Abstract
Hypoxia constricts the pulmonary vessels. An increase in pulmonary vascular resistance
is seen in normal subjects during hypoxic breathing at sea level, in acclimatized
lowlanders and in high altitude natives. Hypoxic pulmonary hypertension in all these
circumstances is most generally moderate, except in high altitude natives at exercise.
However, in the absence of high altitude pulmonary edema (HAPE) or chronic mountain
sickness, a right heart failure that would be the human counterpart of brisket disease
described in cattle, apparently never occurs. In adult patients with HAPE, reported
mean pulmonary artery pressures (Ppa) measured during a right heart catheterization
range from 22 to 63 mm Hg with an average of 39 mm Hg. Recent echo-Doppler estimates
of systolic Ppa in patients with a HAPE are at an average of 53 mm Hg, only moderately
higher than in healthy subjects exposed to comparable normobaric or hypobaric hypoxia.
Subjects with a previous HAPE often present with an enhanced pulmonary vascular reactivity
to hypoxia compared to controls when tested ay sea level, but the overlap is great.
Non invasive echo-Doppler pulmonary hemodynamic studies at sea level have not been
reported to reliably discriminate subjects susceptible to HAPE.
Key words
Hypoxic pulmonary vasoconstriction - high altitude pulmonary edema - altitude
