Walter McNicholas

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Introduction

Sleep has well-recognized effects on breathing, which in normal individuals have no adverse impact. These effects include a mild degree of hypoventilation with consequent hypoxaemia and hypercapnia, and a diminished responsiveness to respiratory stimuli. However, in patients with chronic lung disease such as chronic obstructive pulmonary disease (COPD), these physiological changes during sleep may have a profound effect on gas exchange, and episodes of profound hypoxaemia may develop, particularly during rapid-eye-movement (REM) sleep [1], which may predispose to death at night [2]. Furthermore, COPD has an adverse impact on sleep quality itself [3], which may contribute to the complaints of fatigue and lethargy that are well-recognized features of the condition [4] (Table 7.1).

How does COPD affect sleep quality?

Sleep tends to be fragmented in COPD, with frequent arousals and diminished amounts of slow-wave and REM sleep [3]. The mechanism of sleep impairment in COPD is unclear, but probably relates at least in part to the disordered gas exchange. Although there have been many studies of breathing and gas exchange disturbances during sleep in COPD, few studies have focused on sleep quality. Furthermore, sleep impairment is an aspect of COPD that is frequently ignored by many physicians, even in research protocols designed to assess the impact of COPD on quality of life [5-8]. This aspect assumes particular importance in the context of assessing the impact of pharmacological therapy on quality of life in patients with COPD [9], since pharmacological agents that improve sleep quality in COPD [10] are likely to have a beneficial clinical impact over and above that simply associated with improvements in lung mechanics and gas exchange, particularly in terms of fatigue and overall energy levels.

Table 7.1 Impact of chronic obstructive pulmonary disease (COPD) on sleep.

• Disturbed sleep quality

• Diminished slow-wave and rapid-eye-movement (REM) sleep

• Frequent arousals

• Impaired gas exchange

• Hypoxaemia—may be severe in REM sleep

• Hypercapnia—usually mild

Table 7.2 Mechanisms of sleep-related hypoxaemia in chronic obstructive pulmonary disease (COPD).

• Hypoventilation—most important

• Impact of oxyhaemoglobin dissociation curve—amplifies the impact of hypoventilation

• Ventilation-perfusion mismatching

• Coexisting sleep apnoea—present in only 10-15% of patients

When should COPD patients have sleep studies?

The serious and potentially life-threatening disturbances of ventilation and gas exchange that may develop during sleep in patients with COPD raise the question of appropriate investigation of these patients. However, it is widely accepted that sleep studies are not routinely indicated in patients with COPD associated with respiratory insufficiency, particularly since the awake PaO2 level provides a good indicator of the likelihood of nocturnal oxygen desaturation [11]. Sleep studies are only indicated where there is a clinical suspicion of an associated sleep apnoea syndrome or manifestations of hypoxaemia not explained by the awake PaO2 level, such as cor pulmonale or polycythaemia. In most situations in which sleep studies are indicated, a limited study focusing on respiration and gas exchange should be sufficient, and full polysomnography with sleep staging is rarely required (Table 7.2).

What are the mechanisms of sleep-related breathing disturbances in COPD?

Sleep-related hypoxaemia and hypercapnia are well recognized in COPD, particularly during REM sleep, and may contribute to the development of cor pulmonale [1,12] and nocturnal death [2]. These abnormalities are most common in the 'blue bloater' type of patient, who also have a greater degree of awake hypoxaemia and hypercapnia than the 'pink puffer' type of patient [13]. However, many patients with awake arterial PO2 (PaO2) levels in the mildly hypoxaemic range can also develop substantial nocturnal oxygen desaturation, which appears to predispose to the development of pulmonary hypertension [12]. Furthermore, COPD patients develop levels of oxygen desaturation during sleep that are greater than those seen during maximum treadmill exercise testing [14]. There are a number of potential mechanisms for the development of these abnormalities.

Hypoventilation

Studies using non-invasive methods of quantifying respiration have shown clear evidence of hypoventilation, particularly during REM sleep, associated with periods of hypoxaemia in patients with COPD [15,16], but the semiquantitative nature of these measurements makes it difficult to determine if this is the sole mechanism of oxygen desaturation, or whether other factors are involved. A recent report [14] in which ventilation, SaO2, and transcutaneous Pco2 (PtcCO2) were continuously recorded during sleep in a group of patients with severe but stable COPD demonstrated that falls in SaO2 were accompanied by a rise in PtcCO2, and REM sleep, in particular, was frequently characterized by irregular, low tidal volume respiration and a high PtcCO2. These observations support hypoventilation as the major cause of nocturnal desaturation in COPD, particularly during REM sleep.

Impact of the oxyhaemoglobin dissociation curve

There is a close relationship between awake PaO2 and nocturnal oxygen saturation (SaO2) levels, and it has been proposed that nocturnal oxygen desaturation in patients with COPD is largely the consequence of the combined effects of physiologic hypoventilation during sleep and the fact that hypoxaemic patients show a proportionately greater fall in SaO2 with hypoventilation than normoxaemic, because of the effects of the oxyhaemoglobin dissociation curve [14-16]. However, PaO2 has also been shown to fall more during sleep in major desaturators as compared with minor desaturators [14], which indicates that other factors must also play a part in nocturnal oxygen desaturation in patients with COPD.

Altered ventilation-perfusion relationships

The reduction in accessory muscle contribution to breathing particularly during REM sleep result in a decreased functional residual capacity (FRC), and contribute to worsening ventilation-perfusion relationships during sleep, which also aggravate hypoxaemia in COPD [15,16]. We have found that transcutaneous Pco2 (PtcCO2) levels rise to a similar extent in patients who develop major nocturnal oxygen desaturation to that in patients who develop only a minor degree of desaturation [14], which suggests a similar degree

Table 7.3 Management options for chronic obstructive pulmonary disease (COPD) patients with sleep-related respiratory failure.

General measures

Optimize therapy of underlying condition Prompt therapy of infective exacerbations

Supplemental oxygen

Controlled flow to minimize risk of CO2 retention

Pharmacologic therapy

Bronchodilators, particularly anticholinergics

Theophylline

Almitrine

Non-invasive positive pressure ventilation (NIPPV)

of hypoventilation in both groups, despite the different degrees of nocturnal oxygen desaturation. The much larger fall in PaO2 among the major desa-turators as compared with the minor desaturators, in conjunction with the similar rise in PtcCO2 in both patient groups, suggests that in addition to a degree of hypoventilation operating in all patients, other factors such as ventilation-perfusion mismatching must also play a part in the excess desaturation of some COPD patients.

Coexisting sleep apnoea syndrome

The incidence of sleep apnoea in patients with COPD is about 10-15% [17], which is little higher than would be expected in a normal population of similar age. Factors that may predispose to sleep apnoea in patients with COPD include impaired respiratory drive, particularly in the 'blue bloater' type of COPD patient. Patients with coexisting COPD and sleep apnoea typically develop more severe hypoxaemia 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 SaO2 levels in between ap-noeas. Therefore, they are particularly prone to the complications of chronic hypoxaemia, such as cor pulmonale and polycythaemia [17] (Table 7.3).

Can sleep-related breathing abnormalities in COPD be treated?

General principles

The first principle of management of sleep-related breathing disturbance in COPD should be to optimize the underlying condition, since this will almost invariably have beneficial effects on breathing. For example, optimizing bron-chodilator therapy has been shown to improve gas exchange during sleep

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