Chest
Volume 117, Issue 2, Supplement, February 2000, Pages 48S-53S
Journal home page for Chest

Impact of Sleep in COPD

https://doi.org/10.1378/chest.117.2_suppl.48SGet rights and content

Sleep has well-recognized effects on breathing, including changes in central respiratory control, airways resistance, and muscular contractility, which do not have an adverse effect in healthy individuals but may cause problems in patients with COPD. Sleep-related hypoxemia and hypercapnia are well recognized in COPD and are most pronounced in rapid eye movement sleep. However, sleep studies are usually only indicated in patients with COPD when there is a possibility of sleep apnea or when cor pulmonale and/or polycythemia are not explained by the awake Pao2 level. Management options for patients with sleep-related respiratory failure include general measures such as optimizing therapy of the underlying condition; physiotherapy and prompt treatment of infective exacerbations; supplemental oxygen; pharmacologic treatments such as bronchodilators, particularly ipratropium bromide, theophylline, and almitrine; and noninvasive positive pressure ventilation.

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,

References (49)

  • B Gothe et al.

    Effect of quiet sleep on resting and CO2-stimulated breathing in humans

    J Appl Physiol

    (1981)
  • NJ Douglas et al.

    Respiration during sleep in normal man

    Thorax

    (1982)
  • J Krieger et al.

    Breathing during sleep in normal young and elderly subjects: hypopneas, apneas and correlated factors

    Sleep

    (1983)
  • B Gothe et al.

    Effect of progressive hypoxia on breathing during sleep

    Am Rev Respir Dis

    (1982)
  • JR Stradling et al.

    Changes in ventilation and its components in normal subjects during sleep

    Thorax

    (1985)
  • HD Kerr

    Diurnal variation of respiratory function independent of air quality

    Arch Environ Health

    (1973)
  • MR Hetzel et al.

    Comparison of normal and asthmatic circadian rhythms in peak expiratory flow rate

    Thorax

    (1980)
  • K Tusiewicz et al.

    Mechanics of the ribcage and diaphragm during sleep

    J Appl Physiol

    (1977)
  • MW Johnson et al.

    Accessory muscle activity during sleep in chronic obstructive pulmonary disease

    J Appl Physiol

    (1984)
  • RD Ballard et al.

    Influence of sleep on lung volume in asthmatic patients and normal subjects

    J Appl Physiol

    (1990)
  • DW Hudgel et al.

    Decrease in functional residual capacity during sleep in normal humans

    J Appl Physiol

    (1984)
  • WT McNicholas et al.

    Nocturnal death among patients with chronic bronchitis and emphysema

    Br Med J

    (1984)
  • EC Fletcher et al.

    Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep

    Chest

    (1989)
  • JR Caterall et al.

    Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema

    J Appl Physiol

    (1985)
  • Cited by (106)

    • Use of Positive Airway Pressure in the Treatment of Hypoventilation

      2022, Sleep Medicine Clinics
      Citation Excerpt :

      COPD patients with low baseline pulse O2 saturation (SpO2) are especially prone to O2 desaturation in sleep because they find themselves on the steepest part of the oxyhemoglobin dissociation curve where any given change in Pao2 will result in a greater decline in SpO2.40 O2 desaturations during sleep in COPD can stem from hypoventilation, ventilation-perfusion mismatches, or coexisting OSA.37 The overlap syndrome refers to the co-occurrence of COPD and OSA, both of which are highly prevalent conditions.14

    • COPD-OSA Overlap Syndrome: Evolving Evidence Regarding Epidemiology, Clinical Consequences, and Management

      2017, Chest
      Citation 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.

    View all citing articles on Scopus
    View full text