recovery and ischemic neuronal injury were not improved.
探讨体外心肺复苏与溶栓治疗联合应用对长时间心脏骤停后重要器官功能恢复的影响。
实验室研究。
大学实验室。
猪。
动物经历30分钟未经处理的室颤性心脏骤停,随后进行6小时的体外心肺复苏。动物被分为两个实验组:t-体外心肺复苏(t-ECPR)组,接受100万单位链激酶;对照体外心肺复苏(c-ECPR)组,不接受链激酶。两组的复苏方案均包括以下生理目标:平均动脉压大于70 mmHg,脑灌注压大于50 mmHg,PaO2 150±50 torr(20±7 kPa),PaCO2 40±5 torr(5±1 kPa),核心体温33°C±1°C。体外心肺复苏30分钟后尝试除颤。
根据除颤成功、自主心跳恢复、体外心肺复苏脱机能力以及脱机后的左心室收缩功能评估心脏复苏能力评分。体外心肺复苏联合溶栓显著提高了心脏复苏能力(t-ECPR组为3.7±1.6,c-ECPR组为1.0±1.5)。t-ECPR组的动脉血乳酸清除率高于c-ECPR组(40%±15%对18%±21%)。实验结束时,c-ECPR组的颅内压显著高于t-ECPR组。通过脑电图信号定量分析评估的脑电活动恢复以及组织病理学检查中的缺血性神经元损伤在两组间无差异。t-ECPR组动物未出现包括脑出血在内的出血并发症增加。
在长时间心脏骤停的猪模型中,t-ECPR提高了心脏复苏能力并减轻了脑水肿,且未增加出血并发症。然而,早期脑电图恢复和缺血性神经元损伤并未得到改善。