CHRONIC HYPERCAPNIA IN OBSTRUCTIVE SLEEP APNEA-HYPOPNEA SYNDROME

In order to determine the relationship between chronic hypercapnia and anthropomorphic data, pulmonary function tests and slopes of ventilat ory responses to hypercapnia (HVCR) and hypoxia (HVR), we studied 55 p atients with sleep apnea-hypopnea syndrome (SAHS). Patients were divid ed into hypercapnic, PaCO2, greater than or equal to 45 mm Hg (Group I , n = 23, PaO2 = 61 +/- 10 and PaCO2 = 50 +/- 5 mm Hg, and [HCO-(3)] = 30 +/- 4 mEq/1[means +/- SD]) and normocapnic (or eucapnic), PaCO2 < 45 mm Hg (Group II, n = 32, PaO2 = 76 +/- 10 and PaCO2 = 39 +/- 4 mm H g and [HCO-(3)] = 25 +/- 3 mEq/1 [means +/- SD]) groups. When compared to the normocapnic group, hypercapnic patients were significantly hea vier (with greater body surface area) and had significantly more sever e restrictive and obstructive defects and impaired HVR and HCVR. The m eans (+/-SD) of some of the data follow ( indicates p < 0.05 when Gro up I is compared to Group II): [GRAPHICS] When subgroups of hypercapni c and eucapnic patients with similar lung functions were compared, the subgroups differed significantly in their weights; conversely, in sub groups with comparable weights, lung function tests differed significa ntly. These data suggest that the mechanisms of chronic hypercapnia ar e multifactorial, and we hypothesize that, in the face of repetitive a pneas and hypopneas, increased weight and abnormal lung function tests interact and contribute to the generation and maintenance of hypercap nia.