Pathophysiology of the Upper Airway in Patients With Chronic Obstructive Pulmonary Disease (COPD) and Concomitant Obstructive Sleep Apnea (OSA)

Brief Summary

Detailed Description

This is a physiologic study to assess the effects of lower airway and lung tissue changes of COPD on upper airway collapsibility. Increased in lung volume and destruction of alveolar wall in COPD may have opposite and various effects on the upper airway collapsibility, which is an important factor of OSA development. Chronic obstructive pulmonary disease (COPD) and obstructive sleep apnea (OSA) are very common disorders associated with considerable morbidity, mortality, and healthcare costs. The prevalence of both co-existing conditions is estimated to be \~4% of the general population. This COPD-OSA "overlap" syndrome causes more severe hypoxemia than either COPD or OSA alone and has important clinical consequences, including death. COPD is usually excluded in OSA research and OSA is typically excluded or not assessed in studies of COPD; thus, available information about the "overlap" syndrome is limited. Therefore, it is important to identify patients with both COPD and OSA and determine the mechanisms of poor outcomes for these patients in order to optimize therapy. The pathophysiology of the COPD-OSA syndrome is not well understood. The investigators propose to investigate upper airway (UA) anatomic characteristics and collapsibility as potential underlying mechanisms that may help to explain the negative additive effect of having both conditions. The objectives are to study CT measures of airway anatomy and the critical closing pressure of the upper airway (Pcrit), a gold standard measure of upper airway collapsibility, in patients with COPD-OSA compared with COPD only and normal controls. CT scan of upper airway and chest will allow precise measures of upper airway characteristics and COPD associated alveolar and lower airway ch. angesMeasures of upper airway collapsibility will provide us information about the mechanical nature of the airway and if the patients are more likely to have OSA. Subjects with COPD-OSA may exhibit more upper airway inflammation possibly due to their pre-existing COPD disease and the reoccurring opening and closing of the upper airway due to the OSA. Therefore the investigators would like to assess the degree of inflammation in these patients compared to normal controls.

Primary Outcomes

Secondary Outcomes

• Parapharyngeal fat pad volume(Baseline)
• Emphysema distribution(Baseline)
• Width of hard palate(Baseline)
• Upper airway length(Baseline)
• Nasophayngeal/retropalatal/retroglossal pharyngeal cavity volume(Baseline)
• Tongue volume(Baseline)
• Lower airway wall thickness on chest CT scan(Baseline)
• Forced expiratory volume in 1 second (FEV1)(Baseline)
• Emphysema score(Baseline)
• Lateral airway dimension on hard palate/uvula/epiglottis level(Baseline)
• Cross-sectional airway area on hard palate/uvula/epiglottis level(Baseline)
• Distance between the lower edge of the mandible and the lower edge of the hyoid (MH)(Baseline)
• Volume of retropalatal/retroglossal soft tissue(Baseline)
• Pharyngeal lavage cell count distribution(Baseline)
• Minimal later airway dimension (mLAT)(Baseline)
• Minimal anteroposterior airway dimension (mAP)(Baseline)
• Minimal cross sectional airway area (mCSA)(Baseline)
• Anteroposterior airway dimension on hard palate/uvula/epiglottis level(Baseline)
• Volume within the cervico-mandibular bony frame(Baseline)
• Total lung capacity (TLC)(Baseline)
• Ratio of residual volume / total lung capacity (RV/TLC)(Baseline)
• Diffusing capacity of the lung for carbon monoxide (DLCO)(Baseline)