Key messages

• Acute mountain sickness is associated with relative hypoventilation in relation to high-altitude hypoxia, water and sodium retention, and endothelial cell activation with increased capillary permeability.

• The severity of symptoms correlates with the degree of hypoxemia.

• Possible pathogenetic factors for the development of high-altitude cerebral edema include a depletion reduction in the active outward sodium transport, hydrostatic edema due to the increase in cerebral blood flow, a decrease in intracranial compliance, and hypoxia-induced angiogenesis and osmotic swelling.

• High-altitude pulmonary edema may be due to overperfusion, high permeability, or mechanical damage to pulmonary endothelial and epithelial cells.

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