Improved cerebral perfusion pressures and 24-hr neurological survival in a porcine model of cardiac arrest with active compression-decompression cardiopulmonary resuscitation and augmentation of negative intrathoracic pressure
Improved cerebral perfusion pressures and 24-hr neurological survival in a porcine model of cardiac arrest with active compression-decompression cardiopulmonary resuscitation and augmentation of negative intrathoracic pressure
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DOI：
10.1097/ccm.0b013e318246b9ad
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发表时间：
2012-06-01
影响因子：
8.8
通讯作者：
Yannopoulos, Demetris
中科院分区：
文献类型：
--
作者：
Metzger, Anja K.;Herman, Margot;Yannopoulos, Demetris
目的：在心肺复苏的减压阶段，胸腔内负压的产生增强了心脏的再充盈。我们验证了这一假设，即与每分钟80次的闭胸手动按压相比，以每分钟80次的胸外按压进行主动按压-减压心肺复苏，结合增加胸腔内负压可以降低颅内压并增加脑血流灌注，从而提高长期未经治疗的心脏骤停后神经功能完整的存活率。设计：前瞻性随机动物研究。地点：动物实验设施。对象：总共26头母猪，采用两种不同的方案(n=17和n=9)。干预、测量、主要结果：17头猪在未经治疗的情况下进行8.5分钟的室颤，随机分为两组，一组为心肺复苏组，另一组为心肺复苏组，按压速度为80次/分，主动按压-减压组为80次/分，外加阻抗阈值装置。主动加压-减压心肺复苏+阻抗阈值装置的冠状动脉灌注压(29.5+/-2.7 mm Hg比22.4+/-1.6 mm Hg，p=0.03)、颈动脉血流量(44.0+/-12.2比30.9+/-10.4，p=0.03)和24小时神经功能存活率(88%比22%，p=0.015)更高。在另外9头猪中测得的脑灌注压在主动按压-减压心肺复苏+阻抗阈值装置(21.9+/-1.2 mm Hgvs 8.9+/-0.8 mm Hg，p<；0.0001)中得到改善。主动加压-减压心肺复苏+阻抗阈值装置，减压时平均舒张压较低(12.2+/-0.2 mm Hgvs 16.6+/-1.2 mm Hg，p=0.02)，减压时颅内压曲线下斜率较大(-60.3+/-12.9 mm Hgvs-46.7+/-11.1 mm Hg/sec，p<；结论：主动加压-减压、心肺复苏+阻抗阈值装置在减压期增加了脑灌注压，降低了舒张压和颅内压。这些机制可能是在心脏骤停猪模型中观察到的脑灌流压、颈动脉血流量和存活率增加并具有良好的神经学结果的基础。(Crit Care Med 2012；40：1851-1856)
Objective: Generation of negative intrathoracic pressure during the decompression phase of cardiopulmonary resuscitation enhances the refilling of the heart. We tested the hypothesis that when compared with closed-chest manual compressions at 80 chest compressions per min, treatment with active compression-decompression cardiopulmonary resuscitation at 80 chest compressions/min combined with augmentation of negative intrathoracic pressure would lower intracranial pressure and increase cerebral perfusion, thereby improving neurologically intact survival rates following prolonged untreated cardiac arrest.Design: Prospective, randomized animal study.Setting: Animal laboratory facilities.Subjects: A total of 26 female farm pigs in two different protocols (n = 17 and n = 9).Interventions, Measurements, and Main Results: Seventeen pigs were subjected to 8.5 mins of untreated ventricular fibrillation and prospectively randomized to cardiopulmonary resuscitation at 80 chest compressions/min or active compression-decompression cardiopulmonary resuscitation at 80 chest compressions/min plus an impedance threshold device. Coronary perfusion pressures (29.5 +/- 2.7 mm Hg vs. 22.4 +/- 1.6 mm Hg, p = .03), carotid blood flow (44.0 +/- 12.2 vs. 30.9 +/- 10.4, p = .03), and 24-hr neurological survival (88% vs. 22%, p = .015) were higher with active compression-decompression cardiopulmonary resuscitation + an impedance threshold device. Cerebral perfusion pressures, measured in nine additional pigs, were improved with active compression-decompression cardiopulmonary resuscitation + an impedance threshold device (21.9 +/- 1.2mm Hg vs. 8.9 +/- 0.8 mm Hg, p < .0001). With active compression-decompression cardiopulmonary resuscitation + impedance threshold device, mean diastolic intracranial pressure during decompression was lower (12.2 +/- 0.2 mm Hg vs. 16.6 +/- 1.2 mm Hg, p = .02) and the downward slope of the decompression phase intracranial pressure curve was steeper (-60.3 +/- 12.9 mm Hg vs. -46.7 +/- 11.1 mm Hg/sec, p < .001).Conclusions: Active compression-decompression cardiopulmonary resuscitation + an impedance threshold device increased cerebral perfusion pressures and lowered diastolic intracranial pressure and intracranial pressure rate during the decompression phase. These mechanisms may underlie the observed increase in cerebral perfusion pressure, carotid blood flow, and survival rates with favorable neurologic outcomes in this pig model of cardiac arrest. (Crit Care Med 2012; 40:1851-1856)