Metzler H H, Stenzl W, Rehak P H, Tscheliessnigg K H, List W F
J Thorac Cardiovasc Surg. 1987 Jun;93(6):823-31.
Hemodynamic changes after isolated impairment of right ventricular function (produced by increasing afterload by temporary banding of the pulmonary artery) were studied in 22 ventilated pigs during increased levels of positive end-expiratory pressure (4, 8, 12, and 16 cm H2O). In the open chest group, application of positive end-expiratory pressure produced only a slight decrease of cardiac index. After right ventricular damage a decrease of cardiac index of more than 25% occurred only when higher levels of positive end-expiratory pressure were applied. In contrast to the open chest group, the closed chest group showed more distinct cardiovascular responses after positive end-expiratory pressure. In the damaged right ventricle with a positive end-expiratory pressure of 16 cm H2O, right ventricular end-diastolic pressure increased more than 100%. With positive end-expiratory pressure, cardiac index decreased 34% before and 47% after right ventricular damage. We conclude that positive end-expiratory pressure induces a more pronounced decrease in cardiac index if right ventricular function is impaired. During open chest conditions with lower levels of positive end-expiratory pressure, these changes are only small, however, and probably irrelevant. During closed chest conditions, the hemodynamic changes are much more pronounced. High right ventricular end-diastolic pressures resulting from impaired right ventricular contractility as well as from high levels of positive end-expiratory pressure may have an impact on biventricular function and right ventricular coronary driving pressure.
在22只通气猪中,研究了在呼气末正压(4、8、12和16厘米水柱)升高时,右心室功能单独受损(通过临时结扎肺动脉增加后负荷产生)后的血流动力学变化。在开胸组中,应用呼气末正压仅使心脏指数略有下降。右心室损伤后,仅在应用较高水平的呼气末正压时,心脏指数才会下降超过25%。与开胸组相比,闭胸组在应用呼气末正压后表现出更明显的心血管反应。在呼气末正压为16厘米水柱的受损右心室中,右心室舒张末期压力增加超过100%。应用呼气末正压时,心脏指数在右心室损伤前下降34%,损伤后下降47%。我们得出结论,如果右心室功能受损,呼气末正压会导致心脏指数更明显的下降。然而,在开胸条件下,呼气末正压水平较低时,这些变化很小,可能无关紧要。在闭胸条件下,血流动力学变化更为明显。右心室收缩功能受损以及高水平的呼气末正压导致的高右心室舒张末期压力可能会影响双心室功能和右心室冠状动脉驱动压力。