Obstructive Sleep Apnea in Patients with Chronic Obstructive Pulmonary Disease: Facts and Perspectives

Figures & data

Figure 1. Cumulative number of articles published from 1985 to 2020 related to OS, OSA, and COPD. To identify the number of published articles on OS, OSA, and COPD, searches were performed in MEDLINE using the search terms “chronic obstructive pulmonary disease” AND “obstructive sleep apnea,” “obstructive sleep apnea,” and “chronic obstructive pulmonary disease,” respectively. The numbers of published articles on OS, OSA, and COPD were 7, 119, and 390, respectively in 1985; the cumulative numbers of articles on OS, OSA, and COPD from 1985 to December 2020 were 1514, 41 236, and 79 430, respectively. OS: Overlap syndrome, OSA: Obstructive sleep apnea, COPD: Chronic obstructive pulmonary disease.

Figure 2. Diaphragm electromyogram (EMG) di% (left panel), ventilation (middle panel), and the V_T/EMGdi (right panel) in patients with COPD alone, OS, normal subjects, and patients with OSA. EMGdi% (percentage of maximal diaphragm electromyogram) was used to assess neural respiratory drive. Upper airway resistance was inferred by the ratio of the tidal volume (V_T) to EMGdi (V_T/EMGdi). Ventilation decreases from wakefulness to sleep in all four groups, but the reduction is statistically significant only in patients with COPD, OS, and OSA. EMGdi decreases in patients with COPD alone but increases in patients with OSA from wakefulness to non-rapid eye movement sleep, whereas it remains the same in normal subjects and patients with OS. V_T/EMGdi decreases from wakefulness to sleep in patients with OS and OSA but it changes little in normal subjects and patients with COPD alone. The decrease in ventilation is associated with a reduction of EMGdi in patients with COPD alone, whereas the reduction in ventilation is associated with decreased V_T/EMGdi in patients with both OS and OSA. OSA: Obstructive sleep apnea, COPD: Chronic obstructive pulmonary disease, OS: Overlap syndrome. Adapted from [31] (an open access article distributed in accordance with the Creative Commons Attribution Non Commercial [CC BY-NC 4.0] license).

Figure 3. Markers of inflammation, endothelial dysfunction, and cellular immune function studied in OS patients. Whether these dysfunctions contribute to morbidity, mortality, and comorbidities associated with OS remain to be demonstrated. We did not speculate potential underlying mechanisms that have not been specifically elucidated in OS patients. OS: Overlap syndrome, CRP: C-reactive protein, IL-6: Interleukin-6, sVCAM-1: soluble vascular cell adhesion molecule-1, TNF-α: Tumor necrosis factor-α.

Table

Box 1. Hyperinflation in chronic obstructive pulmonary disease In resting healthy subjects, expiration is passive. The relaxation volume depends upon two opposing pressures: the inward lung and the outward chest wall pressures. The relaxation lung volume is the end-expiratory lung volume (or functional residual capacity, FRC). In the presence of emphysema, lung elastic recoil pressure is diminished, lung elastance is reduced, and lung compliance is increased. Therefore, the expiratory driving pressure is reduced. The relaxation volume occurs at a higher level than that of healthy subjects. Static hyperinflation corresponds to an elevation of the relaxation volume above its predicted value. The expiratory time may be diminished when airway resistance and lung compliance are increased. Expiration may be partial as inspiration occurs before the lungs have returned to their end-expiratory volume. The relaxation volume of the respiratory system is greater than the statically driven relaxation volume. Dynamic hyperinflation is the increase in relaxation volume above the static relaxation volume [147].

Table

Box 2. Upper airway collapsibility Collapsibility can be assessed by measuring the critical closing pressure (Pcrit). The concept of Pcrit arises from modeling the oropharynx as a simple collapsible tube bound by an upstream and downstream segment, the Starling resistor model of OSA (for a review, see Gold and Schwartz [148]). The upstream pressure is the atmospheric pressure (Patm) when the patient breaths room air. The downstream pressure is the tracheal pressure. Airway occlusion occurs when the pressure outside the collapsible tube, i.e., the pressure from the peri-pharyngeal soft tissues, becomes greater than that inside the collapsible tube. The pressure gradient during airflow through the system is defined by Patm − Pcrit. The higher the Pcrit, the more collapsible the airway. When Pcrit is greater than Patm, complete airway occlusion occurs.

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