Culver B H, Marini J J, Butler J
J Appl Physiol Respir Environ Exerc Physiol. 1981 Mar;50(3):630-5. doi: 10.1152/jappl.1981.50.3.630.
To investigate the changes in ventricular function that occur during continuous positive-pressure ventilation, we studied the effects of separate increases in lung volume, pleural pressure, and right ventricular afterload in 15 dogs. Isovolume increases of pleural pressure caused changes in right and left ventricular hemodynamics indistinguishable from those induced by preload reduction. Lung distension with the chest open to atmosphere caused both right and left atrial intracavitary pressures to rise as cardiac output fell, suggesting altered function of both ventricles. Raising right ventricular afterload by pulmonary artery constriction did not reproduce the hemodynamic changes observed during increases of lung volume. These data indicate that the apparent alteration of ventricular function that occurs during continuous positive-pressure ventilation is produced by the associated increase in lung volume and that a right ventricular afterload-ventricular interdependence effect is not the responsible mechanism.
为了研究持续正压通气期间心室功能的变化，我们在15只犬中分别研究了肺容积、胸膜压力和右心室后负荷增加的影响。胸膜压力的等容增加引起的左右心室血流动力学变化与前负荷降低引起的变化无法区分。在胸腔开放于大气的情况下肺扩张导致心输出量下降时左右心房腔内压力均升高，提示两个心室的功能均发生改变。通过肺动脉收缩增加右心室后负荷并未重现肺容积增加时观察到的血流动力学变化。这些数据表明，持续正压通气期间出现的心室功能明显改变是由相关的肺容积增加所致，而右心室后负荷-心室相互依赖效应并非其作用机制。
