Shultz J J, Coffeen P, Sweeney M, Detloff B, Kehler C, Pineda E, Yakshe P, Adler S W, Chang M, Lurie K G
University of Minnesota, Minneapolis.
Circulation. 1994 Feb;89(2):684-93. doi: 10.1161/01.cir.89.2.684.
The mechanisms that underlie cardiopulmonary resuscitation (CPR) in humans remain controversial and difficult to study. This report describes a new human model to evaluate CPR during the first 1 to 2 minutes after the onset of ventricular fibrillation (VF). With this model, standard CPR was compared with active compression-decompression (ACD) CPR, a method that uses a handheld suction device to actively compress and actively decompress the chest.
During routine inductions of VF as part of a transvenous lead cardioverter/defibrillator implantation procedure, CPR was performed in 21 patients if the first defibrillation shock failed and until a successful rescue shock was delivered. Compressions during CPR were performed according to American Heart Association guidelines. For ACD CPR, decompression was performed with up to -30 lbs. Radial arterial and right atrial pressures were measured in all patients. Esophageal pressures, intratracheal pressures, or minute ventilation was measured in the last 13 patients. Application of both CPR techniques increased arterial and right atrial pressures. The mean coronary perfusion pressure was increased throughout the entire CPR cycle with ACD CPR (compression, 21.5 +/- 9.0 mm Hg; decompression, 21.9 +/- 8.7 mm Hg) compared with standard CPR (compression, 17.9 +/- 8.2 mm Hg; decompression, 18.5 +/- 6.9 mm Hg; P < .02 and P < .02, respectively). Ventilation per compression-decompression cycle was 97.3 +/- 65.6 mL with standard CPR and 168.4 +/- 68.6 mL with ACD CPR (n = 7, P < .001). Negative inspiratory pressure was -0.8 +/- 4.8 mm Hg with standard CPR and -11.4 +/- 6.3 mm Hg with ACD CPR (n = 6, P < .04).
Patients undergoing multiple inductions of VF during cardioverter/defibrillator implantation with transvenous leads provide a well-controlled and reproducible model to study the mechanisms of CPR. Using this model, ACD CPR significantly increased arterial blood pressure, coronary perfusion pressure, minute ventilation, and negative inspiratory pressure compared with standard CPR.
人类心肺复苏(CPR)的潜在机制仍存在争议且难以研究。本报告描述了一种新的人体模型,用于评估心室颤动(VF)发作后最初1至2分钟内的心肺复苏情况。利用该模型,将标准心肺复苏与主动按压-减压(ACD)心肺复苏进行了比较,后者是一种使用手持吸引装置对胸部进行主动按压和主动减压的方法。
在经静脉植入心脏转复除颤器的过程中,作为常规诱发心室颤动的一部分,如果首次除颤电击失败且直到成功给予抢救电击,对21例患者进行了心肺复苏。心肺复苏期间的按压按照美国心脏协会的指南进行。对于ACD心肺复苏,减压时施加高达-30磅的力。对所有患者测量了桡动脉和右心房压力。对最后13例患者测量了食管压力、气管内压力或分钟通气量。两种心肺复苏技术的应用均提高了动脉压和右心房压力。与标准心肺复苏相比,在整个心肺复苏周期中,ACD心肺复苏的平均冠状动脉灌注压升高(按压时,21.5±9.0 mmHg;减压时,21.9±8.7 mmHg),而标准心肺复苏为(按压时,17.9±8.2 mmHg;减压时,18.5±6.9 mmHg;P分别<0.0