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Medical > Therapy > General measures

Air travel and altitude exposure

Excessive hypoxic pulmonary vasoconstriction is the hallmark of high altitude pulmonary edema-susceptible subjects. Up to 60 % of climbers with a previous episode of high altitude pulmonary edema repeat it if exposed to altitude without adequate acclimatization (Bärtsch, 1997).

Appetite-suppressive drugs restore hypoxic pulmonary vasoconstriction in dogs (Naeije et al., 1995) and are a risk factor for the development of high altitude pulmonary edema in humans (Naeije et al., 1996). In rats, increased 5-hydroxytriptamine transporter expression that follows discontinuation of dexfenfluramine treatment promotes pulmonary hypertension (Eddahibi et al., 2001). Although reactivity of the pulmonary vasculature to hypoxia has not been tested in patients with pulmonary hypertension, it is likely that environmental hypoxia causes an additional increase in pulmonary vascular resistance, which in turn could precipitate to right heart failure. Thus, patients with pulmonary hypertension in normoxia should not be exposed to altitude and air travel without supplemental oxygen (SaO2 ≥ 90 %) and climbers susceptible to high altitude pulmonary edema should not ascend more than of 300 m/day (sleeping altitude) (Bärtsch, 1997). Should an accurate acclimatization for a high altitude pulmonary edema susceptible subject not be possible, nifedipine has been proven to prevent excessive increase in pulmonary artery pressure and, consequently, high altitude pulmonary edema formation (Bärtsch et al., 1991).

References

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