• P Levi-Valensi, E Weitzenblum, Z Rida, P Aubry, A Braghiroli, C Donner, M Aprill, J Zielinski, and G Würtemberger.
• Depts of pulmonology of Amiens Strasbourg, France.
• Eur. Respir. J. 1992 Mar 1; 5 (3): 301-7.

AbstractIt has been hypothesized that in chronic obstructive pulmonary disease (COPD), sleep-related hypoxaemia could lead to pulmonary hypertension (PH) and cor pulmonale, even in patients with only mild daytime hypoxaemia. We investigated the relationships between sleep variables and daytime pulmonary haemodynamics in 40 COPD patients with daytime arterial oxygen tension (PaO2) between 60-70 mmHg (8-9.3 kPa). Patients were considered as desaturators if they spent at least 30% of the sleep recording time with a transcutaneous O2 saturation (StcO2) less than 90%. Daytime arterial blood gases and pulmonary volumes could not discriminate desaturators "D" (n = 18) from non-desaturators "ND" (n = 22), but awake baseline StcO2, measured just prior to the onset of sleep, was lower in group D. Pulmonary artery mean pressure was significantly higher in group D (19.1 +/- 4.7 vs 16.8 +/- 1.9 mmHg, p less than 0.05) and all patients with PH (6 out of 40) belonged to group D. PH was observed in 6 of the 15 patients whose mean nocturnal StcO2 was less than 90% but in none of the 25 with a mean nocturnal StcO2 greater than 90%. The PH patients (n = 6), all desaturators, differed from the desaturators with no PH (n = 12), and from ND (n = 22) in having higher numbers of desaturation dips, longer durations of dips, and lower mean nocturnal arterial oxygen saturation (SaO2). We conclude that a causal relation between nocturnal desaturation and permanent PH is very likely. Further studies are needed to see whether oxygen therapy can prevent PH in these patients.

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