Vasoconstriction of pulmonary vessels causes an increase in both alveolar capillary pressure and vascular fluid shear stress. Flooding of pulmonary capillaries and increased capillary permeability occur. Fluid and inflammatory cells leak into the air sacs that are normally dry. Pulmonary edema is caused by an imbalance between forces that drive water into the air sacs and the physiologic mechanisms that remove it.
A reaction to lung injury brings about chemical media¬tors of inflammation, vascular endothelial growth factor, interleukin-1, and tumor necrosis factor. These are released from pulmonary structural cells and alveolar macrophages. Neutrophils and platelets are trapped in the pulmonary capillaries. Fluid accumulates in the air sacs resulting in acute shortness of breath.
Hypoxia increases pulmonary vascular resistance and the pulmonary artery pressures rise. Severe exertion further increases pulmonary artery pressures.
Sartori et al. determined that the nasal transepithelial potential difference in persons who were susceptible to high-altitude pulmonary edema was 33% lower than that in individuals who were not susceptible. The susceptible individuals appear to have a defect in transepithelial sodium and water clearance in the lungs, and this may be genetically determined. Severe sudden oxygen lack and exertion appear to render the alveolar-capillary boundary leaky, in susceptible individuals, and fluid with inflamma¬tory cells flood the alveoli.

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