Pulmonary circulation in hypoxia.
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 mmHg with an average of 39 mmHg. Recent echo-Doppler estimates of systolic Ppa in patients with a HAPE are at an average of 53 mmHg, 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 at 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.
Naeije
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Laboratory of Cardiovascular and Respiratory Physiology, Erasme Hospital, Free University of Brussels, Belgium.
D000532:Altitude Sickness / Q000503:physiopathology*; D000818:Animals; D006439:Hemodynamics; D006801:Humans; D000860:Hypoxia / Q000503:physiopathology*; D008168:Lung / Q000098:blood supply; D011652:Pulmonary Circulation / Q000502:physiology*; D011654:Pulmonary Edema / Q000503:physiopathology; D014655:Vascular Resistance / Q000502:physiology; D014661:Vasoconstriction / Q000502:physiology