Current views on the mechanisms of pulmonary oedema

Abstract

Understanding of the causes of pulmonary edema must be based on knowledge of the mechanism responsible for fluid exchange between the several compartments of the normal lung. Recent physiological studies have clarified the main features of these mechanisms. However in 3 areas knowledge is still incomplete, the magnitude of the hydrostatic and oncotic forces responsible for fluid movement within the lung, the means by which protein leaks across the wall of small pulmonary vessels and the routes by which fluid and protein pass between the interstitial tissues of the lung and the alveolar space. On the basis of this physiological knowledge the mode of development of hydrostatic edema, the role of lymphatics in pulmonary edema, and the several stages of pulmonary edema development that may culminate in alveolar flooding are now clearly understood. Knowledge is less complete about edema due to increased vascular permeability. In some experimental models, such as alloxan, leakage is due to irreversible injury to the alveolar wall; in other models, including ANTU .alpha.-apthylthiourea, edema formation depended on minor and reversible changes in pulmonary vascular endothelium similar to those that cause exudate formation in areas of acute inflammation. In no instance is detailed information available of both the rate and magnitude of protein leakage and of the morphological basis of increased vascular permeability. Adequate explanations of the changes that occur in many clinically important types of pulmonary edema, including cardiac failure and neurogenic pulmonary edema are given. Other types of edema, notably that which may complicate traumatic shock or extrapulmonary sepsis and high altitude pulmonary edema, are more complex and the details of their pathogenesis are still obscure.