Yannopoulos Demetris, Aufderheide Tom P, McKnite Scott, Kotsifas Kostantinos, Charris Roussos, Nadkarni Vinay, Lurie Keith G
Department of Cardiology, Cardiac Arrhythmia Center, University of Minnesota, Minneapolis, MN, USA.
Resuscitation. 2006 Jun;69(3):487-94. doi: 10.1016/j.resuscitation.2005.11.005. Epub 2006 May 5.
A new device, the intrathoracic pressure regulator (ITPR), was developed to generate continuous negative intrathoracic pressure during cardiopulmonary resuscitation (CPR) and allow for intermittent positive pressure ventilation. Use of the ITPR has been shown to increase vital organ perfusion and short-term survival rates in pigs. The purpose of this study was to investigate the hemodynamic and blood gas effects of more prolonged (15 min) use of the ITPR during CPR in a porcine model of cardiac arrest.
After 8 min of untreated ventricular fibrillation (VF), 16 female pigs were anaesthetized with propofol, intubated, and randomized prospectively to 15 min of either ITPR-CPR or standard (STD) CPR. Compressions were delivered at a rate of 100/min with a compression to ventilation ratio of 15:2. Ventilations were delivered with a resuscitator bag. Tracheal, aortic, right atrial, intracranial pressures (ICP), common carotid blood flow and respiratory variables were recorded continuously. Arterial and venous blood gases were collected at baseline, and after 5, 10, and 15 min of CPR. Coronary perfusion pressure (CPP) was calculated as diastolic aortic pressure-right atrial pressure. Cerebral perfusion pressure (CerPP) was calculated as mean arterial pressure (MAP)-intracranial pressure. Statistical analysis was performed with unpaired t-test and Friedman's Repeated Measures Analysis.
ITPR-CPR when compared to STD-CPR resulted in a significant decrease in mean decompression phase (diastolic) tracheal pressure (-9+/-0.6 mmHg versus -3+/-0.3 mmHg, p<0.001), diastolic right atrial pressure (DRAP) (-0.1+/-0.2 mmHg versus 2.3+/-0.2 mmHg, p<0.001) and intracranial pressure (20.8+/-0.6 mmHg versus 23+/-0.5 mmHg, respectively, p=0.04) and a significant increase in total mean aortic pressure, coronary and cerebral perfusion pressures and end tidal carbon dioxide (ETCO(2)), (p<0.001). Common carotid artery blood flow was increased by an average of 70%, p<0.001. ABGs showed progressive metabolic acidosis in the ITPR-CPR group, but PaCO(2) remained stable at 34 mmHg for 15 min. In the STD-CPR group, pseudorespiratory alkalosis was observed with PaCO(2) values remaining <20 mmHg (p<0.001). PaO(2) was not different between groups. Following 23 min of cardiac arrest (15 min of CPR) ROSC was achieved in 5/8 ITPR-CPR animals versus 2/8 STD-CPR animals p=0.3.
ITPR-CPR significantly improved hemodynamics, vital organ perfusion pressures and common carotid blood flow compared to STD-CPR in a porcine model of prolonged cardiac arrest and basic life support. The beneficial hemodynamic effects of ITPR-CPR were sustained at least 15 min without any compromise in oxygenation.
一种新装置，即胸腔内压力调节器（ITPR），被研发出来用于在心肺复苏（CPR）期间产生持续的胸腔内负压，并允许进行间歇性正压通气。已证明在猪身上使用ITPR可增加重要器官灌注和短期生存率。本研究的目的是在猪心脏骤停模型中，研究在CPR期间更长时间（15分钟）使用ITPR对血流动力学和血气的影响。
在8分钟未经处理的室颤（VF）后，16只雌性猪用丙泊酚麻醉，插管，并前瞻性随机分为接受15分钟的ITPR-CPR或标准（STD）CPR。按压频率为每分钟100次，按压与通气比例为15:2。使用复苏袋进行通气。持续记录气管、主动脉、右心房、颅内压（ICP）、颈总动脉血流和呼吸变量。在基线以及CPR 5、10和15分钟后采集动脉和静脉血气。冠状动脉灌注压（CPP）计算为舒张期主动脉压减去右心房压。脑灌注压（CerPP）计算为平均动脉压（MAP）减去颅内压。采用非配对t检验和弗里德曼重复测量分析进行统计分析。
与STD-CPR相比，ITPR-CPR导致平均减压期（舒张期）气管压力显著降低（-9±0.6 mmHg对-3±0.3 mmHg，p<0.001）、舒张期右心房压（DRAP）显著降低（-0.1±0.2 mmHg对2.3±0.2 mmHg，p<0.001）和颅内压显著降低（分别为20.8±0.6 mmHg对23±0.5 mmHg，p=0.04），并使总平均主动脉压、冠状动脉和脑灌注压以及呼气末二氧化碳（ETCO₂）显著升高（p<0.001）。颈总动脉血流平均增加70%，p<0.001。血气分析显示ITPR-CPR组出现进行性代谢性酸中毒，但PaCO₂在15分钟内保持稳定在34 mmHg。在STD-CPR组中，观察到假性呼吸性碱中毒，PaCO₂值保持<20 mmHg（p<0.001）。两组间PaO₂无差异。在心脏骤停23分钟（CPR 15分钟）后，5/8接受ITPR-CPR的动物实现了自主循环恢复（ROSC），而接受STD-CPR的动物为2/8，p=0.3。
在延长心脏骤停和基础生命支持的猪模型中，与STD-CPR相比，ITPR-CPR显著改善了血流动力学、重要器官灌注压和颈总动脉血流。ITPR-CPR的有益血流动力学效应至少持续15分钟，且氧合无任何受损。
