叹息样呼吸与猪心肺复苏过程中血流动力学变化的研究

目的 研究CPR的病理生理过程,探讨叹息样呼吸对CPR过程中血流动力学的影响.方法 12头北京长白猪,体质量(30±1)kg,麻醉后气管插管,机械通气,连续记录实时呼吸参数.股动脉置管测量主动脉压(AOP),并抽取动脉血;肺动脉漂浮导管置测最右心房压(RAP)及心输出量(CO).以程控电刺激制作室颤(VF)模型.VF4 min后进行标准30:2 CPR 12 min,记录相关参数.结果 CPR过程中pH,PaCO2及乳酸逐渐升高,而PaO2逐渐降低,但PaO2在整个实验过程中均大于50mmHg.10只动物出现叹息样呼吸,但随时间推移逐渐减弱;未出现叹息样乎吸的2只动物均未复苏成功.标准心外按压在多数动物均可产生大干死腔量(VD)的被动通气,但其潮气量随时间推移逐渐减少.因此人工通气在总分钟通气量中所占比例逐渐增加.CO、冠脉灌注压(CPP)与叹息样呼吸分钟通气量(MVg)呈正相关(r分别等于0.736,0.721,P＜0.01);RAP与MVg呈负相关(r=-0.744,P＜0.01).结论 标准CPR能够维持机体12min的氧合;心外按压能够产生大于VD的被动通气;叹息样呼吸可以通过增加CO、CPP及降低RAP产生对自主循环的恢复产生有益的生理作用.

Abstract：

Objective Gasp was defined as a pathology respiration during cardiac arrest. This study was to investigate its effect on hemodynamics during CPR. Method Twelve domestic pigs, weighening (30 ± 1) kg,were anaesthetized. After tracheal intubation and mechanical ventilation, continuous respiratory variables were recorded. An artery catheter was inserted for reference blood samples and measuring aortic artery pressure (AOP).Right atrial pressure (RAP) and cardiac output (CO) were detected by Swan-Ganz catheter. Ventricular fibrillation (VF) was induced by programmed electrical stimulation instruments. After 4 minutes untreated VF, standard 30:2 CPR was done for 12 minutes and the parameters were recorded. Results pH, PaCO2 and lactic acid increased and PaO2 decreased progressively during CPR, whereas PaO2 was up to 50mmHg during the whole protocol. Gasps were observed in 10 animals, but weaken gradually; the left 2 animals with no gasp did not restore of spontaneous circulation (ROSC). Standard CPR could produce passive ventilation more than dead space (VD), but its tidal volume decreased gradually, which led to the percentage of rescue ventilation increased progressively. Positive correlations were found between CO, coronary perfusion pressure (CPP) and minute ventilation of gasps (MVg) (r was 0.736 and 0.721 respectively, both P ＜0.01); negative correlation were found between RAP and MVg (r= -0. 744, P ＜ 0.01). Conclusions Standard CPR could maintain 12 minutes oxygenation of body; compressions could produce enough passive ventilation more than VD; gasps were benefit to ROSC by increasing CO, CPP and decreasing RAP.

Effect of gasps to hemodynamics during cardiopulmonary resuscitation in a porcine model of prolonged cardiac arrest

Objective Gasp was defined as a pathology respiration during cardiac arrest. This study was to investigate its effect on hemodynamics during CPR. Method Twelve domestic pigs, weighening (30 ± 1) kg,were anaesthetized. After tracheal intubation and mechanical ventilation, continuous respiratory variables were recorded. An artery catheter was inserted for reference blood samples and measuring aortic artery pressure (AOP).Right atrial pressure (RAP) and cardiac output (CO) were detected by Swan-Ganz catheter. Ventricular fibrillation (VF) was induced by programmed electrical stimulation instruments. After 4 minutes untreated VF, standard 30:2 CPR was done for 12 minutes and the parameters were recorded. Results pH, PaCO2 and lactic acid increased and PaO2 decreased progressively during CPR, whereas PaO2 was up to 50mmHg during the whole protocol. Gasps were observed in 10 animals, but weaken gradually; the left 2 animals with no gasp did not restore of spontaneous circulation (ROSC). Standard CPR could produce passive ventilation more than dead space (VD), but its tidal volume decreased gradually, which led to the percentage of rescue ventilation increased progressively. Positive correlations were found between CO, coronary perfusion pressure (CPP) and minute ventilation of gasps (MVg) (r was 0.736 and 0.721 respectively, both P ＜0.01); negative correlation were found between RAP and MVg (r= -0. 744, P ＜ 0.01). Conclusions Standard CPR could maintain 12 minutes oxygenation of body; compressions could produce enough passive ventilation more than VD; gasps were benefit to ROSC by increasing CO, CPP and decreasing RAP.