Sleep disordered breathing and chronic obstructive pulmonary disease: a narrative review on classification, pathophysiology and clinical outcomes

Abstract

Chronic obstructive pulmonary disease (COPD) causes load-capacity-drive imbalance in both wakefulness and sleep, principally driven by expiratory flow limitation and hyperinflation. Sleep imposes additional burdens to the respiratory muscle pump, driven by changes in respiratory muscle tone, neural respiratory drive and consequences of the supine position. COPD patients are therefore at higher risk of decompensation during sleep, which may manifest as altered sleep architecture, isolated nocturnal desaturation, sleep hypoventilation and restless legs. Each form of sleep disordered breathing in COPD is associated with adverse clinical and patient-reported outcomes, including increased risk of exacerbations, hospitalisation, cardiovascular events, reduced survival and poorer quality of life. COPD-obstructive sleep apnoea (OSA) overlap syndrome represents a distinct clinical diagnosis, in which clinical outcomes are significantly worse than in either disease alone, including increased mortality, risk of cardiovascular events, hospitalisation and exacerbation frequency. Sleep disordered breathing is under-recognised by COPD patients and their clinicians, however early diagnosis and management is crucial to reduce the risk of adverse clinical outcomes. In this narrative review, we describe the pathophysiology of COPD and physiological changes that occur during sleep, manifestations and diagnosis of sleep disordered breathing in COPD and associated clinical outcomes.

Keywords: COPD-obstructive sleep apnoea (OSA) overlap; Chronic obstructive pulmonary disease (COPD); pulmonary mechanics; respiratory physiology; sleep; sleep disordered breathing.

Figure 1

Illustration of the bidirectional relationship between sequelae of sleep-disturbance and adverse clinical outcomes in chronic obstructive pulmonary disease (COPD).

Figure 2

Schematic representation of load-capacity-drive imbalance of the respiratory muscle pump during exacerbations of chronic obstructive pulmonary disease (COPD).

Figure 3

Physiological changes during wakefulness and rapid eye movement (REM) sleep including diaphragm electromyography (EMG_di pairs 1–5) from a multipair oesophageal electrode catheter, air flow at the mouth from a pneumotachograph, transcutaneous carbon dioxide (TcCO₂) and peripheral oxygen saturation (SpO₂). Data obtained from a patient with chronic obstructive pulmonary disease.

Figure 4

Example of overnight oximetry in a patient with nocturnal hypoxia. Episodes of nocturnal desaturation that are likely related to rapid eye movement (REM) stage sleep are highlighted in green.

Figure 5

Excess load-capacity-drive imbalance during rapid eye movement (REM)-sleep in COPD leading to nocturnal hypoventilation. Abbreviations: VT, tidal volume; VE, minute ventilation; VD, dead space volume.