肺栓塞致猪心脏骤停期间和自主循环恢复后的血流动力学研究

Study of hemodynamics during cardiac arrest and after restoration of spontaneous circulation in a porcine cardiac arrest model induced by acute pulmonary embolism

目的观察急性肺栓塞致猪心脏骤停期间和自主循环恢复后的血流动力学变化。方法近交系北京长白猪14只，通过颈外静脉注入血栓制作急性肺栓塞致心脏骤停（CA）模型，随后给予心肺复苏和溶栓治疗（尿激酶，15000U／kg，iv）。5只动物恢复自主循环（ROSC）。分别于造模前、CA、ROSC、ROSC后0．5、1、1．5、2、2．5、4、6h监测血流动力学参数。结果①急性肺栓塞致CA时平均动脉压较基线显著下降（P〈0．05），平均肺动脉压和右室压显著升高（P〈0．05）。②ROSC后平均动脉压恢复，但ROSC后4h较基线显著下降（P〈0．05）；在ROSC时和ROSC后0．5～2h心率较基线显著增快（P〈0．05）；平均肺动脉压于ROSC后恢复至基础水平；在ROSC后2,5h和4h右室压较CA时显著下降f（26．5±11．4）mmHgvs．（46．2±13．0）mmHg，（24．8±9_3）mmHg vs．（46．2±13．0）mmHg，均P〈0．05]。③ROSC后4h外周血管阻力达峰值，肺血管阻力于ROSC时明显高于基线[（96．5±24．8）DS／cm^5 vs．（26．5±13．4）DS／cm^5，P〈0．05]，ROSC后1、2h下降，4、6h再次升高[（98．5±0.7）DS／cm^5和（98．0±1．4）DS／cm^5]。④心功能变化：与基线相比，ROSC、ROSC后1～6h左心功能均显著下降（均P〈0．05），右心排出量于ROSC、ROSC后4、6h均显著降低（均P〈0．05），左右心室功能指数于ROSC后1、2h均显著降低（均P〈0．05）。结论急性肺栓塞致CA时平均动脉压下降，平均肺动脉压、右室压、肺血管阻力明显升高，左右心室功能均下降；ROSC后左右心室功能先出现代偿，后失代偿。

Objective To observe the hemodynamic change during cardiac arrest （CA） and after restoration of spontaneous circulation （ROSC） in a porcine acute pulmonary embolism model. Methods A total of 14 inbred Beijing Landraces were used to estalish the model of CA and ROSC induced by acute pulmonary embolism through injection of thrombus followed by cardiopulmonary resuscitation and thrombolytic therapy （urokinase, 15 000 U/kg, iv）. Five resuscitated pigs restored spontaneous circulation. Hemodynamic changes were determined at baseline, CA, ROSC, and 0.5, 1, 1.5, 2, 2.5, 4, and 6 h after ROSC. Results Compared with the baseline, mean arterial pressure was decreased significantly, mean pulmonary arterial pressure and right ventricular pressure were increased significantly, and the heart rate had no change during CA induced by acute pulmonary embolism. The mean arterial pressure restored normal level gradually after ROSC, but was decreased at 4 h after ROSC compared with the baseline （P〈0.05）. The heart rate was faster at ROSC and 0.5-2 h after ROSC than the baseline （P〈0.05）. The mean pulmonary arterial pressure restored the baseline level after ROSC; The right ventricular pressure were decreased at 2.5 h （26.5±11.4） mmHg and 4 h （24.8±9.3） mmHg after ROSC compared with the level during CA （46.2±13.01） mmHg （P〈0.05）. The systemic vascular resistance peaked at 4 h after ROSC. The pulmonary vascular resistance level at ROSC was higher than the baseline [（96.5±24.8）DS/cm^5 vs. （26.5±13.4）DS/cm^5, P〈0.05], and was decreased at 1 h and 2 h after ROSC, but was increased at 4 h and 6 h after ROSC [（98.5±0.7）DS/cm^5 and （98.0±1.4）DS/cm^5]. The changes of heart function： compared with the baseline, the left ventricular fixnction at ROSC and 1-6 h after ROSC were declined significantly （all P〈0.05）, and right cardiac output declined at ROSC and 4 h and 6 h after ROSC （all P〈0.05）, and the level of cardiac ftmction index was dropped at 1 h and 2 h after ROSC （P〈0.05）. Conclusions The mean arterial pressure was declined, mean pulmonary arterial pressure, right ventricular pressure and pulmonary vascular resistance were increased, cardiac function was decreased during CA induced by acute pulmonary embolism; After ROSC, hemodynamic changes were described as compensated in the early stage （1-2 h after ROSC） and decompensated （4 h after ROSC） with time.