Mouth-opening Increases Upper-airway Collapsibility without Changing Resistance during Midazolam Sedation

Abstract

Sedative doses of anesthetic agents affect upper-airway function. Oral-maxillofacial surgery is frequently performed on sedated patients whose mouths must be as open as possible if the procedures are to be accomplished successfully. We examined upper-airway pressure-flow relationships in closed mouths, mouths opened moderately, and mouths opened maximally to test the hypothesis that mouth-opening compromises upper-airway patency during midazolam sedation. From these relationships, upper-airway critical pressure (Pcrit) and upstream resistance (Rua) were derived. Maximal mouth-opening increased Pcrit to −3.6 ± 2.9 cm H2O compared with −8.7 ± 2.8 (p = 0.002) for closed mouths and −7.2 ± 4.1 (p = 0.038) for mouths opened moderately. In contrast, Rua was similar in all three conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, maximum mouth-opening produced an inspiratory airflow limitation at atmosphere that was eliminated when nasal pressure was adjusted to 4.3 ± 2.7 cm H2O. We conclude that maximal mouth-opening increases upper-airway collapsibility, which contributes to upper-airway obstruction at atmosphere during midazolam sedation.

The impacts of open-mouth breathing on upper airway space in obstructive sleep apnea: 3-D MDCT analysis

“…Meurice et al [23] reported this phenomenon by measuring upper airway collapsibility in open-and closed-mouth positions in healthy sleeping volunteers and showed that sleeping with the mouth open increases upper airway collapsibility. In addition, Ayuse et al [24] tested the hypothesis that opening the mouth during sleep compromises upper airway patency during midazolam sedation by examining the relationship between pressure and flow in the upper airway in open-and closed-mouth positions. They concluded that maximal mouth opening increases upper airway collapsibility and can cause difficulties during midazolam sedation.…”

The compensatory responses to upper airway obstruction in normal subjects under propofol anesthesia

“…We have previously reported that passive measurements of upper airway collapsibility in sedated subjects were similar to non-REM sleep (Ayuse et al, 2004; Inazawa et al, 2005; Ikeda et al, 2006). Active compensatory neuromuscular responses, however, have not been characterized in anesthetized subjects.…”

“…At each level of P N , breaths were evaluated for the presence of inspiratory airflow limitation, as previously described (Schwartz et al, 1988, 1989; Boudewyns et al, 2000; Ayuse et al, 2004). Inspiratory flow limitation was defined as the presence of a plateau in inspiratory airflow in association with a continued fall in esophageal pressure by at least 1 cm H 2 O beyond the onset of the plateau.…”

Risk Factors With Intravenous Sedation for Patients With Disabilities

“…Decreased SpO 2 can be caused by occlusion of the upper respiratory tract following motion suppression, sedative drug overdose, or deep sedation 16 ; transient glossoptosis caused by choking or cough reflex 17 ; or the use of instruments such as those used for maintaining mouth opening during oral manipulations.…”