Yannopoulos Demetris, Metzger Anja, McKnite Scott, Nadkarni Vinay, Aufderheide Tom P, Idris Ahamed, Dries David, Benditt David G, Lurie Keith G
University of Minnesota, Division of Cardiology, MN, USA.
Resuscitation. 2006 Sep;70(3):445-53. doi: 10.1016/j.resuscitation.2006.02.005. Epub 2006 Aug 9.
The intrathoracic pressure regulator (ITPR) was created to improve hemodynamics by generating continuous negative airway pressure between positive pressure ventilations to enhance cardiac preload in apnoeic animals. In normovolemic and hypovolemic pigs, we tested the hypothesis that continuous negative intrathoracic pressure set at -5 or -10mmHg, interrupted only for intermittent positive pressure ventilations, would decrease intracranial (ICP) and right atrial (RAP) pressure, and increase mean arterial pressure (MAP).
Twelve pigs were anesthetized with propofol and ventilated with a bag. The ITPR was used to vary baseline endotracheal pressures (ETPs) for 5min periods in the following sequence: 0, -5, 0, -10, 0mmHg under normovolemic conditions. Six pigs were bled 50% (32.5+/-mL/kg) of their estimated blood volume and the airway pressure sequence was repeated. Six other pigs were bled 35% (22.75+/-mL/kg) of their estimated blood volume and the same airway pressure sequence was repeated. Intracranial, aortic, right atrial pressures, arterial blood gases, end tidal CO(2) (ETCO(2)), were measured. ANOVA was used for statistical analysis. Linear regression analysis was performed for ETP and ICP.
Mean arterial and vital organ perfusion pressures were significantly improved and RA pressure significantly decreased with the use of the ITPR; the effect was greater with the more negative ETPs and lower circulating blood volume. The change of ICP was linearly related to the ETP and blood loss: DeltaICP=[1.22-0.84(1-%blood loss/100)]xETP, r(2)=0.88 (in mmHg), p<0.001. There were no adverse device effects and there was a significant increase of ETCO(2) with the use of ITPR.
The ITPR decreased RAP and ICP significantly and improved mean arterial and cerebral and coronary perfusion pressures without affecting acid base balance severely. The decrease in ICP was directly proportional to the reduction in intrathoracic pressure. The effects were more pronounced in severe hypovolemic and hypotensive states with more negative ETP pressure.
胸腔内压力调节器（ITPR）的设计目的是通过在正压通气之间产生持续的气道负压来改善血流动力学，以增加呼吸暂停动物的心脏前负荷。在正常血容量和低血容量猪中，我们测试了以下假设：设定为-5或-10mmHg的持续胸腔内负压，仅在间歇性正压通气时中断，会降低颅内（ICP）和右心房（RAP）压力，并增加平均动脉压（MAP）。
12只猪用丙泊酚麻醉并用袋子通气。在正常血容量条件下，按以下顺序使用ITPR在5分钟内改变基线气管内压力（ETP）：0、-5、0、-10、0mmHg。6只猪失血估计血容量的50%（32.5±mL/kg），并重复气道压力序列。另外6只猪失血估计血容量的35%（22.75±mL/kg），并重复相同的气道压力序列。测量颅内、主动脉、右心房压力、动脉血气、呼气末二氧化碳（ETCO₂）。采用方差分析进行统计分析。对ETP和ICP进行线性回归分析。
使用ITPR时，平均动脉压和重要器官灌注压显著改善，RAP压力显著降低；ETP越负且循环血容量越低，效果越明显。ICP的变化与ETP和失血呈线性相关：ΔICP = [1.22 - 0.84(1 - %失血/100)]×ETP，r² = 0.88（单位为mmHg），p < 0.001。没有不良的设备影响，并且使用ITPR时ETCO₂显著增加。
ITPR显著降低了RAP和ICP，改善了平均动脉压以及脑和冠状动脉灌注压，且未严重影响酸碱平衡。ICP的降低与胸腔内压力的降低成正比。在严重低血容量和低血压状态下，ETP压力越负，效果越明显。
