Pathophysiology of altitude illness

The pathophysiology of altitude illness is related to the body’s response to hypoxia. Atmospheric pressure falls with increasing altitude, so less oxygen is available to breathe. The threshold altitude for developing symptoms due to reduced oxygen availability is usually about 2500 metres, although altitude illness can occur at lower elevations.

The normal process of acclimatisation to high altitude occurs gradually over weeks. Within minutes of entering an hypoxic environment, the earliest processes of acclimatisation begin. These include hyperventilation, increased heart rate, blood pressure and cardiac output, as well as variable (organ-dependent) vasoconstriction and vasodilation. Within days, haemoglobin production increases and diuresis occurs; together, these elevate haematocrit. Muscle mass decreases and tissues become more vascularParise, 2017. Features of normal acclimatisation include mild headache (high-altitude headache), shortness of breath and diuresis; these usually settle over 24 to 48 hours, but may last up to 5 days after first exposure to high altitude.

Pathological altitude illness occurs when ascent occurs too quickly, and the body does not have sufficient time to acclimatise to the changed environment. The exact mechanisms by which altitude illness develops are not clearParise, 2017. Marked cerebral vasodilation and increased capillary fluid leakage are understood to cause symptoms of acute mountain sickness (AMS) and high-altitude cerebral oedema (HACE). Marked pulmonary vasoconstriction and capillary fluid leakage are thought to cause symptoms of high-altitude pulmonary oedema (HAPE).