Nasal obstruction may cause sleep apnea and changes in breathing routes, but it remains unclear how breathing route changes affect obstructive sleep apnea syndrome (OSAS). We evaluated the relationship between breathing route and OSAS severity. We conducted polysomnography on 45 subjects with OSAS but no nasal obstruction in awake state using simultaneous multipoint pressure measurement. Pressure sensors were placed in the pharyngeal cavity such at the epipharynx, the oropharynx immediately below the soft palate, the hypopharynx next to the posterior tongue, and in the esophagus. Subjects were divided based on negative pressure epipharynx into 3 groups—nasal breathing with nasal obstruction (n=13), normal nasal breathing (n=16), and oral breathing (n=16). The apnea hypopnea index (AHI) of the oral breathing group was 52.0/h—significantly higher than in the nasal obstruction group at 32.1/h and the normal nasal breathing group at 24.4/h. The pressure study indicated that oral breathing obstructs the upper airway in the oral cavum and at tongue base, and that nasal obstruction in turn generates negative pressure in the epipharynx collapsing the lower upper airway. In contrast, nasal breathing normally obstructs the upper airway only via the uvula in OSAS during sleep.
Severity thus clearly differs between oral and nasal breathing during sleep. Subjects with OSAS breathing orally during sleep tend to have a higher AHI than subjects with nasal breathing due to severe hypopharynx airway obstruction.
