Coexistence of Obstructive Sleep Apnea and Chronic Obstructive Pulmonary Disease

Abstract

Background: Obstructive sleep apnea (OSA) and chronic obstructive pulmonary disease (COPD) may lead to chronic alveolar hypoventilation. The coexistence of OSA and COPD has been termed the ‘overlap syndrome’. The aim of the study was to determine the relationship between the severity of COPD and the occurrence of chronic alveolar hypoventilation in patients with OSA and to evaluate the impact of chronic alveolar hypoventilation in patients with the overlap syndrome on the severity of breathing disorders during sleep. Material and methods: The study included 64 obese patients (BMI 40.0 ± 6.5 kg/m2) with OSA (AHI > 15; mean AHI 52 ± 22) coexisting with COPD. We analysed the results of polysomnography, spirometry and arterial blood gas analysis. Results: Chronic alveolar hypoventilation was present in 67% of the patients, including 60.5%, 85% and 100% of patients with moderate, severe and very severe COPD by spirometry, respectively. Patients with chronic alveolar hypoventilation had lower values of FVC (2.7 ± 0.8 l vs. 3.6 ± 0.9 l; p < 0.001), FEV1 (1.7 ± 0.6 l vs. 2.2 ± 0.5 l; p < 0.001) and mean SaO2 at the end of obstructive sleep apneas and hypopneas (75% ± 10% vs. 84% ± 5%; p < 0.001). Conclusions: Chronic alveolar hypoventilation is observed in the majority of obese patients with moderate to severe OSA and coexisting COPD, including moderate COPD. The occurrence of chronic alveolar hypoventilation in obese patients with OSA coexisting with COPD is associated with a marked arterial hypoxia during obstructive sleep apneic and hypopneic episodes.

The Interactions between Smoking and Sleep

“…Smokers also seem to present more severe OSAHS, at least in the majority of the studies [5,7,[80][81][82][83][84], compared to non-smokers. Numerous OSA indices were deteriorated in smokers including ODI, mean and minimum SaO2, total sleep time and sleep time ratio with SaO2 below 90%, mean apnoea duration, nocturnal hypoxia index and COHb levels [5,7,[80][81][82][83][84][85][86][87][88][89]. However, the relationship of AHI with smoking is not clear.…”

“…However, the relationship of AHI with smoking is not clear. Many studies concluded that AHI is deteriorated or affected in a dosedependent manner with smoking, even after adjusting for covariates [5,7,[80][81][82][83][84], while in other studies AHI seems not to be related with smoking [85][86][87][88][89][90][91][92]. As far as Epworth sleepiness scale (ESS), the majority of the studies concluded that it is worse in smokers [80,82,85,87], although there were also a few notable exceptions in this topic [7,91].…”

“…Furthermore, it is rather clear that smokers with OSAHS present significantly more frequently cardiovascular, metabolic, respiratory and gastrointestinal co-morbidities compared to non-smokers [5,7,80,82,84,85,93]. Additionally, it seems that smoking ameliorates the beneficial effect of the treatment of OSAHS with continuous positive airway pressure (CPAP) [92].…”

“…Moreover, orexin-A levels were significantly lower in never smokers with OSAHS compared to ex-or current smokers [115]. The co-existence of OSA or short sleep duration with smoking has been related not only with excess body weight, but also with metabolic diseases such as resistance to insulin or type II diabetes mellitus, increased triglycerides, increased low density lipoprotein (LDL) cholesterol and decreased high-density lipoprotein (HDL) cholesterol levels and also with cardiovascular diseases such as hypertension and coronary artery disease [9,12,13,82,84,[116][117][118][119][120]. Furthermore, in patients with OSAHS, current smoking determines the circulating levels of myeloperoxidase (MPO), an oxidative stress marker, and matrix metalloproteinase-9 (MMP-9), a plaque destabilizer, both signaling a worse prognosis [121].…”