Chest
Impact of Sleep in COPD
Section snippets
Effects of Sleep on Respiration
The effects of sleep on respiration include changes in central respiratory control, airways resistance, and muscular contractility. A schematic outline of the effects of sleep on respiration is given in Figure 1.
Central Respiratory Effect
Sleep is associated with a diminished responsiveness of the respiratory center to chemical, mechanical, and cortical inputs,23 particularly during REM sleep. Furthermore, the responsiveness of the respiratory muscles to respiratory center outputs are also diminished during sleep, particularly during REM, although the diaphragm is less affected than the accessory muscles in this regard.2 There is a decrease in minute ventilation during non-REM sleep and more so during REM sleep,456 predominantly
Airway Resistance
Most normal subjects have circadian changes in airway caliber with mild nocturnal bronchoconstriction.89 Such bronchoconstriction may be exaggerated in patients with asthma, who can demonstrate falls in peak flow rate of ≥ 50%, compared with an average of 8% in normal subjects.9
Ribcage and Abdominal Contribution to Breathing
A reduction in ribcage contribution to breathing has been reported during REM sleep compared with wakefulness and non-REM sleep because of a marked reduction in intercostal muscle activity,10 whereas diaphragmatic contraction is little affected. This fall in intercostal muscle activity assumes particular clinical significance in patients who are particularly dependent on accessory muscle activity to maintain ventilation, such as those with COPD where lung hyperinflation reduces the efficacy of
Functional Residual Capacity
A modest fall in functional residual capacity (FRC) has been noted in both non-REM and REM sleep,1213 which does not cause significant ventilation to perfusion mismatching in healthy subjects, but can do so, with resulting hypoxemia, in patients with chronic lung disease.12 Possible mechanisms responsible for this reduction in FRC include respiratory muscle hypotonia, cephalad displacement of the diaphragm, and a decrease in lung compliance.4
Sleep in COPD
Sleep-related hypoxemia and hypercapnia are well recognized in COPD, particularly during REM sleep, and may contribute to the development of cor pulmonale14 and nocturnal death.15 These abnormalities are most common in “blue–bloater”-type patients, who also have a greater degree of awake hypoxemia and hypercapnia than “pink–puffer”-type patients.314 However, many patients with awake Pao2 levels in the mildly hypoxemic range can also develop substantial nocturnal oxygen desaturation, which
1. Hypoventilation
Studies using noninvasive methods of quantifying respiration have shown clear evidence of hypoventilation, particularly during REM sleep, associated with periods of hypoxemia in patients with COPD,17181920 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.
2. Impact of the Oxyhemoglobin Dissociation Curve
There is a close relationship between awake Pao2 and nocturnal arterial oxygen saturation (Sao2) levels, and it has
Investigation of Sleep-Related Breathing Disturbances in COPD
The serious and potentially life-threatening disturbances in 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.2324 Sleep studies are only
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 Sao2 in addition to sleep quality in patients with COPD,29 although other studies have shown conflicting results on the ability of ipratropium to block nocturnal bronchoconstriction in asthma.3031
2. Theophylline
In addition to being a bronchodilator,
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2017, ChestCitation Excerpt :These adaptations include diminished respiratory drive, reduced skeletal muscle activity that is particularly relevant to accessory muscle contraction,13 and changes in lung mechanics, such as reduced functional residual capacity,14 that adversely affect ventilation-perfusion relationships (Fig 1). These physiological adaptations do not produce clinically significant changes in gas exchange in normal subjects but may result in major oxygen desaturation in patients with COPD,15 which may result in serious clinical consequences, including an increased risk of death at night during acute exacerbations.16 The possibility that COPD may predispose to OSA and OSA to COPD has been explored in many studies over the past 2 decades, but the comparison of epidemiology between reports is made difficult by methodological differences in recording techniques and study populations and differing definitions of sleep apnea and SDB.