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Eur Respir J 2001; 17:848-855
Copyright ©ERS Journals Ltd 2001


Outcome of COPD patients with mild daytime hypoxaemia with or without sleep-related oxygen desaturation

A. Chaouat1, E. Weitzenblum1, R. Kessler1, R. Schott1, C. Charpentier1, P. Levi-Valensi2, J. Zielinski3, L. Delaunois4, R. Cornudella5 and J. Moutinho dos Santos6

1 Dept of Pneumology, University Hospital, Strasbourg, France, 2 Dept of Pneumology, University Hospital, Amiens, France, 3 Institute of Tuberculosis and Lung Diseases, Warsaw, Poland, 4 Cliniques Universitaires UCL, Yvoir, Belgium, 5 University Hospital, Barcelona, Spain and 6 Dept of Pulmonology, Coimbra, Portugal

CORRESPONDENCE: A. Chaouat, Service de Pneumologie, Hôpital de Hautepierre, 1,Avenue Molière, 67098, Strasbourg Cedex, France. Fax: 33 388127827

Keywords: chronic obstructive pulmonary disease, hypercapnia, hypoxaemia, pulmonary hypertension, sleep-related hypoxaemia

Received: July 26, 2000
Accepted January 9, 2001

This study was partly supported by agrant "Programme Hospitalier de Recherche Clinique" (PHRC 1995) promoted by Hôpitaux Universitaires de Strasbourg.

The aim of the present study was to compare the evolution of pulmonary haemodynamics and of arterial blood gases in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate hypoxaemia, with or without sleep-related oxygen desaturation.

COPD patients with daytime arterial oxygen partial pressure in the range 56–69 mmHg were included prospectively. Sleep-related oxygen desaturation was defined as spending ≥30% of the nocturnal recording time with arterial oxygen saturation <90%.

From the 64 patients included, 35 were desaturators (group 1) and 29 were nondesaturators (group 2). At baseline (t0), patients with sleep-related desaturation had a significantly higher daytime (mean±sd) arterial carbon dioxide partial pressure (Pa,CO2) (44.9±4.9 mmHg versus 41.0±4.1 mmHg, p=0.001) whereas mean pulmonary artery pressure (mPAP) was similar in the two groups. After 2 yrs (t2) of follow-up, 22 desaturators and 14 nondesaturators could be re-evaluated, including pulmonary haemodynamic measurements. None of the nondesaturator patients became desaturators at t2. The difference between the two groups in terms of daytime Pa,CO2 was still present at t2. The mean changes in mPAP from t0 to t2 were similar between the two groups, as were the rates of death or requirement for long-term oxygen therapy (American Thoracic Society criteria) during follow-up of up to 6 yrs.

The presence of sleep-related oxygen desaturation is not a transitional state before the worsening of daytime arterial blood gases, but is a characteristic of some chronic obstructive pulmonary disease patients who have a higher daytime arterial carbon dioxide partial pressure. Such isolated nocturnal hypoxaemia or sleep-related worsening of moderate daytime hypoxaemia does not appear to favour the development of pulmonary hypertension, nor to lead to worsening of daytime blood gases.







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