VENTILATION AND GAS-EXCHANGE DURING SLEEP AND EXERCISE IN SEVERE COPD

Ventilation and gas exchange were studied during sleep and incremental treadmill exercise in 19 patients with severe stable COPD with the pr imary aim of comparing the pathophysiology of oxygen desaturation in t he two conditions. A secondary aim was to determine whether exercise s tudies could aid in the prediction of sleep desaturation. Full polysom nography was used, and ventilation, arterial oxygen saturation (SaO(2) ), and transcutaneous PCO2 (PtcCO(2)) mere monitored continuously duri ng sleep. No patient had significant sleep apnea. Mean (SD) FEV(1) was 32 (9.1)% predicted, PaO2 was 71.2 (12.4) mm Hg, and PaCO2 was 44.5 ( 4.6) mm Hg. SaO(2) fell twice as much during sleep as during maximum e xercise: 13.1 (8.9) vs 6.0 (3.6)% (p<0.001). The mean sleep and exerci se SaO(2), and minimum sleep and exercise SaO(2) were well correlated on linear regression (r=0.81 and 0.78, respectively, p<0.001), but on multiple regression analysis, awake PaO2 was a better predictor of sle ep desaturation than was exercise desaturation. The 12 major desaturat ors (minimum sleep SaO(2) <85%) had twice as great a fall in exercise SaO(2) as the 7 minor desaturators (3.6+/-2.8 vs 7.4+/-3.3%, p<0.05). The major desaturators also had a greater fall in estimated sleep PaO2 : 19.8 (5.1) vs 6.4 (7.1) mm Hg (p<0.01), which suggests that their gr eater sleep desaturation is not simply due to their position on the st eep portion of the oxyhemoglobin dissociation curve. The rise in PtcCO (2) during sleep was similar among major and minor desaturators: 7.5 ( 2.9) vs 5.8 (3.7) mm Hg (p=NS), suggesting that all patients had a sim ilar degree of hypoventilation during sleep, and that the greater fall in SaO(2) and estimated PaO2 among some patients was secondary to oth er factors such as increased ventilation-perfusion mismatching.