Stress failure of the blood-gas barrier

Abstract

The blood-gas barrier must be extremely thin because oxygen and carbon dioxide cross the alveolar-capillary membrane by passive diffusion, and the diffusion resistance is proportional to thickness. Despite its remarkable size (harmonic mean thickness approximately 0.6 microm) the membrane must be immensely strong, because maintenance of its integrity is fundamental for pulmonary gas exchange. The basement membrane is probably the principal anatomical structure providing the strength of the blood-gas barrier. Experimental studies have demonstrated that wall stress of the capillaries can become very high when perfusion pressure is increased to 5.2 kPa (39 mmHg) or more, which was associated with breaks of the capillary endothelium, the alveolar epithelium, or both. These values are potentially reached or exceeded in different cardiac or pulmonary diseases, or in healthy humans subjected to heavy exercise. Stress failure of pulmonary capillaries may play a role in neurogenic pulmonary oedema, high-altitude pulmonary oedema, re-expansion pulmonary oedema, and some forms of the adult respiratory distress syndrome. Increased alveolar pressure due to lung inflation potentiates damage of the blood-gas barrier, suggesting that increases in capillary transmural pressure and transpulmonary pressure are equivalent in terms of their effects on capillary wall stress. These data may have importance for the management of patients with acute respiratory failure requiring mechanical ventilation.