Sibbald W J, Anderson R R, Holliday R L
Can Med Assoc J. 1979 Feb 17;120(4):445-50.
Pulmonary edema is common cause of acute respiratory failure and can be seen in not only cardiac but also noncardiac diseases. The pathophysiologic mechanism for the development of acute pulmonary edema in any clinical situation can usually be explained alterations in the forces governing the transvascular flux of fluid in the pulmonary microvasculature, according to the Starling equation. "Cardiac" pulmonary edema is primarily due to an increase in the capillary hydrostatic pressure of sufficient magnitude to overcome the forces maintaining fluid within the vessel and the ability of the lymphatics to drain the transudated fluid. On the other hand, pulmonary edema occurring in association with noncardiac disease (e.g., sepsis, aspiration or shock) is secondary to an increase in the permeability of the pulmonary microvasculature and is referred to as noncardiogenic pulmonary edema or the adult respiratory distress syndrome. This article examines the mechanisms for the development of pulmonary edema and discusses the differences between the cardiac and noncardiac types.
肺水肿是急性呼吸衰竭的常见病因，不仅可见于心脏疾病，也可见于非心脏疾病。根据斯塔林方程，在任何临床情况下，急性肺水肿发生发展的病理生理机制通常都可以用肺微血管中控制液体跨血管流动的力的改变来解释。“心源性”肺水肿主要是由于毛细血管静水压升高到足以克服维持血管内液体的力以及淋巴管引流渗出液的能力。另一方面，与非心脏疾病（如脓毒症、误吸或休克）相关的肺水肿是由于肺微血管通透性增加所致，被称为非心源性肺水肿或成人呼吸窘迫综合征。本文探讨了肺水肿发生发展的机制，并讨论了心源性和非心源性肺水肿类型之间的差异。
