Fig. 7.1 Sao2 and transcutaneous CO2 levels in non-REM and REM sleep on and off supplemental oxygen. Adapted from  with permission.
[10,18] Respiratory infections in these patients should be treated promptly and vigorously.
The role of oxygen therapy in COPD is covered in another chapter, but it is important to summarize the impact of oxygen supplementation in COPD during sleep. Oxygen therapy effectively corrects sleep-related hypoxaemia in COPD , but at the cost of some degree of CO2 retention. However, this retention is usually modest (approximately 1 kPa) and non-progressive during the night. Oxygen therapy can also improve sleep quality (Fig. 7.1).
Anticholinergics. Cholinergic tone is increased at night, and it has been proposed that this contributes to airflow obstruction and deterioration in gas exchange during sleep in patients with obstructive airways disease. There is recent evidence that ipratropium improves arterial SaO2 in addition to sleep quality in patients with COPD .
Theophylline. Theophylline improves gas exchange during sleep in COPD , which may reflect the fact that in addition to being a bronchodilator, theophylline has important effects on respiration, including central respira tory stimulation and improved diaphragmatic contractility . However, theophyllines have an adverse effect on sleep quality, and also have a relatively high incidence of gastrointestinal intolerance, which limits their usefulness in this setting.
b2-agonists. There are only limited data on the efficacy of b2-agonists on the management of sleep-related breathing abnormalities in COPD. One report found that a long-acting theophylline was superior to salbutamol in terms of nocturnal gas exchange and overnight fall in spirometry . However, there are no studies of the impact of long-acting b2-agonists on sleep and breathing in COPD.
Almitrine. Almitrine lessens hypoxaemia both awake and asleep, by means of carotid body stimulation and improved ventilation-perfusion matching within the lung , and it is beneficial in hypoxaemic patients with COPD . Important side effects include pulmonary hypertension, dyspnoea and peripheral neuropathy .
The role of non-invasive ventilation in acute exacerbations of COPD is covered in Chapter 16. However, in the past decade, increasing attention has been directed towards non-invasive methods of ventilatory support of COPD patients with chronic respiratory insufficiency, particularly during sleep [25,26]. Beneficial effects on gas exchange during wakefulness have been widely reported in patients treated with nocturnal ventilatory support in addition to improvements in respiratory muscle strength and endurance [27,28]. The mechanism by which non-invasive positive-pressure ventilation (NIPPV) produces improvements in daytime blood gases likely involve a number of factors, which include resting of the respiratory muscles, resetting of respiratory drive, particularly at the chemoreceptor level and a reduction in residual volume and in the degree of gas trapping.
The findings from studies of NIPPV during sleep in COPD offer exciting new prospects for the management of such patients with advanced disease who are in chronic respiratory failure. However, the health-care resource implications of this therapy are potentially very great, because of the high prevalence of COPD. While it is clear from the literature that NIPPV will play an increasing role in the management of patients with advanced COPD over coming years, it is likely that only a subset of patients with advanced COPD will benefit from this therapy. These considerations emphasize the importance of outcome studies that evaluate the efficacy of this therapy in different patient populations.
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