Non-Cardiogenic Pulmonary Edema

T he barrier between pulmonary capillaries and alveolar gas consists of a series of three anatomical layers with distinct structural characteristics. The cytoplasmic projections of the capillary endothelial cells represent the first layer of this barrier and overlap to form a continuous cytoplasmic tube. At the overlapping junctions of these cytoplasmic projections are clefts of varying sizes (averaging approximately 4 nm in width), which provide communication between pulmonary capillaries and the interstitial space (loose junctions). The interstitial space represents the second layer and contains connective tissue, fibroblasts, macrophages, small arteries, veins and lymphatic channels. The third layer is the alveolar wall which is continuous with the bronchial epithelium and is composed of large squamous cells with thin cytoplasmic projections. These projections overlap in a similar way to the projections of capillary endothelium. In contrast to the endothelial junctions, which allow for variable continuity between capillaries and interstitial space, the alveolar epithelial clefts are obliterated by complete fusion of the membranes of the adjacent cells, so as to demand greater forces for their disruption (tight junctions). The tightness of these junctions helps to forestall alveolar flooding, which represents the final stage of pulmonary edema. In other tissues there is normally a continuous exchange of liquid and colloids between the vascular bed and the interstitium. The lymphatics serve to continuously remove colloids and fluid from the interstitial space to the systemic venous circulation, so as to ensure that the volume of interstitial space remains constant. Pulmonary edema develops when the movement of liquid from the blood vessels to the interstitial space and in some instances to the alveoli exceeds the return of liquid to the blood by way of the lymphatics. Whether initiated by an imbalance of Starling forces or by primary damage to the various components of the alveolarcapillary membrane, the sequence of liquid exchange and accumulation in the lungs is the same and can be represented as three separate stages. In stage 1, there is an increase in transfer of liquid from blood capillaries to the interstitial space. The pulmonary capillary endothelial junctions are widened by an increase in filtrative forces or by toxic damage of the membrane. Despite the increased filtration, there is no increase in interstitial volume because there is an equal increase in lymphatic drainage. When the filtered load from the pulmonary capillaries to the interstitial space is increased beyond a limit, the lymphatics cannot follow this rapid rhythm and liquid and colloid begin to accumulate in the more compliant interstitial compartment surrounding bronchioles, arterioles and venules (stage 2). With further increase in filtered load, the volume limits of the more compliant Non-Cardiogenic Pulmonary Edema