By J. B. West (auth.), T. H. Stanley, R. J. Sperry (eds.)
Anesthesia and the Lung 1992 offers contemporary advances within the analysis, pre-, intra-, and postoperative anesthetic administration of sufferers with lung affliction, offering for pulmonary and non-pulmonary surgical procedure. It additionally offers with ventilation-perfusion concerns, the lung as a metabolic organ, the consequences of anesthesia on pulmonary mechanics and pulmonary blood movement. additionally, there are chapters that concentrate on hypoxia; nearby adjustments within the lung; pulmonary surfactant; fresh advances within the knowing of pulmonary edema; excessive altitude illness; anesthesia and the regulate of respiring; fresh improvement in oximetry; instrumentation designed to degree pulmonary oxygen stress, pO2 and pCO2 transcutaneously; differential lung air flow; reactive airlines; septic surprise; the grownup respiration misery syndrome and diverse elements of ventilatory aid.
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Additional info for Anesthesia and the Lung 1992
This may contribute to the circumferential tension of the alveolar wall depending on the geometry. The capillary wall stress can be calculated for typical conditions at failure. 3 microns (6). Gehr et a1. 4 microns. Using these figures, the calculated wall stress is about 8 x 105 dyn/cm2 (8 x 104 N/m 2 ). This is an extremely high stress being approximately the same as the wall stress of the normal aorta which is predominantly composed of collagen and elastin. By contrast, the thin side of the blood-gas barrier has approximately half of its thickness made up of the single layers of capillary endothelial and alveolar epithelial cells, the other half being composed of the extra-cellular matrix.
Finally, stress failure can be expected when either the capillary transmural pressure is abnormally high, or the strength of the extracellular matrix is abnormally low. The later probably occurs in Goodpasture's Syndrome where the collagen-IV is cleaved by auto antibodies which specifically attack this molecule. The result is bleeding both into the lung and the kidney, the two microcirculations most at risk from a raised capillary pressure. It is also conceivable that the break down of alveolar walls 50 seen in alpha 1 antitrypsin deficiency where the collagen is attacked by neutrophil elastase could be considered stress failure though this takes place over years rather than days or seconds.
We attributed the changes to the high mechanical stresses to which the capillary walls were exposed. An analysis was made of the three principal forces acting on the capillary wall. The first is the circumferential or hoop tension caused by the transmural pressure, and determined by the Laplace law. The second force is the surface tension of the alveolar lining layer because, since the capillaries bulge into the alveolar spaces, this surface tension supports the capillary walls and tends to prevent stress failure.