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Hypoxic pulmonary vasoconstriction and high altitude pulmonary edema
The American Review of Respiratory Disease
|August 1, 1986
Summary
Pulmonary vasoreactivity testing at sea level does not reliably predict susceptibility to high altitude pulmonary edema. This study found normal responses in a patient who later developed the condition.
Area of Science:
- Cardiovascular Physiology
- Altitude Medicine
- Respiratory Physiology
Background:
- High altitude pulmonary edema (HAPE) is a life-threatening condition.
- Pulmonary vasoreactivity testing assesses the lung's response to hypoxia.
- Predicting HAPE susceptibility is crucial for mountaineers and high-altitude dwellers.
Observation:
- A 51-year-old male underwent pulmonary hemodynamic testing during normobaric inspiratory hypoxia (FiO2 0.125).
- Testing was performed 11 months before and 3 weeks after a HAPE episode at 5,700m.
- Pulmonary vascular resistance increased significantly, consistent with normal volunteer responses.
Findings:
- The patient's pulmonary hemodynamic response to hypoxia at sea level was within the normal range.
- Despite a prior HAPE episode, the vasoreactivity test did not indicate increased susceptibility.
- Arterial PO2 decreased to 40-43 mmHg during hypoxic challenge.
Implications:
- Pulmonary vasoreactivity testing to hypoxia at sea level may not be a reliable indicator for HAPE risk.
- Individual susceptibility to HAPE might depend on factors beyond acute hypoxic pulmonary vasoconstriction.
- Further research is needed to identify accurate biomarkers for HAPE susceptibility.