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[持续正压呼吸下右心损伤的血流动力学。开胸实验研究]

[Hemodynamics in right heart damage under continuous positive pressure respiration. An experimental study of the open thorax].

作者信息

Metzler H

出版信息

Anaesthesist. 1985 Feb;34(2):72-8.

PMID:3885780
Abstract

The haemodynamic effects of isolated right ventricular damage (produced by pressure overloading from temporary banding of the pulmonary artery) under increased positive end-expiratory pressure were investigated in 12 pigs. Under controlled ventilation and anaesthesia with fentanyl and pancuronium bromide the experimental study was performed with an open chest and pericardium; under these circumstances high levels of PEEP resulted primarily in an increase of right ventricular afterload. RAP (+30,2%, p less than 0.05) and RVEDP (+196%, p less than 0,01) of the damaged right ventricle were increased markedly, dRVp/dt is decreased (-18%, p less than 0,05) with a corresponding endsystolic pressure-volume relationship. The decrease of CI after moderate right ventricular lesion is more distinct under PEEP (-27%, p less than 0,01) than previously (-13%). Because of an elevation of TPR-I (+24%) there was no significant fall of systemic arterial pressure (-6,6%); heart rate also remained constant (+3%). Accordingly, with the open chest, haemodynamic changes related to increased positive end-expiratory pressure are very discrete, both in intact and damaged right ventricles; only with high levels of PEEP, elevation of pulmonary vascular resistance--under open chest conditions the predominant factor--limits myocardial performance of the damaged right ventricle and results in a significant reduction of cardiac output.

摘要

在12头猪身上研究了呼气末正压增加时孤立性右心室损伤(由肺动脉临时扎带造成压力过载所致)的血流动力学效应。在芬太尼和潘库溴铵控制通气和麻醉下,通过开胸和心包进行实验研究;在这些情况下,高水平的呼气末正压主要导致右心室后负荷增加。受损右心室的右房压(+30.2%,p<0.05)和右室舒张末期压力(+196%,p<0.01)显著升高,右室压力变化率(dRVp/dt)降低(-18%,p<0.05),伴有相应的收缩末期压力-容积关系。中度右心室损伤后,在呼气末正压下心脏指数(CI)的降低(-27%,p<0.01)比之前(-13%)更明显。由于总外周阻力-指数(TPR-I)升高(+24%),体循环动脉压无显著下降(-6.6%);心率也保持恒定(+3%)。因此,开胸时,无论是完整的还是受损的右心室,与呼气末正压增加相关的血流动力学变化都非常不明显;只有在高水平呼气末正压时,肺血管阻力升高——在开胸条件下这是主要因素——限制了受损右心室的心肌功能,导致心输出量显著降低。

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