Who Gets High Altitude Pulmonary Edema And Why?

This paper focuses on high altitude pulmonary edema (HAPE) that occurs in individuals who are free of any pre-existing disease. An exaggerated hypoxic pulmonary vasoconstriction (HPV) is a hallmark of susceptibility to HAPE. In addition, a low hypoxic ventilatory response and defective sodium-dependent absorption of water from the alveoli may contribute to HAPE-susceptibility. However, excessive pulmonary artery hypertension appears to be crucial for the development of HAPE, since lowering pulmonary artery pressure by drugs, such as nifedipine or tadalafil (phospho-diesterase-5-inhibitor), will in most cases prevent HAPE. There is increasing evidence that the excessive pulmonary artery pressure response in HAPE-susceptible individuals is due to a reduced NO bioavailability. HAPE-susceptible individuals show an endothelial dysfunction in the systemic circulation in hypoxia. Lower levels of exhaled NO in hypoxia before and during HAPE in susceptible individuals suggest that this abnormality also occurs in the lungs and polymorphisms of the eNOS gene are associated with susceptibility to HAPE in the Indian and Japanese population.

Keywords: high altitude pulmonary edema; hypoxia; pulmonary circulation; endothelial dysfunction; NO; pathophysiology