Congestive heart failure probably results in pleural eflusions because of increased leakage of fluid into the pulmonary interstitium, which collects in the pleural space, and increased systemic venous pressure, which decreases lymphatic flow and therefore decreases pleural fluid absorption. Diuretics could lead to fluid resolution through multiple mechanisms. By decreasing left atrial pressure, less fluid would leak from the pulmonary microvasculature, leading to decreased fluid formation and eventual resolution by lymphatic drainage. Also, by decreasing systemic venous pressure, the lymphatic drainage would be increased. Finally, decreasing systemic arterial pressure could lead to a pressure gradient that favored fluid reabsorption via the pleural microvessels.
Exudative causes for effusions usually involve some type of inflammation and compromise of the pulmonary or pleural microvasculature, which leads to increased leakage of fluid that has a higher concentration of protein. Therefore, the gradient between serum and fluid protein will be low. Figure 1 shows that measuring the fluid-to-serum protein ratio or the albumin gradient will lead to a highly significant separation of transudates from exudates.
Chakko et al showed that treatment of patients with congestive heart failure and pleural effusions with diuretics leads to a concentration of pleural fluid protein which can be in the exudative range. Five patients in our series, four of whom had had previous diuretic therapy, were misclassified as “pseudoexudates” by Lights criteria. By applying the criterion of an albumin gradient greater than 1.2 g/dl to indicate a transudate, all five patients were correctly classified. In our series the albumin gradient criterion for exudates was 100 percent specific, while Lights criteria were 72 percent specific.