闭胸复苏犬的血流动力学特点的研究

Characteristics of hemodynamics during closed chest cardiopulmonary resuscitation

目的 研究闭胸复苏犬的血流动力学特点,分析其机制.方法 健康杂种犬12只,采用电击致犬室颤的动物模型.心跳停止4 min后,按照国际心肺复苏指南2005标准开始心肺复苏.复苏2 min后,静注肾上腺素1 mg.致颤前及复苏过程中对主动脉内压、中心静脉压、心电图进行有创同步监测.方法 用Chart5Ch软件做统计图,计算冠脉灌注压,分析闭胸复苏犬的血流动力学特点.用配对t检验比较静注肾上腺素前后血流动力学变化,P＜0.05为差异具有统计学意义.结果 闭胸复苏犬的血流动力学效应表现为两种类型：8只犬（8/12）表现为主动脉内压（AOP）与中心静脉压（CVP）同步变化,而冠脉灌注压（CPP）几乎为0;4只犬（4/12）表现为主动脉内压升高而中心静脉压不变.静注肾上腺素后,AOP及CPP显著增大,其中,主动脉收缩压（ASP）[（66±14）mmHg和（107±28）mmHg,P＜0.01];主动脉舒张压（ADP）[（25±2.2）mmHg和（45±13）mmHg,P=0.001],CPP[（2.8±3.8）mmHg和（29±13）mmHg,P＜0.001];ASP,ADP及CPP增加值的95%可信区间分别是（21.1～59.1）,（10.2～28.3）及（16.7～35.7）.结论 胸泵机制是闭胸复苏的主要机制.肾上腺素可以打破心肺复苏时主动脉内压与中心静脉压的平衡,增加冠脉灌注压,可能增加复苏成功率.

Objective To study the hemodynamics during closed chest cardiopulmonary resuscitation （CCCPR） in dogs in order to unravel the mechanism. Method Twelve healthy mongrel dogs were selected to make animal model of ventricular fibrillation induced by electric shock on the chest wall. Closed-chest cardiopulmonary resuscitation （CCCPR） was initiated four minutes after ventricular fibrillation appeared according to American Heart Guidelines in 2005 for Cardiopulmonary Resuscitation and Emergency Cardiovascular Rescue. After CPR for 2 minutes, 1mg epinephrine was injected intravenously. The central venous pressure （CVP）, the aortic pressure （AOP）and the invasive electrocardiogram （ECG） were used to monitor continuously before ventricular fibrillation and the entire course of CPR. The coronary perfusion pressure （CPP） was calculated. The changes in aortic diastolic pressure （ADP） and CPP produced by chest compression or the injection of epinephrine were analyzed. The aortic pressure and the central venous pressure were recorded simultaneously during CPR. A chart was made and the CPP was calculated with the software Chart5Ch. The hemodynamic changes produced by the administration of epinephrine were studied. Data were analyzed with paired Student t test. P 〈 0.05 was considered as a significant difference. Results Two kinds of hemodynamic effects of CPR were observed. In 8 dogs （8/12） , the aortic pressure changed synchronously with the CVP, and the CPP was almost zero, and in other 4 dogs （4/12）, the aortic pressure increased and the CVP remained unchanged with presence of the CPP. After the administration of epinephrine, the AOP and the CPP increased significantly. The Aortic systolic pressure（ASP） increased from （66± 14） mmHg to（107 ± 28） mmHg, （P = 0. 001）. The Aortic diastolic pressure （ADP） increased from （25 ±2.2） mmHg to（45 ± 13） mmHg （P =0.001）. And the coronary perfusion pressure （CPP） increased from （2.8± 3.8） mmHg to （29 ± 13） mmHg （P 〈 0.001）. The 95 % confidential interval of the added value of the ASP,ADP and CPPwere （21.1-59.1）, （10.2-28.3） and （16.7-35.7）, respectively. Conclusions The thoracic pump mechanism is the primary role in the closed chest Cardiopulmonary resuscitation. Epinephrine can increase ADP and CPP and has the capability to break the balance between aortic pressure and central venous pressure, increasing the rate of successful cardiopulmonary resuscitation.