Fluid Interchange at the Pulmonary Capillary Wall in Lung Edema †

Although pulmonary edema has been studied as an entity by clinicians and physiologists since the time of Albertini,1 confusion about the course of events leading to the recognizable clinical signs has persisted until the present. Some of this confusion has been due to the tendency on the part of medical scientists to favor a unitary hypothesis for any phenomenon which seems to be circumscribed within a single organ and physiologic framework. By now the multiplicity of events leading to the phenomenon of lung edema has been thoroughly aired,2'8 but there still remains a common focus for all types of pulmonary edema-the excessive accumulation of fluid in the pulmonary pericapillary tissue spaces. In a broad sense, edema is a state in which the normal balance of fluid interchange between blood capillaries and tissue spaces or body cavities is disturbed, leading to an accumulation of plasma filtrate. Although edema is frequently a generalized phenomenon, it is most dramatic when it affects the lung and pleural spaces, the pericardial space, or the brain. This is not because of any fundamental difference in the mechanism of the edema, but rather in the nature of the target organ. Furthermore, the anatomical structure and physiological function of each organ will determine the variable importance of the numerous factors responsible for edema formation. A few years ago, a report from this laboratory posed several questions which had to do with the role of vascular pressure, anoxia, nervous vasomotor control, and ventilation in the genesis of edema of the lung.' Since the studies of Welch in 1878,' these and other questions have guided investigators into countless experiments. The answers to these questions are gradually developing, but we are beginning to see that many of the factors which have been implicated can be quite variable, and all need not be present at any one time.