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At the end of 19th century, Starling and Tubby,' in Aa landmark study, interpreted microvascular a landmark fluid and solute exchange as resulting from the balance between hydrostatic and colloidosmotic pressures, according to the following formula:
OF = LP X A [(PCAP - PPL) - (sigma)D(piCAP - piPL)]
where, QF is fluid movement, and LP, A, (sigma)D, P, and pi are filtration coefficient, surface area of the pleura, reflection coefficient for protein movement across the pleura (PL), hydrostatic pressure of the pulmonary capillary bed (CAP), and oncotic pressure of pleural space, respectively.
Thirty years later, Neergard,2 using the Starling equation, offered an explanation for the pleural fluid turnover. He proposed a hypothesis claiming that pleural fluid filters at parietal pleura and is reabsorbed trough the visceral pleura. This hypothesis was further explored by Agostoni and Setnikar,3 who found that the difference between hydrostatic and colloidosmotic pressure in the pulmonary capillaries was large enough to account for the subatmospheric pressure of the pleural liquid. Based on the present state of knowledge, this old hypothesis is no longer valid. According to more recent data, the lung interstitium and the pleural space under physiologic conditions behave as functionally independent compartments due to the low water and solute permeability of the visceral pleura. Pleural fluid is produced at parietal pleural level, mainly in the less dependent region of the cavity. Reabsorption is accomplished by parietal pleural lymphatics in the most dependent part of the cavity, on the diaphragmatic surface and in the mediastinal regions.4
Although most pulmonary and cardiology textbooks claim that either right-sided or biventricular heart failure is necessary for the development of transudative pleural effusion, data suggest that pleural effusions in heart failure are more closely related to left than to right ventricular dysfunction and are mainly due to interstitial pulmonary edema.5,6 Pleural effusion secondary to congestive heart failure (CHF) may be bilateral (60 to 88%) or unilateral (right-sided effusions twice as common as left-sided effusions [8 to 28% vs 4 to 15%, respectively]), free flowing and, using Light's criteria,7 usually transudative.11-10 There is a strong correlation between heart failure and pleural effusion; for this reason, the diagnostic thoracocentesis usually is not recommended. Indeed, in the presence of CHF, a thoracocentesis is recommended only if there is...