Abdominal compression increases upper airway collapsibility during sleep in obese male obstructive sleep apnea patients.

STUDY OBJECTIVES: Abdominal obesity, particularly common in centrally obese males, may have a negative impact on upper airway (UA) function during sleep. For example, cranial displacement of the diaphragm with raised intra-abdominal pressure may reduce axial tension exerted on the UA by intrathoracic structures and increase UA collapsibility during sleep. DESIGN: This study aimed to examine the effect of abdominal compression on UA function during sleep in obese male obstructive sleep apnea patients. SETTING: Participants slept in a sound-insulated room with physiologic measurements controlled from an adjacent room. PARTICIPANTS: Fifteen obese (body mass index: 34.5 +/- 1.1 kg/m2) male obstructive sleep apnea patients (apnea-hypopnea index: 58.1 +/- 6.8 events/h) aged 50 +/- 2.6 years participated. INTERVENTIONS: Gastric (PGA) and transdiaphragmatic pressures (P(DI)), UA closing pressure (UACP), UA airflow resistance (R(UA)), and changes in end-expiratory lung volume (EELV) were determined during stable stage 2 sleep with and without abdominal compression, achieved via inflation of a pneumatic cuff placed around the abdomen. UACP was assessed during brief mask occlusions. MEASUREMENTS AND RESULTS: Abdominal compression significantly decreased EELV by 0.53 +/- 0.24 L (P=0.045) and increased PGA (16.2 +/- 0.8 versus 10.8 +/- 0.7 cm H2O, P < 0.001), P(DI) (11.7 +/- 0.9 versus 7.6 +/- 1.2 cm H2O, P < 0.001) and UACP (1.4 +/- 0.8 versus 0.9 +/- 0.9 cm H2O, P = 0.039) but not R(UA)(6.5 +/- 1.4 versus 6.9 +/- 1.4 cm H2O x L/s, P=0.585). CONCLUSIONS: Abdominal compression negatively impacts on UA collapsibility during sleep and this effect may help explain strong associations between central obesity and obstructive sleep apnea.

Upper airway surface tension but not upper airway collapsibility is elevated in primary Sjögren's syndrome.

STUDY OBJECTIVES: Primary Sjögren's syndrome is an autoimmune disease typified by xerostomia (dry mouth) that, in turn, could lead to increased saliva surface tension (gamma) and increased upper airway collapsibility. Fatigue, of unknown etiology, is also frequently reported by patients with primary Sjögren's syndrome. Recent preliminary data indicate a high prevalence of obstructive sleep apnea in healthy-weight women with primary Sjögren's syndrome. Concurrent research highlights a significant role of gamma in the maintenance of upper airway patency. The aim of this study was to compare oral mucosal wetness, saliva gamma, and upper airway collapsibility during wake and sleep between women with primary Sjögren's syndrome and matched control subjects. SETTING: Participants slept in a sound-insulated room with physiologic measurements controlled from an adjacent room. PARTICIPANTS: Eleven women with primary Sjögren's syndrome and 8 age- and body mass index-matched control women. INTERVENTIONS: Upper airway collapsibility index (minimum choanal-epiglottic pressure expressed as a percentage of delivered choanal pressure) was determined from brief negative-pressure pulses delivered to the upper airway during early inspiration in wakefulness and sleep. MEASUREMENTS AND RESULTS: Patients with primary Sjögren's syndrome had significantly higher saliva gamma ("pull-off" force method) compared with control subjects (67.2 +/- 1.1 mN/m versus 63.2 +/- 1.7 mN/m, P < 0.05). Upper airway collapsibility index significantly increased from wake to sleep (Stage 2 and slow wave sleep) but was not different between groups during wake (primary Sjögren's syndrome versus controls; 36.3% +/- 8.0% vs 46.0 +/- 13.8%), stage 2 sleep (53.1% +/- 11.9% vs 63.4% +/- 7.2%), or slow-wave sleep (60.8% +/- 12.2% vs 60.5% +/- 9.3%). CONCLUSIONS: Despite having a significantly "stickier" upper airway, patients with primary Sjögren's syndrome do not appear to have abnormal upper airway collapsibility, at least as determined from upper airway collapsibility index.