Determinants of chronic hypercapnia in Japanese men with obstructive sleep apnea syndrome

Study objective: To identify the determinants of chronic hypercapnia (ie, PaCO2, greater than or equal to 45 mm Hg) in men with obstructive sleep apnea syndrome (OSAS) without airflow obstruction. Design: An analysis was conducted of 143 male patients with OSAS, which had been diagnosed by polysomnography (PSG), who had been referred to a university hospital. Patients were classified as hypercapnic (ie, PaCO2, greater than or equal to 45 mm Hg) and normocapnic (ie, PaCO2, < 45 mm Hg), and obese (ie, body mass index [BMI], greater than or equal to 30 kg/m(2)) or nonobese (ie, BMI, < 30 kg/m(2)). Patients with airflow obstruction (ie, FEV1/FVC ratio, < 70%) were excluded from the study. Baseline clinical characteristics, pulmonary function, PSG data, and blood gas data were compared between hypercapnic and normocapnic patients. Correlations between PaCO2 and several anthropometric, respiratory, and polysomnographic variables were determined by stepwise multiple regression analysis. Results: Fifty-five patients (38%) were hypercapnic. Hypercapnic patients were younger and heavier, and had more abnormalities on pulmonary and PSG testing. Stepwise multiple regression analysis revealed that the PaCO2 level was influenced significantly by the mean level of arterial oxygen saturation (SaO(2)) during sleep and by the percent of vital capacity (%VC) (R-2 = 0.430; p < 0.0001), indicating that 43% of the total variance in the PaCO2 could be explained by the mean SaO(2) and %VC in hypercapnic patients. In contrast, only 13% of the total variance in the PaCO2 was accounted for by the mean SaO(2) and BMI in normocapnic patients (R-2 = 0.134; p = 0.0034). The mean SaO(2), %VC, and PaO2 were selected as independent variables for predicting the PaCO2 in obese patients. These variables explained 41% of the total variance in the PaCO2 (R-2 = 0.407; p < 0.0001), whereas the mean SaO(2) only accounted for 13% of the total variance in PaCO2 levels in nonobese patients (R-2 = 0.134; p = 0.0064). Conclusion. Nocturnal desaturation and restrictive pulmonary impairment play major roles in determining the PaCO2 in hypercapnic and obese OSAS patients without airflow obstruction.