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Review
. 2019 Sep 25;28(153):190064.
doi: 10.1183/16000617.0064-2019. Print 2019 Sep 30.

Sleep in chronic respiratory disease: COPD and hypoventilation disorders

Walter T McNicholas  1   2 , Daniel Hansson  3   4 , Sofia Schiza  5 , Ludger Grote  3   4
Affiliations
Review

Sleep in chronic respiratory disease: COPD and hypoventilation disorders

Walter T McNicholas et al. Eur Respir Rev. .

Abstract

COPD and obstructive sleep apnoea (OSA) are highly prevalent and different clinical COPD phenotypes that influence the likelihood of comorbid OSA. The increased lung volumes and low body mass index (BMI) associated with the predominant emphysema phenotype protects against OSA whereas the peripheral oedema and higher BMI often associated with the predominant chronic bronchitis phenotype promote OSA. The diagnosis of OSA in COPD patients requires clinical awareness and screening questionnaires which may help identify patients for overnight study. Management of OSA-COPD overlap patients differs from COPD alone and the survival of overlap patients treated with nocturnal positive airway pressure is superior to those untreated. Sleep-related hypoventilation is common in neuromuscular disease and skeletal disorders because of the effects of normal sleep on ventilation and additional challenges imposed by the underlying disorders. Hypoventilation is first seen during rapid eye movement (REM) sleep before progressing to involve non-REM sleep and wakefulness. Clinical presentation is nonspecific and daytime respiratory function measures poorly predict nocturnal hypoventilation. Monitoring of respiration and carbon dioxide levels during sleep should be incorporated in the evaluation of high-risk patient populations and treatment with noninvasive ventilation improves outcomes.

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Conflict of interest statement

Conflict of interest: W.T. McNicholas has nothing to disclose. Conflict of interest: D. Hansson reports non-financial support from Itamar, during the conduct of the study. Conflict of interest: S. Schiza has nothing to disclose. Conflict of interest: L. Grote reports non-financial support from Itamar, personal fees from AstraZeneca, during the conduct of the study; and personal fees from Resmed, Philips, Fisher and Paykel, Itamar outside the submitted work. In addition, Dr. Grote has a patent on drug treatment in sleep apnea licensed.

Figures

FIGURE 1
FIGURE 1
Interactions between COPD and obstructive sleep apnoea (OSA) that may influence the prevalence of the overlap syndrome. BMI: body mass index; REM: rapid eye movement.
FIGURE 2
FIGURE 2
Different patterns of oxygen desaturation during sleep in patients with a) COPD, b) obstructive sleep apnoea and c) overlap syndrome. SaO2: arterial oxygen saturation; SpO2: arterial oxygen saturation measured by pulse oximetry; PtcCO2: transcutaneous carbon dioxide tension; REM: rapid eye movement.
FIGURE 3
FIGURE 3
Sleep-related hypoventilation in COPD. Image shows ∼30 min of respiration during non-rapid and rapid eye movement (NREM and REM) sleep in a female patient with stable, advanced COPD. The level of arterial oxygen saturation (SaO2) and transcutaneous carbon dioxide tension (PtcCO2) is already reduced during NREM stage 2 sleep compared to values during wakefulness (SaO2 90%). No repetitive apnoea/hypopnea occurred. In the transition to REM sleep a physiological reduction in respiratory efforts (reduced amplitude in the thoracic effort signal) with a corresponding decrease in airflow amplitude occurred. A further reduction in SaO2 and a significant increase in PtcCO2 (a qualitative, non-calibrated signal) is the consequence of the REM sleep hypoventilation. Heart rate increases as an indirect sign of increased sympathetic activity.
FIGURE 4
FIGURE 4
Pathophysiology of sleep-related hypoventilation in neuromuscular diseases. PaO2: arterial carbon dioxide tension.
See this image and copyright information in PMC

References

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MeSH terms