In order to clarify whether nocturnal hypoxaemia (arterial oxygen saturation, SaO₂ <90% may exist in the long-term before daytime hypoxaemia (PaO₂ <8·0 kPa) occurs in chronic obstructive pulmonary disease (COPD), 21 patients with stable severe COPD without daytime hypoxaemia (PaO₂ ≥8·0 kPa) were studied prospectively. Subjects were monitored twice by polysomnography (PSG) 12 months apart. Spirometry was performed, and diffusion capacity (DlCO) and hypercapnic respiratory drive response ΔPi_0·1 ΔPCO₂⁻¹) were measured during the daytime in conjunetion with polysomnography.

At the start of the study our subjects had FEV₁%P (FEV₁ as a percentage of predicted value) of 26·1 ± 7·2%, a mean nocturnal nadir SaO₂ of 83 ± 5%, and a mean SaO₂ during nocturnal hypoxaemic episodes of 88·0 ± 0·7%. The patients' ΔPi_0·1 ΔPCO₂⁻¹ was 1·8 ± 1·4 cm H₂O kPa⁻¹ (within the normal range). For the entire study group, no significant change in any lung function or blood gas parameter was noted during the year of observation, and nocturnal SaO₂ remained unaltered. Stage I sleep decreased (P<0·05) after 12 months. Prolonged stage I sleep was associated with nocturnal hypoxaemia at the second PSG. Five subjects developed daytime hypoxaemia and they showed poorer lung function but similar nocturnal hypoxaemia and ΔPi_0·1 ΔPCO₂⁻¹ level compared to the rest of the patients. Patients with sudden SaO₂ dips had more pronounced nocturnal hypoxaemia and prolonged wakefulness than ‘non-dippers’.

In conclusion, the mean level of nocturnal hypoxaemia may persist unaltered for at least 1 yr. COPD patients with exclusively nocturnal hypoxaemia have a hypercapnic drive response within the normal range. Prolonged nocturnal hypoxaemia and reduced whole night oxygenation are associated with increased superficial sleep. Sleep fragmentation and high carbon dioxide sensitivity may be important defence mechanisms against sleep-related hypoxaemia.

The appearance of daytime hypoxaemia is preceded by a substantial deterioration in lung function, but by only a minor deterioration of nocturnal hypoxaemia.