Patients with COPD have a higher prevalence of insomnia, nightmares and daytime sleepiness than the general population , with close to 50% of patients reporting significant disturbance in sleep quality.
Polysomnographic studies show sleep fragmentation with frequent arousals and diminished slow wave and REM sleep .
Sleep disturbance is probably a consequence of the underlying lung disease, although adverse effects of drug therapy may also contribute.
Sleep disturbance probably contributes to the nonspecific daytime symptoms of chronic fatigue, lethargy and overall impairment in quality of life described by these patients [7, 8].
The potential effects of chronic sleep disturbance on pulmonary function in COPD are unknown but 1 night’s sleep deprivation leads to small transient falls in forced vital capacity and forced expiratory volume in one second .
Mechanisms of Oxygen Desaturation During Sleep in COPD
Sleep-related hypoventilation has been demonstrated in COPD, particularly during REM, with associated oxygen desaturation . There is a close relationship between the awake arterial oxygen tension (Pa,O2) and nocturnal arterial oxygen saturation (Sa,CO2) levels [2, 11], although hypercapnia is associated with more pronounced nocturnal oxygen desaturation than normocapnia for any given level of awake Sa,CO2 in some studies [11, 12] but not in others .
Nocturnal oxygen desaturation in COPD is probably the consequence of the combined effects of physiological hypoventilation during sleep and the fact that hypoxaemic patients show a proportionately greater fall in Sa,CO2 with hypoventilation because they are on, or close to, the steep portion of the oxyhaemoglobin dissociation curve. However, some patients with awake Pa,O2 levels in the mildly hypoxaemic range can also develop clinically significant nocturnal oxygen desaturation, which may predispose to pulmonary hypertension .
The mechanisms of hypoventilation in sleep include a diminished responsiveness of the respiratory centre to chemical, mechanical and cortical inputs, particularly during REM sleep. Furthermore, there is a normal circadian change in airway calibre resulting in mild nocturnal bronchoconstriction.
Altered ventilation/perfusion relationships
The accessory muscle contribution to breathing is reduced in sleep, particularly during REM, which results in a decreased functional residual capacity. This contributes to worsening ventilation/perfusion relationships, which also aggravates hypoxaemia. This fall in intercostal muscle activity is particularly significant in patients who are dependent on accessory muscle activity to maintain ventilation, such as those with COPD, where lung hyperinflation reduces the efficiency of diaphragmatic contraction.
Effect of Oxygen Desaturation During Sleep on Haemodynamics, Morbidity and Mortality
Studies of COPD patients with nocturnal desaturation and mild daytime hypoxemia have demonstrated higher daytime pulmonary artery pressures in these patients than in a similar group of patients who did not desaturate at night .
REM-associated falls in Sa,CO2 are associated with increases in pulmonary artery pressure during sleep that can be reversed by supplemental oxygen, although most COPD patients with sustained pulmonary hypertension are also hypoxaemic during the daytime. However, there is no convincing evidence that isolated nocturnal pulmonary hypertension in COPD is a significant independent predictor of survival.
Patients with COPD have also been reported to have an increase in premature ventricular contractions during sleep, which decrease in frequency with supplemental oxygen . Furthermore, hypoxaemia in REM sleep may have myocardial effects similar to those found during maximal exercise .
There is evidence that nocturnal oxygen desaturation contributes to mortality, particularly during acute exacerbations. Two studies have demonstrated a significant relationship between nocturnal desaturation and long-term survival, although the data are less clear on whether the relationship is independent of other factors such as lung function or awake blood gases [11, 16]. Furthermore, there is no clear evidence that correction of nocturnal oxygen desaturation improves survival . However, there is evidence that patients with exacerbations are more likely to die at night, particularly those with hypercapnia .
The prevalence of sleep apnoea in patients with COPD is about the same as a normal population of similar age . However, patients with co-existing COPD and sleep apnoea typically develop more severe oxygen desaturation during sleep because such patients may be hypoxaemic at the commencement of each apnoea, whereas patients with pure sleep apnoea tend to resaturate to normal Sa,CO2 levels in between apnoeas. Therefore, they are particularly prone to the complications of chronic hypoxaemia, such as cor pulmonale and polycythaemia.