The effect of increased lung volume in chronic obstructive pulmonary disease on upper airway obstruction during sleep

Abstract

Patients with chronic obstructive pulmonary disease (COPD) exhibit increases in lung volume due to expiratory airflow limitation. Increases in lung volumes may affect upper airway patency and compensatory responses to inspiratory flow limitation (IFL) during sleep. We hypothesized that COPD patients have less collapsible airways inversely proportional to their lung volumes, and that the presence of expiratory airflow limitation limits duty cycle responses to defend ventilation in the presence of IFL. We enrolled 18 COPD patients and 18 controls, matched by age, body mass index, sex, and obstructive sleep apnea disease severity. Sleep studies, including quantitative assessment of airflow at various nasal pressure levels, were conducted to determine upper airway mechanical properties [passive critical closing pressure (Pcrit)] and for quantifying respiratory timing responses to experimentally induced IFL. COPD patients had lower passive Pcrit than their matched controls (COPD: -2.8 ± 0.9 cmH2O; controls: -0.5 ± 0.5 cmH2O, P = 0.03), and there was an inverse relationship of subject's functional residual capacity and passive Pcrit (-1.7 cmH2O/l increase in functional residual capacity, r(2) = 0.27, P = 0.002). In response to IFL, inspiratory duty cycle increased more (P = 0.03) in COPD patients (0.40 to 0.54) than in controls (0.41 to 0.51) and led to a marked reduction in expiratory time from 2.5 to 1.5 s (P < 0.01). COPD patients have a less collapsible airway and a greater, not reduced, compensatory timing response during upper airway obstruction. While these timing responses may reduce hypoventilation, it may also increase the risk for developing dynamic hyperinflation due to a marked reduction in expiratory time.

Pathogenesis of obstructive sleep apnea in individuals with the COPD + OSA Overlap syndrome versus OSA alone

“…We suspect this is due to the fact that a collapsible upper airway is requisite for OSA to be present. Similar to a previous study (Biselli et al, ), we did not find a difference in P crit between OVS and OSA alone, but in contrast we did not see a relationship between P crit and FRC, perhaps because we considered FRC relative to body size (i.e., percent predicted). We did observe an association between increased total lung capacity and lower V passive , which did not meet significance but encompassed a potentially important effect size.…”

“…With respect to anatomical factors, stability of the upper airway is dependent on traction from the trachea, thus increases in lung volumes can improve upper airway collapsibility (i.e., stiffen the airway) (Owens, Malhotra, Eckert, White, & Jordan, 2010;Van de Graaff, 1988). Consequently, increased lung volumes in COPD may have a protective effect on upper airway closing pressure and thus may reduce the apnea-hypopnea index (Biselli et al, 2015;Krachman et al, 2016). However, a loss of elastic recoil related to emphysema may decrease tracheal traction forces, and thus the net effect of COPD on upper airway collapsibility is difficult to predict.…”

Non-invasive ventilation with intelligent volume-assured pressure support versus pressure-controlled ventilation: effects on the respiratory event rate and sleep quality in COPD with chronic hypercapnia

“…Higher backup breathing rates also seem to have no relevant effect on pCO 2 reduction during NIV in hypercapnic COPD 31. COPD patients who also have coexisting obstructive sleep apnea (overlap syndrome) demonstrated an increase in functional residual capacity (FRC) due to shortened or aggravated inspiration 32. Looking at basic pathophysiology, it is possible to conclude that patients with obstructive airway disease could benefit from a low breathing rate because this might reduce the extent of overinflation by shifting the FRC to inspiration 33.…”

The overlaps of asthma or COPD with OSA: A focused review

“…In the case of COPD, it was not clear that lung parenchymal destruction from emphysema and reduced tissue elastance would exert the same pull on the large airways. However, Biselli et al 41 measured upper airway collapsibility and found that patients with hyperinflation did have less upper airway collapsibility, and indeed, radiographical signs of hyperinflation were associated with reduced OSA severity. 42 These data would refute the hypothesis that tissue destruction causing hyperinflation in severe COPD would contribute to OSA pathogenesis.…”