Physiology

Misconceptions or Recent Advances

• Visceral pleural blood from pulmonary circuit - really from bronchial supply
• Absorption of protein-free fluid via visceral pleura - really absorbed through stomata on parietal surface.
• High rate of normal fluid and protein turnover - actually very low rate

True Concepts

• Fluid formed at parietal surface - Pressure gradient from parietal pleural intestinum to pleural space due to subatmospheric pleural space pressure. Little from visceral surface.
• Pleural protein filtered to 0.3-9.4 g/dl, then water reabsorbed leaving 1-1.5 g/dl
• Lower filtration rate found with radiolabeled albumin studies in sheep by Staub, et al. Old data, likely due to model (dog) and inflammation from pleural catheters. Lymphatics with large reserve - if fluid accumulates, there is both increased fluid formation and decreased clearance
• Six mechanisms of pleural fluid accumulation
  • Increased hydrostatic pressure, especially systemic venous pressure combined with capillary wedge pressure in CHF
  • Decreased oncotic pressure - by itself not a huge problem because of lymphatic reserves
  • Decreased (more negative) pleural pressure - collapsed or trapped lung
  • Increased permeability of microvasculature, inflammatory fluid formation
  • Impaired lymphatic drainage - blockage of channels with tumor, fibrosis, etc.
  • Fluid from peritoneal space - ascites moves via diaphragmatic lymphatics or diaphragmatic defects (less than 1 cm)
• Gas absorption - dependent on N2 gradient. In pneumothorax, 02 therapy increases gradient of N2 from pleural space to venous blood