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High-altitude pulmonary hypertension: a pathophysiological entity to different diseases
1Intensive Care Unit of the Dept of Internal Medicine, University Hospital, Zurich, Switzerland. klinmax@usz.unizh.ch
The European Respiratory Journal
|December 19, 2003
Summary
Pulmonary hypertension at high altitudes causes high-altitude pulmonary oedema (HAPE) and right heart failure. Structural changes in pulmonary arteries, not just functional, drive these conditions, necessitating revised terminology.
Area of Science:
- Altitude sickness
- Cardiopulmonary physiology
Background:
- Pulmonary hypertension is key in high-altitude pulmonary oedema (HAPE) and right heart failure (subacute/chronic mountain sickness).
- Alveolar hemorrhage from elevated pulmonary artery pressure/flow is a proposed HAPE mechanism.
- Extended acclimatization prevents HAPE but not right heart failure at 6,000m.
Purpose of the Study:
- To explore the pathophysiological mechanisms of high-altitude pulmonary hypertension and related conditions.
- To propose revised terminology for altitude-induced cardiopulmonary issues.
Main Methods:
- Review of existing studies on high-altitude pulmonary hypertension, HAPE, and mountain sickness.
- Analysis of acclimatization effects on HAPE and right heart failure.
- Assessment of pulmonary hypertension response to oxygen and altitude changes.
Main Results:
- Rapid arterial remodeling may prevent HAPE but not right heart failure.
- Pulmonary hypertension is largely unresponsive to oxygen at altitude.
- Complete resolution of pulmonary hypertension occurs only after prolonged low-altitude stays, suggesting structural changes.
Conclusions:
- Structural changes in pulmonary arteries are the likely mechanism for high-altitude pulmonary hypertension.
- Pulmonary hypertension drives HAPE and high-altitude right heart failure.
- Current terminology should be adjusted to reflect the driving role of pulmonary hypertension.