[Pulmonary hypertension in patients with pure obstructive sleep apnea]. / Nadcisnienie plucne u chorych na niepowiklany obturacyjny bezdech senny.

UNLABELLED: Patients with obstructive sleep apnoea (OSA) every night experience recurrent episodes of alveolar hypoxia. Alveolar hypoxia is the most potent pulmonary vasoconstrictor causing remodeling of pulmonary arteries and pulmonary hypertension. Development of pulmonary hypertension in patients with OSA is rather rarely observed but still discussed. We studied pulmonary haemodynamics, using Swan Ganz thermodilution catheter, in 67 patients (64 M and 3 F, mean age 45 years) with severe OSA (in full polysomnography mean AHI = 62) and normal pulmonary function data. We observed normal mean haemodynamic values at rest: PPA 15,8 mm Hg, PW 6.8 mm Hg, CO 5.6 L/min. PVR 150 dyn.sec.cm(-5). In 11 pts (16%) the pulmonary artery pressure at rest was elevated (PPA 23.9 mm Hg and PVR 234 dyn.sec.cm(-5)), they were younger, more obese and had higher number of apneic episodes per hour of sleep. During mild exercise (44 pts) PPA rose from 15.8 mm Hg to 29.8 mm Hg and was abnormally high in 17 pts. IN CONCLUSION: we observed pulmonary hypertension at rest in 16% patients with severe OSA, but during exercise in about 40%.

Effects of intermittent exposure to high altitude on pulmonary hemodynamics: a prospective study.

Chronic alveolar hypoxia due to disease or low atmospheric pressure at high altitude results in the development of hypoxic pulmonary hypertension. The effects of intermittent hypoxia on pulmonary hemodynamics in healthy men have not been studied. We aimed to investigate, prospectively, pulmonary hemodynamics in workers commuting between an elevation of 3700 and 4200 m (4-week working shift) and lowland, below 500 m (4 weeks of holiday). Pulmonary hemodynamics has been investigated by Doppler echocardiography in 26 healthy Caucasian males, mean age 42 +/- 9 yr. First at lowland (760 m) and next during the fourth week of work at high altitude. Investigations were repeated in 21 subjects 1 year later at the end of the high-altitude exposure. The third series of investigations was performed 2 yr after the initial ones in 10 subjects who earlier had shown the strongest hypoxic vasoconstriction. At lowland, subjects presented with normal pulmonary hemodynamics. At high altitude, mean pulmonary artery pressure (PAPm) rose from 14.7 +/- 2.7 mmHg to 25.8 +/- 8.3 mmHg. One year later the PAPm remained unchanged in hypoxic conditions (25.0 +/- 7.3 mmHg). At the end of a 2-year follow-up of 10 "hyperreactors," PAPm measured at the end of the hypoxic exposure was the same as at the initial investigation, averaging 28 +/- 4.0, 28 +/- 3.5, and 29 +/- 2.5 mmHg at the beginning and at 1 and after 2 yr of intermittent exposure to high altitude. We concluded that intermittent exposure to 4000 m lasting 3 yr does not lead to development of permanent pulmonary hypertension.