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High altitude pulmonary oedema.

Peter Bärtsch1, Heimo Mairbäurl, Erik R Swenson

  • 1Department of Internal Medicine, Medical University Clinic Heidelberg, Germany. peter_bartsch@med.uni-heidelberg.de

Swiss Medical Weekly
|August 30, 2003
PubMed
Summary

High altitude pulmonary oedema (HAPE) is caused by rapid ascent and high altitudes. Slow ascent, typically under 350m daily above 2500m, prevents HAPE.

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Area of Science:

  • Physiology
  • Altitude Medicine
  • Pulmonary Medicine

Background:

  • High altitude pulmonary oedema (HAPE) is a serious condition affecting individuals ascending to high elevations.
  • It typically manifests within the first few days of exposure to altitudes above 2500-3000 meters.
  • Elevated pulmonary artery pressure is a key factor in HAPE development.

Purpose of the Study:

  • To investigate the pathophysiology of incipient high altitude pulmonary oedema (HAPE).
  • To identify key determinants and preventative strategies for HAPE.

Main Methods:

  • Utilized right heart catheterization to measure pressures.
  • Employed bronchoalveolar lavage (BAL) to analyze alveolar fluid and cells.
  • Investigated fluid dynamics within the alveoli.

Main Results:

  • HAPE is characterized as hydrostatic oedema with normal left atrial pressure.
  • Demonstrated high permeability leakage of the alveolocapillary barrier and mild alveolar hemorrhage.
  • Evidence suggests decreased alveolar fluid clearance contributes to non-cardiogenic pulmonary oedema.
  • Inflammatory responses may occur in advanced HAPE cases.

Conclusions:

  • HAPE is primarily determined by altitude, ascent profile, and individual susceptibility.
  • Gradual acclimatization, with ascent gains not exceeding 300-350 m/day above 2500 m, is crucial for prevention.
  • Treatment involves supplemental oxygen or immediate descent; nifedipine is an alternative if descent is not feasible.

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