Overview

• High-altitude illnesses can occur at altitudes above 2000–2500 m (∼ 6500–8000 feet) as a result of unsuccessful acclimatization
• Manifestations range from acute mountain sickness to high-altitude pulmonary edema and high-altitude cerebral edema.
• Initial management includes supplemental oxygen and cessation of ascent or rapid descent.

Risk factors for altitude illness

• Patient-related: age < 50 years, history of migraines, previous altitude illness
• Rapid ascent pattern: e.g.,
  • Ascent to > 3500 m (∼ 11,500 feet) from < 1200 m in one day
  • Increase in sleeping altitude of > 500 m/day (∼ 1650 feet) above 3000 m (∼ 9850 feet)

Acute mountain sickness (AMS)

Pathophysiology

PiO2 and oxygenation decrease at high altitudes. Acclimatization (a normal compensatory process that occurs in response to the low level of oxygen at high altitude) occurs in different organ systems during the first hours to days. Physiological changes typically become significant at elevations > 2500 m (∼ 8000 feet);

• Early changes: Hypobaric hypoxia triggers ventilation → tachypnea and respiratory alkalosis → increased glycolysis → increased 2,3-BPG synthesis → right shift of oxygen dissociation curve → enhanced tissue oxygenation
• Late changes
  • Polycythemia
  • Arterial pH returns to normal through bicarbonate excretion (renal compensation).
  • Pulmonary hypertension
  • Cor pulmonale and right ventricular hypertrophy

High-altitude pulmonary edema (HAPE)

High-altitude pulmonary edema is a noncardiogenic pulmonary edema occurring shortly after rapid ascent, typically to > 4500 m (∼ 14,500 feet), and is the most common cause of death in individuals ascending rapidly to high altitude.

Pathophysiology

• Similar to acute mountain sickness: a decrease in the partial pressure of arterial oxygen causes vasoconstriction in different organ systems
• Hypoxic pulmonary vasoconstriction → increased pulmonary arterial and capillary pressures → pulmonary hypertension
• Pulmonary hypertension and inflammatory responses → accumulation of extravascular fluid and proteins in the alveolar spaces → pulmonary edema