SLEEP-RELATED O-2 DESATURATION AND DAYTIME PULMONARY HEMODYNAMICS IN COPD PATIENTS WITH MILD HYPOXEMIA

It has been hypothesized but not firmly established that sleep-related hypoxaemia could favour the development of pulmonary hypertension in chronic obstructive pulmonary disease (COBB) patients without marked d aytime hyperaemia, We have investigated the relationships between pulm onary function data, sleep-related desaturation and daytime pulmonary haemodynamics in a group of 94 COPD patients not qualifying for conven tional O-2 therapy (daytime arterial oxygen tension (Pa,O-2) in the ra nge 7.4-9.2 kPa (56-69 mmHg)), Nocturnal desaturation was defined by s pending greater than or equal to 30% of the recording time with a tran scutaneous O-2 Saturation <90%. An obstructive sleep apnoea syndrome w as excluded by polysomnography, Sixty six patients were desaturators ( Group 1) and 28 were nondesaturators (Group 2). There was no significa nt difference between Groups 1 and 2 with regard to pulmonary volumes and Pa,O-2 (8.4+/-0.6 vs 8.4+/-0.4 kPa (63+/-4; vs 63+/-3 mmHg)) but a rterial carbon dioxide tension (Pa,CO2) was higher in Group 1 (6.0+/-0 .7 vs 5.3+/-0.5 kPa (45+/-5 vs 40+/-4 mmHg); p<0,0001), Mean pulmonary artery pressure (<(P)over bar pa>) was very similar in the two groups (2.6+/-0.7 vs 2.5+/-0.6 kPa (19+/-5 vs 19+/-4 mmHg)). No individual v ariable or combination of variables could predict the presence of pulm onary hypertension. It is concluded that in these patients with chroni c obstructive pulmonary disease with modest daytime hypoxaemia, functi onal and gasometric variables (with the noticeable exception of arteri al carbon dioxide tension) cannot predict the presence of nocturnal de saturation; and that mean pulmonary artery pressure is not correlated with the degree and duration of nocturnal hypoxaemia. These results do not support the hypothesis that sleep-related hypoxaemia favours the development of pulmonary hypertension.