Study of hemodynamics during cardiac arrest and after restoration of spontaneous circulation in a porcine cardiac arrest model induced by acute pulmonary embolism / 中华急诊医学杂志

ABSTRACT

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, 15000 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/cm5 vs. (26.5±13.4)DS/cm5, 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/cm5 and (98.0±1.4)DS/cm5]. The changes of heart function compared with the baseline, the left ventricular function 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 function 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.