Pathophysiology Ĭurrently proposed pathophysiology of HAPE. Future genomic testing could provide a clearer picture of the genetic factors that contribute to HAPE. Genes implicated in the development of HAPE include those in the renin-angiotensin system (RAS), NO pathway, and hypoxia-inducible factor pathway (HIF). ĭata on the genetic basis for HAPE susceptibility is conflicting and interpretation is difficult. Įndothelial tissue dysfunction has also been linked to development of HAPE, including reduced synthesis of NO (a potent vasodilator), increased levels of endothelin (a potent vasconstrictor), and an impaired ability to transport sodium and water across the epithelium and out of the alveoli. Microneurographic recordings in these individuals developed a direct link between PAP rise and sympathetic nervous system over-activation, which could explain the exaggerated response to hypoxia in these persons. In these individuals, the pulmonary artery pressure (PAP) and pulmonary vascular resistance (PVR) were shown to be abnormally high. In studies performed at sea level, HAPE-s people were found to have exaggerated circulatory response to both hypoxia at rest and during exercise. There is currently no indication or recommendation for people with PFO to pursue closure prior to extreme altitude exposure. HAPE-susceptible (HAPE-s) individuals were also found to be four times more likely to have a patent foramen ovale (PFO) than those who were HAPE-resistant. Anatomic abnormalities that are predisposing include congenital absence of pulmonary artery, and left-to-right intracardiac shunts (e.g., atrial and ventricular septal defects), both of which increase pulmonary blood flow.

There are multiple factors that can contribute to the development of HAPE, including sex (male), genetic factors, prior development of HAPE, ascent rate, cold exposure, peak altitude, intensity of physical exertion, and certain underlying medical conditions (e.g., pulmonary hypertension). The most reliable sign of HAPE is severe fatigue or exercise intolerance, especially in a climber that was previously not displaying this symptom. Crackles or wheezing (while breathing) in at least one lung fieldĪcute mountain sickness and high altitude cerebral edema may also be present in conjunction with HAPE, however these symptoms may be subtle or not present at all.Weakness or decreased exercise performance.In the presence of a recent gain in altitude, the presence of the following: The Lake Louise Consensus Definition for high-altitude pulmonary edema has set widely used criteria for defining HAPE symptoms. Physiological and symptomatic changes often vary according to the altitude involved. HAPE remains the major cause of death related to high-altitude exposure, with a high mortality rate in the absence of adequate emergency treatment. There are many factors that can make a person more susceptible to developing HAPE, including genetic factors, but detailed understanding is lacking and currently under investigation. It is severe presentation of altitude sickness. Re-entry HAPE is also an entity that has been described in persons who normally live at high altitude but who develop pulmonary edema after returning from a stay at low altitude. However, cases have also been reported between 1,500–2,500 metres or 4,900–8,200 feet in more vulnerable subjects.Ĭlassically, HAPE occurs in persons normally living at low altitude who travel to an altitude above 2,500 meters (8,200 feet). High-altitude pulmonary edema ( HAPE) is a life-threatening form of non-cardiogenic pulmonary edema that occurs in otherwise healthy people at altitudes typically above 2,500 meters (8,200 ft). High-altitude pulmonary oedema (HAPO) Ĭhest x-ray of HAPE showing characteristic patchy alveolar infiltrates with right middle lobe predominance. Medical condition High-altitude pulmonary edema

Symptoms of altitude sickness