Chronic Obstructive Pulmonary Disease See Also Chapter 20

COPD affects approximately 14 million adult Americans. COPD patients often report multiple problems with sleep, including insomnia and frequent awakenings. Sleep studies of COPD patients have revealed decreased total sleep time, frequent arousals and awakenings, and reduced amounts of slow-wave and rapid eye movement (REM) sleep. Impaired sleep quality likely results from a combination of factors, including chronic shortness of breath, nocturnal cough, and sleep-associated hypoxemia. In 1962, Trask and Cree (25) reported oximetry data from seven COPD patients, demonstrating oxygen desaturation to as low as 37% during subjective sleep. Pierce et al. (26) subsequently used electroencephalographic sleep staging and indwelling arterial catheters in 19 COPD patients to demonstrate a mean maximal fall in arterial partial pressure of oxygen (PaO2) of 7.4 mmHg from wakefulness to sustained sleep. Douglas et al. (27) reported that 10 COPD patients all reduced their oxygen saturation by more than 10% during sleep, and eight of these patients demonstrated oxygen saturations that dipped below 50%. The lowest PaO2s dropped into the range of 26 to 44 mmHg, which occurred predominantly during REM sleep. It has been widely observed that the most severe hypoxemia typically occurs during

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FIGURE 3 Overnight changes in sleep stage, oxygen saturation, and transcutaneous partial pressure of oxygen (PO2), with intermittent measurement of arterial partial pressure of oxygen (PaO2) in a chronically hypoxic chronic obstructive pulmonary disease patient. Note severe rapid eye movement (black bars on EEG Sleep Stage graph) associated hypoxemia. Abbreviations: EEG, electroencephalogram; kPa, kilopascals. Source: From Ref. 82.

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FIGURE 3 Overnight changes in sleep stage, oxygen saturation, and transcutaneous partial pressure of oxygen (PO2), with intermittent measurement of arterial partial pressure of oxygen (PaO2) in a chronically hypoxic chronic obstructive pulmonary disease patient. Note severe rapid eye movement (black bars on EEG Sleep Stage graph) associated hypoxemia. Abbreviations: EEG, electroencephalogram; kPa, kilopascals. Source: From Ref. 82.

REM sleep, when there is reduced inspiratory muscle activity and periods of hypoventilation characterized by small tidal volumes and variable respiratory effort. REM-associated hypoventilation can trigger severe hypoxemia even when the patient's waking PaO2 is greater than 60 mmHg. However, COPD patients with lower levels of waking ventilation, manifested by higher arterial partial pressure of carbon dioxide (PaCO2) with lower PaO2, are likely to have the most severe nocturnal desaturation (Fig. 3).

Both episodic and relatively fixed pulmonary hypertension has been demonstrated in COPD patients with significant nocturnal oxygen desaturation, and nocturnal oxygen therapy can subsequently improve these abnormalities (28). Nocturnal supplemental oxygen can also improve sleep quality in COPD patients with nocturnal hypoxemia (29). The administration of low-flow supplemental oxygen by nasal cannula to COPD patients with a PaO2 less than 55 mmHg was assessed in both the Nocturnal Oxygen Treatment Trial (30) and the Medical Research Council Working Party study (31). These studies demonstrated improved long-term survival in hypoxic COPD patients when supplemental oxygen was administered for at least 12 to 15 hours daily, which typically included the sleeping hours. It has therefore become standard care to administer 24-hour oxygen therapy in COPD patients with a waking resting PaO2 of less than 55 mmHg, or in the range of 55 to 59 mmHg with evidence of end-organ damage (pedal edema, elevated hematocrit, or evidence of cor pulmonale). It has not been clearly established that nocturnal supplemental oxygen benefits COPD patients who have a waking PaO2 of at least 60 mmHg with only isolated nocturnal arterial oxygen desaturation.

Although there is no evidence that COPD increases the risk for concurrent OSA, COPD can certainly be seen in association with OSA, which in combination has been termed the "overlap syndrome" (32). Treating such patients with nocturnal supplemental oxygen alone are unlikely to alleviate OSA-related symptoms of sleep disruption and nonrestorative sleep, and may actually increase apnea duration and contribute to greater sleep-associated increases in PaCO2. These patients warrant therapy with CPAP, which reverses upper airway obstruction, improves gas exchange, and reduces inspiratory muscle work during sleep. There is some evidence that patients with "overlap syndrome" may be better candidates for bilevel positive airway pressure than standard CPAP (33).

Airflow obstruction in COPD frequently worsens in the early morning hours, in a fashion similar to asthmatic patients (34). Medical therapy for these worsening and associated symptoms usually consists of bronchodilator therapy, including long acting beta-adrenergic agents, anticholinergics, and theophylline. Berry et al. (35) observed in 12 normocapnic COPD patients that sustained-release theophylline improved morning FEV1 and oxygen saturation plus PaCO2 during non-REM (NREM) sleep, without adversely affecting sleep quality. Martin et al. (36) evaluated 36 patients with moderate-to-severe COPD during treatment with either four times daily nebulized ipratropium or placebo. Four weeks of treatment with ipratropium improved nocturnal oxygen saturation and perceived sleep quality, and increased time spent in REM sleep. McNicholas et al. (37) more recently assessed the utility of once daily inhaled tiotropium in 95 patients with moderate-to-severe COPD. Tiotropium improved FEV1 and oxygen saturation during sleep, although there was no detected improvement in sleep quality. It appears that all of these bronchodila-tors may be useful for treatment of troublesome nocturnal symptoms in COPD patients. However, given the risks for potential side effects versus potential benefit from each medication, a reasonable approach is to initiate therapy at bedtime with tiotropium, to be followed by the administration of an inhaled long acting beta-adrenergic agent if warranted, with sustained-release theophylline reserved for those patients who continue to have troublesome night-time symptoms.

Nocturnal noninvasive positive pressure ventilatory support has been administered to many patients with COPD. Although this approach has been found quite useful in the treatment of acutely exacerbated COPD patients, those with severe but stable COPD have not as clearly benefited. Wijkstra et al. (38) conducted a meta-analysis of randomized controlled trials that assessed nocturnal noninvasive positive pressure ventilation in stable COPD patients. It was concluded that noninvasive ventilatory support did not improve lung function, gas exchange, or sleep efficiency. This therapy is therefore currently not widely advocated in patients with stable COPD, although it should be considered in patients with waking hypoventilation, especially in conjunction with the "overlap syndrome."

Sleeping Sanctuary

Sleeping Sanctuary

Salvation For The Sleep Deprived The Ultimate Guide To Sleeping, Napping, Resting And  Restoring Your Energy. Of the many things that we do just instinctively and do not give much  of a thought to, sleep is probably the most prominent one. Most of us sleep only because we have to. We sleep because we cannot stay awake all 24 hours in the day.

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