Pulmonary hypertension and hypoxemia in obstructive sleep apnea syndrome

To determine whether pulmonary hypertension (PH) can occur in obstructive sleep apnea syndrome (OSAS) in the absence of lung or primary cardiac disease, we studied 27 patients (26 males, mean age 49 ± 10 yr) with OSAS (respiratory disturbance index [RDI] > 10 events/h) in whom clinically significant lung or cardiac diseases were excluded. Pulsed Doppler measurements of pulmonary hemodynamics, pulmonary function tests, arterial blood gas analysis, and polysomnography were performed. A total of 11 OSAS patients (41%) were found to have pulmonary hypertension. The levels of PH were relatively mild (Ppa ≤ 26 mm Hg). There were no differences between PH and non-PH patients in body mass index (BMI), smoking history, or lung function. PH patients were more hypoxemic when awake than non-PH patients (Pa(O₂) = 72.2 ± 7.6 versus 77.6 ± 7.3 mm Hg, respectively; p < 0.05) but did not differ in severity of sleep apnea (RDI = 51.9 ± 25.1 versus 56.8 ± 26.2 events/h, respectively, p = NS) or indices of sleep desaturation. The hypoxemia in PH patients could not be explained by impairment of lung function, greater body mass, or a higher prevalence of smoking, and Pa(O₂) in the study population was significantly correlated with Ppa (r = -0.46, p < 0.02) but not with FEV₁ or BMI. We conclude that lung disease is not a prerequisite for PH in OSAS. We speculate that the development of PH in OSAS patients depends more on individual differences in the response of the pulmonary circulation to the episodic alveolar hypoxia and respiratory acidosis associated with sleep apneas than on differences in the frequency or severity of the apneas. Repetitive elevation of Ppa during sleep into the PH range may lead to pulmonary vascular remodeling in 'responders' and thereby daytime PH and hypoxemia.