Xu Nana, Zhang Jiabi, Luo Jialin, Wang Li, Chen Yong, Zhou Lijun, Chen Bihua, Luo Lan, Liu Xiaolu, Luo Shuju, Wang Yong, Luo Zunwei, Ding Li, Li Mei, Zhou Manhong
Department of Emergency, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou, China.
Department of Nursing, Affiliated Hospital of Zunyi Medical University, Zunyi 563000, Guizhou, China.
Zhonghua Wei Zhong Bing Ji Jiu Yi Xue. 2025 May;37(5):472-476. doi: 10.3760/cma.j.cn121430-20250124-00083.
To compare the effects of different chest compression rates (60-140 times/min) on hemodynamic parameters, return of spontaneous circulation (ROSC), resuscitation success, and survival in a porcine model of cardiac arrest (CA) followed by cardiopulmonary resuscitation (CPR).
Forty healthy male domestic pigs were randomly divided into five groups based on chest compression rate: 60, 80, 100, 120, and 140 times/min (n = 8). All animals underwent standard anesthesia and tracheal intubation. A catheter was inserted via the left femoral artery into the thoracic aorta to monitor aortic pressure (AOP), and another via the right external jugular vein into the right atrium to monitor right atrial pressure (RAP). In each group, animals were implanted with a stimulating electrode via the right external jugular vein to the endocardium, and ventricular fibrillation (VF) was induced by delivering alternating current stimulation, resulting in CA. After a 1-minute, manual chest compressions were performed at the assigned rate with a compression depth of 5 cm. The first defibrillation was delivered after 2 minutes of CPR. No epinephrine or other pharmacologic agents were administered during the entire resuscitation process. From 1 minute before VF induction to 10 minutes after ROSC, dynamic monitoring of AOP, coronary perfusion pressure (CPP), and partial pressure of end-tidal carbon dioxide (PCO). Cortical ultrastructure was examined 24 hours post-ROSC using transmission electron microscopy.
With increasing compression rates, both the total number of defibrillations and cumulative defibrillation energy significantly decreased, reaching their lowest levels in the 120 times/min group. The number of defibrillations decreased from (4.88±0.83) times in the 60 times/min group to (2.25±0.71) times in the 120 compressions/min group, and energy from (975.00±166.90)J to (450.00±141.42)J. However, both parameters increased again in the 140 times/min group [(4.75±1.04)times, (950.00±207.02)J], the differences among the groups were statistically significant (both P < 0.01). As compression frequency increased, PCO, pre-defibrillation AOP and CPP significantly improved, peaking in the 120 times/min group [compared with the 60 times/min group, PCO (mmHg, 1 mmHg≈0.133 kPa): 18.69±1.98 vs. 8.67±1.30, AOP (mmHg): 95.13±7.06 vs. 71.00±6.41, CPP (mmHg): 14.88±6.92 vs. 8.57±3.42]. However, in the 140 times/min group, these values declined significantly again [PCO, AOP, and CPP were (10.59±1.40), (72.38±11.49), and (10.36±4.57) mmHg, respectively], the differences among the groups were statistically significant (all P < 0.01). The number of animals achieving ROSC, successful resuscitation, and 24-hour survival increased with higher compression rates, reaching a peak in the 120 times/min group (compared with the 60 times/min group, ROSC: 7 vs. 2, successful resuscitation: 7 vs. 2, 24-hour survival: 7 vs.1), then decreased again in the 140 times/min group (the animals that ROSC, successfully recovered and survived for 24 hours were 3, 3, and 2, respectively). Transmission electron microscopy revealed that in the 60, 80, and 140 times/min groups, nuclear membranes in cerebral tissue were irregular and incomplete, nucleoli were indistinct, and mitochondria were swollen with reduced cristae and abnormal morphology. In contrast, the 100 times/min and 120 times/min groups exhibited significantly attenuated ultrastructural damage.
Among the tested chest compression rates of 60-140 times/min, a chest compressions frequency of 120 times/min is the most favorable hemodynamic profile and outcomes during CPR in a porcine CA model. However, due to the wide spacing between groups, further investigation is needed to determine the optimal compression rate range more precisely.
在猪心脏骤停(CA)后进行心肺复苏(CPR)的模型中,比较不同胸外按压速率(60 - 140次/分钟)对血流动力学参数、自主循环恢复(ROSC)、复苏成功率及生存率的影响。
40只健康雄性家猪根据胸外按压速率随机分为五组:60、80、100、120和140次/分钟(n = 8)。所有动物均接受标准麻醉和气管插管。通过左股动脉插入导管至胸主动脉监测主动脉压(AOP),通过右颈外静脉插入另一根导管至右心房监测右心房压(RAP)。每组动物经右颈外静脉植入刺激电极至心内膜,通过施加交流电刺激诱发心室颤动(VF),导致心脏骤停。1分钟后,以指定速率进行人工胸外按压,按压深度为5厘米。心肺复苏2分钟后进行首次除颤。在整个复苏过程中未使用肾上腺素或其他药物。从诱发心室颤动前1分钟至自主循环恢复后10分钟,动态监测主动脉压、冠状动脉灌注压(CPP)和呼气末二氧化碳分压(PCO₂)。自主循环恢复后24小时,使用透射电子显微镜检查皮质超微结构。
随着按压速率增加,除颤总次数和累积除颤能量均显著降低,在120次/分钟组达到最低水平。除颤次数从60次/分钟组的(4.88±0.83)次降至12次/分钟组的(2.25±0.71)次,能量从(975.00±166.90)焦耳降至(450.00±141.42)焦耳,但在140次/分钟组这两个参数再次升高[(4.75±1.04)次,(950.00±207.02)焦耳],组间差异具有统计学意义(均P < 0.01)。随着按压频率增加,呼气末二氧化碳分压、除颤前主动脉压和冠状动脉灌注压显著改善,在120次/分钟组达到峰值[与60次/分钟组相比,呼气末二氧化碳分压(mmHg,1 mmHg≈0.133 kPa):18.69±1.98 vs. 8.67±1.30,主动脉压(mmHg):95.13±7.06 vs. 71.00±6.41,冠状动脉灌注压(mmHg):14.88±6.92 vs. 8.57±3.42]。然而,在140次/分钟组,这些值再次显著下降[呼气末二氧化碳分压、主动脉压和冠状动脉灌注压分别为(10.59±1.40)、(72.38±11.49)和(10.36±4.57)mmHg],组间差异具有统计学意义(均P < 0.01)。实现自主循环恢复、成功复苏及24小时存活的动物数量随着按压速率升高而增加,在120次/分钟组达到峰值(与60次/分钟组相比,自主循环恢复:7 vs. 2,成功复苏:7 vs. 2,24小时存活:7 vs. 1),然后在140次/分钟组再次下降(自主循环恢复、成功复苏并存活24小时的动物分别为3、3和2只)。透射电子显微镜显示,在60、80和140次/分钟组,脑组织中的核膜不规则且不完整,核仁模糊,线粒体肿胀,嵴减少且形态异常。相比之下,100次/分钟和120次/分钟组的超微结构损伤明显减轻。
在60 - 140次/分钟的胸外按压速率测试中,120次/分钟的胸外按压频率在猪心脏骤停模型的心肺复苏过程中具有最有利的血流动力学特征和结果。然而,由于组间间距较大,需要进一步研究以更精确地确定最佳按压速率范围。