Abstract

The pleural space is bounded by two membranes, the visceral pleura covering the lung and the parietal pleura covering the chest wall and diaphragm. Pleural pressure is subatmospheric and ensures inflation of the lung. In the normal state, liquid filters from the systemic pleural microvessels, mostly from the parietal pleura, into the pleural space along the pressure gradient across a leaky mesothelium. The liquid exits via the parietal pleural lymphatics, which open directly into the pleural space via holes called stomata. The lymphatics can increase their rate of liquid clearance approximately 30-fold and thus can accommodate increases in the entry of pleural liquid without allowing accumulation. An abnormal collection of pleural liquid can accumulate if both the pleural liquid entry rate increases and pleural liquid exit rate decreases. The pleural liquid may originate from a wide variety of sources and reach the pleural space because of (1) the subatmospheric pleural pressure, (2) the leaky pleural membranes, and (3) the high capacitance of the pleural space. Because removal of pleural liquid via the lymphatics does not change the protein concentration, the protein of pleural effusions gives information on the formation of the liquid. Depending on the protein and lactate dehydrogenase concentrations of the liquid, these effusions can be categorized as exudates or transudates. By their mechanical effects, pleural effusions can impair ventilatory function by expanding the chest wall and inverting the diaphragm and can impair cardiac function to the point of tamponade by reducing venous return and diastolic filling of the heart.

Full Text
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