[Clinical aspects and pathophysiology of altitude sickness]

Headache, nausea, vomiting, insomnia and peripheral edema are the most important symptoms of acute mountain sickness (AMS), which occur within 6 to 12 h. after exposure to altitudes of more than 2500 m a. s. l. Usually, these symptoms resolve spontaneously; however, they may progress to life-threatening cerebral edema in some cases. High-altitude pulmonary edema (HAPE) is a noncardiogenic edema, which is often preceded by acute mountain sickness. Frequency and severity of these illnesses depend on the altitude, the rate of ascent and the degree of individual susceptibility. A low hypoxic ventilatory drive, sodium and water retention as well as increased capillary permeability are the most important pathophysiological factors which contribute to hypoxemia and edema formation in AMS. They are also important in the pathophysiology of HAPE. In addition, excessive hypoxic pulmonary artery hypertension is most likely crucial in the pathogenesis of HAPE. Constitutional factors which regulate ventilation and pulmonary artery pressure under hypoxia are considered the most important determinants of susceptibility to AMS and HAPE.