| Abstract: | Summary. Nocturnal hypoxaemia is often noted in COLD patients with a daytime PaO2 above 8.0 kPa. It has been assumed that ventilation-perfusion inequality contributes to nocturnal hypoxaemia. 10 patients with advanced COLD [median FEV1 0.73 (range 0.50-1.32)1], but without daytime hypoxaemia [median PaO2 8.35 (range 8.0–12.2) kPa] were investigated with regard to possible nocturnal hypoxaemia using polysomnography. Daytime lung function was assessed by spirometry and carbon monoxide diffusion capacity (DLCO). Daytime ventilation-perfusion (VA/Q) relationships were measured by the multiple inert gas elimination technique. Dispersion of perfusion and ventilation distributions was increased [log SDQ 1.01 (range 0.80-1.35) and log SDV 0.91 (range 0.69-1.86) resp.]. Around 8% of the ventilation was directed towards high VA/Q areas (10< VA/Q<100). All subjects reached all sleep stages, and all but one had a nadir nocturnal oxygen saturation (SaO2) of below 90%. Their median lowest nocturnal SaO2 was 84.0 (range 70.93)% and their mean oxygen saturation in the course of desaturation episodes (Mmin SaO2) was 86.4 (range 83.6–91.5)%. An increased mean VA/Q ratio of ventilation distribution was associated with a reduced DLco Increased nocturnal episodes of wakefulness and of stage I sleep correlated with increased dead space ventilation and dispersion of the ventilation distribution. Patients with deep nocturnal desaturations had a low mean VA/Q ratio of the perfusion distribution (Q mean) (r=0.87, P<0.01) and increased perfusion of inferior VA/Q areas (0.1 VA/Q<0.3). Low Mmin SaO2 was associated with low morning PaO2 and a low Q mean. COLD patients with solely nocturnal hypoxaemia have a high degree of pulmonary hyperinflation and emphysema. Increased sleep disruption is associated with more severe small airway disease. Increased perfusion of sparsely ventilated areas is associated with more pronounced nocturnal desaturations. |
