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急性油酸肺损伤后生理死腔对呼气末正压反应的机制

Mechanisms of physiological dead space response to PEEP after acute oleic acid lung injury.

作者信息

Coffey R L, Albert R K, Robertson H T

出版信息

J Appl Physiol Respir Environ Exerc Physiol. 1983 Nov;55(5):1550-7. doi: 10.1152/jappl.1983.55.5.1550.

DOI:10.1152/jappl.1983.55.5.1550
PMID:6358162
Abstract

In acute increased-permeability edema, the Bohr physiological dead space (VD/VTCO2) can be influenced by changes in anatomic dead space, ventilation-perfusion (VA/Q) heterogeneity, shunt, and the Haldane effect. We used the multiple inert gas elimination technique to assess the effect of positive end-expiratory pressure (PEEP) on each of these components of VD/VTCO2 in 14 pentobarbital-anesthetized dogs with increased permeability edema induced by infused oleic acid. PEEP of 5, 10, 15, and 20 cmH2O was applied in random sequence. Following injury VD/VTCO2 increased. It decreased with 5 or 10 cmH2O PEEP but increased progressively at higher PEEP levels. The decrease in VD/VTCO2 at 5 or 10 cmH2O PEEP was due to reductions in shunt and midrange VA/Q heterogeneity. The increase in VD/VTCO2 that occurred with higher PEEP levels was due to increased ventilation to high VA/Q regions and a larger anatomic dead space. Haldane effect magnified the shunt component of VD/VTCO2 but reduced the influence of midrange VA/Q heterogeneity.

摘要

在急性通透性增加性水肿中,玻尔生理死腔(VD/VTCO2)可受解剖死腔、通气-灌注(VA/Q)不均一性、分流及哈代效应变化的影响。我们采用多种惰性气体消除技术,评估呼气末正压(PEEP)对14只戊巴比妥麻醉、因输注油酸诱导产生通透性水肿的犬的VD/VTCO2各组成部分的影响。以随机顺序施加5、10、15和20 cmH2O的PEEP。损伤后VD/VTCO2升高。在5或10 cmH2O PEEP时其降低,但在更高PEEP水平时逐渐升高。5或10 cmH2O PEEP时VD/VTCO2降低是由于分流及中等范围VA/Q不均一性的减少。更高PEEP水平时VD/VTCO2升高是由于高VA/Q区域通气增加及解剖死腔增大。哈代效应放大了VD/VTCO2的分流部分,但减少了中等范围VA/Q不均一性的影响。

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