Tang W, Weil M H, Noc M, Sun S, Gazmuri R J, Bisera J
Institute of Critical Care Medicine, UHS/Chicago Medical School, North Chicago, Ill. 60064.
Circulation. 1993 Oct;88(4 Pt 1):1916-21. doi: 10.1161/01.cir.88.4.1916.
After prolonged cardiac arrest, conventional methods of closed-chest cardiac compression are ineffective. This is primarily because of failure to generate minimal threshold levels of coronary perfusion pressure for cardiac resuscitation. This report introduces a new option for cardiac resuscitation by use of a combination of intermittent ascending aortic balloon occlusion, aortic infusion, and precordial compression to increase the pressure gradient for coronary perfusion.
Twenty anesthetized, mechanically ventilated, normovolemic domestic pigs were investigated. A 10F balloon catheter was advanced from the left femoral artery into the ascending aorta. Ventricular fibrillation was induced with an AC current delivered through an electrode catheter advanced into the right ventricle. Precordial compression was initiated after 7 minutes of untreated ventricular fibrillation. The animals were randomized to one of four groups: (1) balloon occlusion with proximal infusion of oxygenated saline, (2) balloon occlusion alone, (3) proximal aortic infusion together with epinephrine without balloon occlusion, and (4) injection of epinephrine without balloon occlusion or proximal infusion. For balloon occlusion, the balloon was inflated for 30 seconds during each minute of cardiopulmonary resuscitation. In the subsets of animals that received infusions, oxygenated saline (30 mL) was injected into the proximal aorta immediately after balloon occlusion. Epinephrine was used in two subsets: It was injected as a bolus in amounts of 30 micrograms/kg into the right atrium at 30 seconds after start of precordial compression and repeated as required to maintain coronary perfusion pressure within the range of 25 to 30 mm Hg. Defibrillation was attempted at 1 minute after start of precordial compression and at 1-minute intervals thereafter. Resuscitation attempts were continued until there was return of spontaneous circulation or for a total of 30 minutes after start of precordial compression. Coronary perfusion pressure generated by precordial compression was significantly increased after balloon occlusion. Each of 10 animals was successfully resuscitated and survived for 48 hours after balloon occlusion whether or not it was combined with infusion. Three of five animals were resuscitated by a combination of infusion and epinephrine in the absence of aortic occlusion, but none survived for 48 hours (P = .02). Only one epinephrine-treated animal was successfully resuscitated and survived for 48 hours in the absence of balloon occlusion or infusion (P < .05).
Ascending aortic balloon occlusion with or without proximal aortic infusion strikingly increased resuscitability and 48-hour survival after cardiac arrest under conditions when conventional methods failed.
长时间心脏骤停后,传统的闭胸心脏按压方法无效。这主要是因为未能产生用于心脏复苏的最低冠状动脉灌注压阈值水平。本报告介绍了一种通过间歇性升主动脉球囊闭塞、主动脉灌注和心前区按压相结合来增加冠状动脉灌注压力梯度的心脏复苏新方法。
对20只麻醉、机械通气、血容量正常的家猪进行了研究。将一根10F球囊导管从左股动脉推进至升主动脉。通过推进至右心室的电极导管输送交流电诱发室颤。在未治疗的室颤7分钟后开始心前区按压。将动物随机分为四组之一:(1)球囊闭塞并近端注入氧合盐水,(2)单纯球囊闭塞,(3)近端主动脉灌注并联合肾上腺素但无球囊闭塞,(4)注射肾上腺素但无球囊闭塞或近端灌注。对于球囊闭塞,在每一分钟的心肺复苏过程中球囊充气30秒。在接受灌注的动物亚组中,球囊闭塞后立即向近端主动脉注入30 mL氧合盐水。肾上腺素用于两个亚组:在心前区按压开始30秒后以30微克/千克的剂量作为推注注入右心房,并根据需要重复注射以维持冠状动脉灌注压在25至30毫米汞柱范围内。在心前区按压开始1分钟后及此后每隔1分钟尝试除颤。复苏尝试持续进行,直至自主循环恢复或在心前区按压开始后总共持续30分钟。球囊闭塞后,心前区按压产生的冠状动脉灌注压显著增加。无论是否联合灌注,10只动物中有每只在球囊闭塞后均成功复苏并存活48小时。在无主动脉闭塞的情况下,五只动物中有三只通过灌注和肾上腺素联合成功复苏,但无一存活48小时(P = 0.02)。在无球囊闭塞或灌注的情况下,仅一只接受肾上腺素治疗的动物成功复苏并存活48小时(P < 0.05)。
在传统方法失败的情况下,无论有无近端主动脉灌注的升主动脉球囊闭塞显著提高了心脏骤停后的复苏能力和48小时生存率。