In COPD patients, suffering from moderate to severe emphysema without severe blood gas impairment, no correlation was shown between the extent of emphysema, as assessed by HRCT, and the severity of ventilation-perfusion inequality. A substantial collateral ventilation in severe emphysema may be a mechanism that prevents a deterioration in V(A)/Q relationships and in blood gas levels.

An elevated V mean and probably shunting are important contributing factors for the reduced PaO(2) and hypercapnic ventilatory response is a major determinant of PaCO(2) in eucapnic stable hypoxaemic COPD. Six months of LTOT does not affect blood gases, CO(2) sensitivity or ventilation-perfusion relationships.

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 > or = 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 delta PI0.1 delta PCO2(-1)) were measured during the daytime in conjunction 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' delta PI0.1 delta PCO2(-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 delta PI0.1 delta PCO2(-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.

Forced expiratory volumes are reduced in chronic obstructive pulmonary disease (COPD), mainly as a result of inflammatory and morphological changes in the small airways (with a diameter < 2 mm) and in the alveoli. However, it is difficult to detect minor changes in small airways by spirometry measurements. To study the effects on small airways of inhaled corticosteroids (ICS), 19 stable COPD patients were investigated; 15 were evaluated by ventilation-perfusion (V(A)/Q) relationships, assessed by the multiple inert gas elimination technique, and by diffusing capacity for carbon monoxide (DL(CO)), assessed by the single breath technique. Measurements were repeated after 2 months of budesonide inhalations (800 microg) twice daily. Before ICS treatment: mean forced expiratory volume in 1 sec (FEV1) as a percentage of predicted (% P) was 40.1 (+/- 16.0)%, DL(CO)% P was 45.7 (+/- 25.0)% and 6.0 (+/- 6.4)% of the ventilation was directed at high V(A)/Q areas. The mean of the V(A)/Q ratio for ventilation (V-mean) was 2.7 times higher than normal. After 2 months of ICS: the mean of DL(CO)% P increased by 8.6 (+/- 19.4)%, and FEV1/vital capacity decreased by 6.9 (+/- 11.3)%. Basal morning and ACTH-stimulated S-cortisol levels were significantly reduced. All the V(A)/Q relationships remained unchanged. In conclusion, a significant increase in diffusion capacity for carbon monoxide levels after treatment with corticosteroid inhalations for 2 months was shown, but no significant improvements were found in forced expiratory airflow, lung volumes, or V(A)/Q relationships.