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High altitude pulmonary edema. Med. Sci. Sports Exerc., Vol. 31, No. 1 (Suppl.), pp. S23-S27, 1999. Altitude, speed and mode of ascent, and, above all, individual susceptibility are the most important determinants for the occurrence of high altitude pulmonary edema (HAPE). This illness usually occurs only 2-5 d after acute exposure to altitudes above 2500-3000 m. Chest radiographs and CT scans show a patchy predominantly peripheral distribution of edema. Wedge pressure is normal at rest, and there is an excessive rise of pulmonary artery pressure (PAP) that precedes edema formation and appears to be a crucial pathophysiologic factor for HAPE. Additional factors such as an inflammatory response and/or a decreased fluid clearance from the lung may, however, be necessary for the development of this noncardiogenic pulmonary edema. Bronchoalveolar lavage in patients with mostly advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data to decide whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Supplemental oxygen is the primary treatment in areas with medical facilities whereas the treatment of choice in remote mountain areas is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible. Even susceptible individuals can avoid HAPE when they ascend slowly with an average gain of altitude not exceeding 300-350 m·d−1 above an altitude of 2500 m.