High Altitude Pulmonary Edema

Abstract

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 days after acute exposure to altitudes above 2,500-3,000 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 in pulmonary artery pressure (Ppa) which precedes edema formation. Bronchoalveolar lavage in patients with advanced HAPE shows evidence of inflammatory response with increased capillary permeability. There are, however, no prospective data indicating whether the inflammatory response is a primary cause of HAPE or a consequence of edema formation. Excessive rise in Ppa appears to be a crucial pathophysiologic factor for HAPE. Recent observations of high Ppa in HAPE-susceptible sujects who did not develop pulmonary edema after rapid ascent to high altitude suggest either that Ppa does not necessarily reflect capillary pressure in these individuals or else that additional factors, such as an inflammatory response and/or a decreased fluid clearance from the lung, are necessary for the development of pulmonary edema. The treatment of choice is immediate descent. When this is impossible and supplemental oxygen is not available, treatment with nifedipine is recommended until descent is possible.

Assessment of High Altitude Tolerance in Healthy Individuals

“…An abnormal rise of pulmonary artery pressure plays a crucial role in the pathophysiology of HAPE (Bärtsch, 1997;Bärtsch, 1999). Studies using right-heart catheterization have demonstrated that HAPE-susceptible subjects have an abnormal rise in pulmonary artery pressure during brief exposure to hypoxia (FIO 2 5 0.12) at low altitude (Hultgren, Grover, and Hartley, 1971;Eldridge et al, 1996), and also during exercise in normoxia (Eldridge et al, 1996;Kawashima et al, 1989).…”

Rare Mitochondrial DNA Polymorphisms are Associated with High Altitude Pulmonary Edema (HAPE) Susceptibility in Han Chinese

“…This condition normally occurs at altitudes above 3000 m and affects many people including previously fit individuals. [1][2][3][4] Advances in the understanding of the biochemical pathways involved in the physiologic response to hypoxia have led to greater insights into the pathogenesis of HAPE.…”

Letter from Denali: Pulmonary Edema at High Altitude

“…Several reviews are available to trace that history (Schoene, 1987;Hackett and Roach, 1990;Richalet, 1995;Bartsch, 1997). Pioneered by Hultgren, studies in the 1960s and 1970s focused on pulmonary and cardiac hemodynamics to determine if there was left ventricular dysfunction and/or excessive pulmonary hypertension that led to a breakdown in the pulmonary vascular barrier, resulting in diffuse pulmonary edema and hypoxemia.…”