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在猪心脏骤停模型中,止血带辅助心肺复苏可增加心肌灌注。

A tourniquet assisted cardiopulmonary resuscitation augments myocardial perfusion in a porcine model of cardiac arrest.

作者信息

Yang Zhengfei, Tang David, Wu Xiaobo, Hu Xianwen, Xu Jiefeng, Qian Jie, Yang Min, Tang Wanchun

机构信息

Weil Institute of Critical Care Medicine, Rancho Mirage, CA, United States; Sun Yat-sen Memorial Hospital, Sun Yat-sen University, Guangzhou, China.

Weil Institute of Critical Care Medicine, Rancho Mirage, CA, United States; Eisenhower Medical Center, Rancho Mirage, CA, United States.

出版信息

Resuscitation. 2015 Jan;86:49-53. doi: 10.1016/j.resuscitation.2014.10.009. Epub 2014 Oct 23.

Abstract

OBJECTIVE

During cardiopulmonary resuscitation (CPR), myocardial blood flow generated by chest compression rarely exceeds 35% of its normal level. Cardiac output generated by chest compression decreases gradually with the prolongation of cardiac arrest and resuscitation. Early studies have demonstrated that myocardial blood flow during CPR is largely dependent on peripheral vascular resistance. In this study, we investigated the effects of chest compression in combination with physical control of peripheral vascular resistance assisted by tourniquets on myocardial blood flow during CPR.

METHODS

Ventricular fibrillation was induced and untreated for 7 min in ten male domestic pigs weighing between 33 and 37 kg. The animals were then randomized to receive CPR alone or a tourniquet assisted CPR (T-CPR). In the CPR alone group, chest compression was performed by a miniaturized mechanical chest compressor. In the T-CPR group, coincident with the start of resuscitation, the thin elastic tourniquets were wrapped around the four limbs from the distal end to the proximal part. After 2 min of CPR, epinephrine (20 μg/kg) was administered via the femoral vein. After 5 min of CPR, defibrillation was attempted by a single 150 J shock. If resuscitation was not successful, CPR was resumed for 2 min before the next defibrillation. The protocol was continued until successful resuscitation or for a total of 15 min. Five minutes after resuscitation, the elastic tourniquets were removed. The resuscitated animals were observed for 2h.

RESULTS

T-CPR generated significantly greater coronary perfusion pressure, end-tidal carbon dioxide and carotid blood flow. There was no difference in both intrathoracic positive and negative pressures between the two groups. All animals were successfully resuscitated with a single shock in both groups. There were no significant changes in hemodynamics observed in the animals treated in the T-CPR group before-and-after the release of tourniquets at post-resuscitation 5 min.

CONCLUSIONS

T-CPR improves myocardial and cerebral perfusion during CPR. It may provide a new and convenient method for augmenting myocardial and cerebral blood flow during CPR.

摘要

目的

在心肺复苏(CPR)期间,胸外按压产生的心肌血流量很少超过其正常水平的35%。胸外按压产生的心输出量会随着心脏骤停和复苏时间的延长而逐渐下降。早期研究表明,CPR期间的心肌血流量很大程度上取决于外周血管阻力。在本研究中,我们调查了胸外按压结合使用止血带辅助对外周血管阻力进行物理控制对CPR期间心肌血流量的影响。

方法

对10头体重在33至37千克之间的雄性家猪诱发室颤并使其持续7分钟不予处理。然后将这些动物随机分为单纯接受CPR组或止血带辅助CPR(T-CPR)组。在单纯CPR组中,通过小型化机械胸外按压装置进行胸外按压。在T-CPR组中,在复苏开始的同时,将薄弹性止血带从四肢远端向近端缠绕。CPR 2分钟后,经股静脉给予肾上腺素(20μg/kg)。CPR 5分钟后,尝试单次150J电击除颤。如果复苏未成功,则在下次除颤前继续进行CPR 2分钟。该方案持续进行,直至复苏成功或总共持续15分钟。复苏后5分钟,去除弹性止血带。对复苏后的动物观察2小时。

结果

T-CPR产生了显著更高的冠状动脉灌注压、呼气末二氧化碳分压和颈动脉血流量。两组之间的胸内正压和负压均无差异。两组所有动物均通过单次电击成功复苏。在复苏后5分钟松开止血带前后,T-CPR组处理的动物的血流动力学未观察到显著变化。

结论

T-CPR可改善CPR期间的心肌和脑灌注。它可能为在CPR期间增加心肌和脑血流量提供一种新的便捷方法。

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