|Ph.D Student||Dotan Yaniv|
|Subject||Control of Upper Airway Dilator Muscles Activity during|
Sleep and Anesthesia in Patients with Obstructive
Sleep Apnea Syndrome
|Department||Department of Medicine||Supervisors||Professor Giora Pillar|
|Professor Arie Oliven|
|Full Thesis text|
Introduction: Pharyngeal collapsibility in Obstructive Sleep Apnea (OSA) syndrome is believed to increase due to a decline in upper airway dilator muscle (UADM) activity. We demonstrated in preliminary studies that during mild anesthesia, upper airway collapse was not explained by sleep-induced decline in UADM activation, as UADM ElectroMyoGraphy (EMG) activity increased during apneas and hypopneas, but failed to improve airflow. The present study was undertaken to evaluate the hypothesis that failure of intense activation of UADM to prevent pharyngeal obstruction may be associated with sleep-induced changes in UADM coordination.
Material and Methods:
1) Studies under propofol anesthesia: 17 patients with OSA were evaluated from termination of propofol administration to awakening. Genioglossus (GG)-EMG, airflow, esophageal pressure (Pes) and pharyngeal area (pharyngoscopy) were monitored. GG-Electrical stimulation (ES) was used to evaluate possible mechanical dysfunction.
2) Studies during sleep: 15 patients with OSA were evaluated. GG and tongue retractors (TR) EMG, airflow, and Pes were monitored. While awake, GG/TR-EMG were compared to Biceps/Triceps EMG. EMG/Pes was assessed while patients breathed through variable resistors, to estimate the EMG required to prevent pharyngeal collapse. During sleep, Pre-arousal EMG (sleepEMG) was compared to EMG at the same Pes during wakefulness (awakeEMG). SleepEMG/awakeEMG >1 indicated EMG level sufficient to prevent pharyngeal collapse.
1) Studies under propofol anesthesia: Prolonged hypopneas triggered an increase in GG-EMG, reaching 62.2 ± 32.7% of maximal GG-EMG obtained during wakefulness. This activity failed to increase flow and pharyngeal cross-sectional area (CSA). Awakening resulted in pharyngeal enlargement and restoration of flow, with marked reduction in GG-EMG. GG-ES under anesthesia increased the inspiratory pharyngeal CSA (p<0.01) and flow (p<0.001), indicating adequate mechanical response.
2) Studies during sleep: During wakefulness, the pattern of tongue muscles activation differed considerably from arm muscles, as both GG/TR were activated similarly during all tongue movements. During sleep, GG-EMG before arousal was significantly higher than during wakefulness at equal Pes (p<0.01). TR-EMG levels were significantly lower than during wakefulness (p<0.05).
Conclusions: In OSA patients during propofol anesthesia, pharyngeal occlusion persists despite large increases in GG-EMG, in the presence of a preserved mechanical response to ES. In OSA patients during sleep, GG-EMG may increase to levels by far higher than those required to prevent pharyngeal collapse during wakefulness, but fails to improve airflow. Co-activation of TR is deficient during sleep. This alteration in the pattern of tongue muscle activation may be involved in the pathogenesis of pharyngeal obstruction during sleep.