Figures
- Figure 1.
Pathophysiology of sleep-related respiratory changes in chronic obstructive pulmonary disease. Sleep has negative effects on various aspects of respiration resulting in worsening hypoxaemia. FRC: functional residual capacity; FEV1: forced expiratory volume in 1 s; V′/Q′: ventilation/perfusion ratio.
- Figure 2.
Pathophysiological interactions between chronic obstructive pulmonary disease (COPD), sleep and obstructive sleep apnoea syndrome (OSAS). Interactions between COPD, sleep and OSAS are shown, highlighting factors relating to COPD that may promote or inhibit the development of obstructive apnoea and hypopnoea (OAH). BMI: body mass index; REM: rapid eye movement. Reproduced from [50] with permission from the publisher.
- Figure 3.
Arterial oxygen saturation (SaO2) patterns during sleep in obstructive sleep apnoea (OSA) alone and the overlap syndrome. SaO2 patterns in a patient with a) OSA alone and b) overlap syndrome demonstrating the persisting pattern of desaturation in the overlap patient whereas the OSA patient returns to normal SaO2 between apnoea events.
- Figure 4.
Kaplan–Meier survival curves for outcomes among chronic obstructive pulmonary disease (COPD) patients without obstructive sleep apnoea (OSA) (COPD group), patients with COPD and coexisting OSA (overlap group), and patients with overlap syndrome treated with continuous positive airway pressure (CPAP) since enrolment (overlap with CPAP group). a) Survival and b) severe COPD exacerbation-free survival curves among the three study groups. The differences between curves from the COPD only and COPD with OSA treated with CPAP groups are statistically significant from the curve of patients with COPD and untreated OSA (p<0.001). Reproduced from [57] with permission from the publisher.
