High altitude-induced pulmonary oedema

Cardiovasc Res. 2006 Oct 1;72(1):41-50. doi: 10.1016/j.cardiores.2006.07.004. Epub 2006 Jul 12.

Abstract

Almost one mountain trekker or climber out of two develops several symptoms of high altitude illness after a rapid ascent (> 300 m/day) to an altitude above 4000 m. Individual susceptibility is the most important determinant for the occurrence of high altitude pulmonary oedema (HAPE). Symptoms associated with HAPE are incapacitating fatigue, chest tightness, dyspnoea at the slightest effort, orthopnoea, and cough with due to haemoptysis in an advanced stage of the disease pink frothy sputum. The hallmark of HAPE is an excessively elevated pulmonary artery pressure (mean pressures of 35 and 55 mm Hg), which precedes the development of pulmonary oedema. Elevated pulmonary capillary pressure and protein- as well as red blood cell-rich oedema fluid without signs of inflammation in its early stage are characteristic findings. Furthermore, decreased fluid clearance from the alveoli may contribute to this non-cardiogenic pulmonary oedema. Immediate descent or supplemental oxygen and nifedipine are recommended until descent is possible. Susceptible individuals can prevent HAPE by slow ascent: an average gain of altitude not exceeding 400 m/day above an altitude of 2500 m. If progressive high altitude acclimatization is not possible, a prophylaxis with nifedipine should be recommended.

Publication types

  • Review

MeSH terms

  • Acclimatization
  • Altitude Sickness / etiology*
  • Altitude Sickness / prevention & control
  • Disease Susceptibility
  • Humans
  • Hypertension, Pulmonary / complications
  • Hypertension, Pulmonary / prevention & control
  • Nifedipine / therapeutic use
  • Pulmonary Artery / physiopathology
  • Pulmonary Edema / etiology*
  • Pulmonary Edema / prevention & control
  • Vasodilator Agents / therapeutic use

Substances

  • Vasodilator Agents
  • Nifedipine