Daytime pulmonary hemodynamics in patients with obstructive sleep apnea without lung disease.

It is controversial whether obstructive sleep apnea (OSA) causes pulmonary hypertension (PH) in the absence of hypoxemic lung disease. To investigate this further we measured awake pulmonary hemodynamics, pulmonary gas exchange, and small airways function in 32 patients with OSA (apnea- hypopnea index, mean +/- SE, 46.2 +/- 3. 9/h) who had normal screening lung function. Pulmonary artery pressure (Ppa) and cardiac output were measured by Doppler echocardiography at three levels of inspired oxygen (FIO2 0.50, 0.21, and 0.11) and during incremental increases in pulmonary blood flow (10, 20, and 30 microgram/kg/min dobutamine infusions) while breathing 50% oxygen. Eleven patients had PH (mean Ppa >/= 20 mm Hg, Group I). They did not differ from patients without PH (Group II) in lung function, severity of sleep-disordered breathing, age, or body mass. Compared with Group II, Group I patients had increased small airways closure during tidal breathing (FRC-closing capacity: Group I, -0.16 +/- 0.11; Group II, 0.27 +/- 0.09 L; p < 0.05), more ventilation-perfusion inequality (AaPO2: 23.8 +/- 2.8; 19.8 +/- 1.4 mm Hg; p = 0.08), a greater pulmonary artery pressor response to hypoxia (DeltaPpa FIO2, 0.50 to 0.11: 16.4 +/- 1.93; 6.4 +/- 0.77 mm Hg; p < 0.05) and a marked rise in Ppa during increased pulmonary blood flow. We conclude that PH may develop in some patients with OSA without lung disease and that it is associated with small airways closure during tidal breathing and heightened pulmonary pressor responses to hypoxia and during increased pulmonary blood flow. Such changes are consistent with remodeling of the pulmonary vascular bed in affected patients with OSA, seemingly unrelated to severity of sleep-disordered breathing.