Effects of Pulmonary Edema on Lung Mechanics

J. Snapper, J. Sheller
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引用次数: 2

Abstract

It is useful to distinguish between cardiogenic and noncardiogenic pulmonary edema when considering the effects of pulmonary edema on lung mechanics. Pulmonary edema can be caused by an increase in the hydrostatic and oncotic pressures favoring fluid transudation from the capillaries to the pulmonary interstitium and airspaces, or by increased permeability of the pulmonary capillary endothelium. In some patients, a combination of altered driving pressures and permeability may contribute to the development of pulmonary edema. Since left heart failure and increased left atrial pressure are by far the most common causes of increased driving pressures favoring fluid transudation, this type of pulmonary edema is often labelled cardiogenic. In the adult respiratory distress syndrome (ARDS), or noncardiogenic pulmonary edema, pulmonary edema develops in the setting of normal driving pressures. Considerable clinical and experimental evidence supports the concept that the development of pulmonary edema in ARDS is causally related to increased permeability of the pulmonary capillary endothelium.' Since the alterations in lung mechanics associated with cardiogenic pulmonary edema and ARDS differ, the two types of pulmonary edema will be considered separately. These differences may have clinical implications in the therapy of both cardiogenic pulmonary edema and ARDS.
肺水肿对肺力学的影响
在考虑肺水肿对肺力学的影响时,区分心源性和非心源性肺水肿是有用的。肺水肿可由流体静压和肿瘤压力的增加引起,这有利于液体从毛细血管向肺间质和肺间隙的转运,或由肺毛细血管内皮的渗透性增加引起。在一些患者中,驱动压力和通透性的改变可能导致肺水肿的发生。由于左心衰竭和左房压升高是迄今为止驱动压力升高的最常见原因,这类肺水肿通常被标记为心源性。在成人呼吸窘迫综合征(ARDS)或非心源性肺水肿中,肺水肿是在正常驱动压力下发生的。大量的临床和实验证据支持这一概念,即ARDS中肺水肿的发展与肺毛细血管内皮通透性增加有因果关系。由于与心源性肺水肿和ARDS相关的肺力学改变不同,因此将分别考虑两种类型的肺水肿。这些差异可能对心源性肺水肿和ARDS的治疗具有临床意义。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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