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J Dent Res 83(9):718-722, 2004
© 2004 International and American Associations for Dental Research

RESEARCH REPORT
Clinical

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

T. Ayuse1,*, T. Inazawa1, S. Kurata1, I. Okayasu1, E. Sakamoto1, K. Oi1, H. Schneider2, and A.R. Schwartz2

1 Nagasaki University Graduate School of Biomedical Science, Dept. of Clinical Physiology, 1-7-1 sakamoto Nagasaki-shi, 852-8588, Japan; and
2 The Johns Hopkins School of Medicine, Division of Pulmonary and Critical Care Medicine and Johns Hopkins Sleep Disorders Center, Baltimore, MD, USA;

* corresponding author, ayuse{at}net.nagasaki-u.ac.jp


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
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.

KEY WORDS: critical pressure • conscious sedation • upper airway • mouth opening • mandibular position • sleep apnea


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Conscious sedation is used, in conjunction with local anesthesia, for patients undergoing oral surgery or dental treatment, to allay their anxiety and to decrease intra-operative awareness. Among the agents available for sedation, the benzodiazepine, midazolam, is widely used to induce brief periods of conscious sedation. Because it is difficult for patients to keep their mouths open during midazolam sedation, mechanical mouth-openers are frequently used to widen the oral aperture and oropharyngeal cavity. The effect of these mouth-openers on oropharyngeal patency, however, has not been well-established.

Previous studies (Morikawa et al., 1961; Kuna and Remmers, 1985; Suratt and Hollowell, 1990; Meurice et al., 1996) have demonstrated that mouth-opening increases upper-airway collapsibility during both sleep and wakefulness. A recent study reported that mouth-opening increased the resistance in the upper airway during sleep and may contribute to the occurrence of sleep-disordered breathing (Meurice et al., 1996). In contrast, Verin et al.(2002) reported that opening the mouth during wakefulness did not significantly influence upper-airway flow dynamics in normal humans. Although the mouth was opened to a similar degree in both studies, differences in the asleep-awake state may have explained the disparate results of these two studies, since mouth-opening may have a greater effect on upper-airway collapsibility when neuromuscular tone is decreased during sleep or sedation. Nevertheless, little is known about the effect of mouth-opening on upper-airway function during midazolam sedation. The purpose of our study, therefore, was to examine the effect of mouth-opening on upper-airway function in patients breathing through their noses under midazolam sedation. We hypothesized that opening the mouth would increase upper-airway resistance and/or collapsibility during midazolam sedation.


   MATERIALS & METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
Subjects
Subjects were eligible for this study if they were healthy and free of any obvious sleep complaints, including snoring. The experimental protocols described below were approved by the Human Investigation Committee of the Nagasaki University School of Dentistry. Informed written consent was obtained from all subjects (n = 13, 22.1 ± 1.9 yrs). All subjects were male.

Experimental Techniques
    Polysomnographic measurements
All subjects underwent routine hemodynamic monitoring and polysomnographic monitoring of sleep with bilateral electro-oculograms (EOGs), electroencephalograms (EEGs) (C3-A2), and submental electromyograms (EMGs) (Fig. 1Go). A standard Hyatt-type esophageal balloon catheter (Ackrad Laboratories, Inc., Cranford, NJ, USA) was passed perinasally and utilized for monitoring esophageal pressure (Pes). Oxygen saturation (SpO2) was measured by pulse oximetry. Thoracic and abdominal movements were also recorded by inductance plethysmography (model TR755T, Nihon Koden, Tokyo, Japan). We used the BIS monitor (Aspect Medical Systems Inc., Natick, MA, USA) to process EEG signals to determine the depth of sedation. Airflow was monitored with a pneumotachometer (model TV112T, Nihon Koden) and differential pressure transducer (model TP-602T, Validyne ± 2 cm H2O). All measurements were displayed and stored simultaneously on a desktop computer equipped with data acquisition software (Windaq, Dataq Instruments, Inc., Akron, OH, USA) and were also recorded on an eight-channel thermal recorder.



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  		Figure 1. Diagram of experimental techniques.

 
    Experimental apparatus
Pressure was controlled at the subject’s nose (Pn) over the range from –15 to 10 cm H2O. Both a bilevel positive-pressure source (BiPAP; Respironics, Murrysville, PA, USA) and a negative-pressure source (smoke cleaner unit, NIIC-Tokyo, Japan) were utilized for this purpose. These pressure sources were connected to a valve that could be turned manually to toggle between them. The outflow from this valve was then connected to the pneumotachometer and nasal mask.

Experimental Protocols
    Sedation
Each subject had a 22G intravenous catheter inserted, and Ringer’s lactate solution was infused at a normal maintenance rate. Initially, midazolam was injected at a rate of 0.5 mg per min. In this phase, the level of sedation was simultaneously evaluated every min according to both the Observer’s Assessment of Alertness and Sedation scale (OAAS) (Chernik et al., 1990) and the output of the BIS monitor. We required an OAAS scale score of 3 to proceed (indicating that the subject no longer responded to a normal tone of voice but did respond to his name being called loudly). Also, the subject’s BIS value had to be between 65 and 85. If the targeted level of sedation had not been achieved after the initial midazolam bolus, an additional dose of midazolam was given, and the sedation level was reconfirmed before further data acquisition proceeded.

    Measurement of upper-airway collapsibility
After an adequate level of sedation was attained, the subjects were initially allowed to breathe under atmospheric pressure while nasal pressure was gradually increased to a holding pressure until inspiratory airflow limitation was eliminated, as previously described (Schwartz et al., 1998b; Boudewyns et al., 2000). Thereafter, nasal pressure was maintained at a holding level and was subsequently lowered progressively by 1 to 2 cm H2O every 5 or 6 breaths until zero flow occurred (Fig. 2Go). At the lowest level, nasal pressure was maintained for only 10 sec, since obstructive apnea was induced. Furthermore, if the value of SpO2 decreased below 90%, the protocol was aborted for reasons of safety. At least 2 series of pressure-flow relationships were generated for each condition, lasting approximately 10–15 min per condition. Prior to repeating a series of pressure-flow relationships, we reconfirmed and/or re-established the subject’s stable state of sedation and breathing. If the subject awoke during the series, we raised the nasal pressure to a holding level and resumed the series once the subject’s stable breathing and sedation had been achieved. The abbreviated nature of our protocol allowed for repeated assessments of the upper-airway pressure-flow relationship under several experimental conditions.



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  		Figure 2. A representative polysomnographic recording is illustrated, showing the change in nasal pressure (Pn) (fourth channel from top) and upper inspiratory airflow (VI) (fifth channel from top). As shown, progressively sub-atmospheric levels of nasal pressure (Pn) were applied in a stepwise manner (left to right) and kept constant at each pressure level for 5 or 6 breaths. At negative Pn values, below –3 cm H2O, inspiratory flow limitation ensued, as indicated by a flattening of the inspiratory airflow contour (see downward arrow from left), while the esophageal pressure (Pes) continued to become increasingly more negative. We obtained maximal inspiratory flow (VImax) by taking the difference between zero inspiratory flow and maximal inspiratory flow, as illustrated by the dotted lines. Of note, electroencephalograms (EEG), bilateral electro-oculograms (EOG), and submental electromyograms (EMG) (Channels 1–3 from top) indicate that moderate sedation was maintained throughout the experiment. Similar findings were observed in all subjects.

 
    Mouth-opening protocols
Prior to the study, 2 different sizes of custom mouth-openers were made. For each subject, the mouth-opener was placed at the first molar by means of a dental bite registration cream agent (Vinyl polysiloxane) (ExabiteII, GC, Inc., Tokyo, Japan). To prevent air from leaking from the subject’s mouth, we sealed it tightly with surgical tape. Each subject was fitted with a nasal mask affixed to his face with a sealing compound. Subjects were monitored in the supine position. A U-shaped pillow was placed under the subject’s head, and a head strap fixed the head into position so that positional changes would not influence upper-airway function. The pressure-flow data were acquired in three different conditions in random order. In condition 1, the pressure-flow relationship was obtained for mouth closed with the chin cap/surgical tape (Condition 1, closed mouth). We used a custom-made mouth-opening device to acquire data from subjects with their mouths opened moderately (1–1.5 cm distance between upper and lower incisors, Condition 2) and with their mouths opened maximally (3.5–4 cm distance between upper and lower incisors, Condition 3).

Data Analysis
    Sleep and sleep-disordered breathing
We used standard polysomnographic techniques to determine sleep stages and sleep-disordered breathing events as previously described (Smith et al., 1983). Apneas were defined by the complete cessation of airflow for more than 10 sec. Hypopneas were defined as a greater than 50% reduction of airflow associated with either an arousal from sleep or greater than 4% oxyhemoglobin desaturation.

    Upper-airway pressure relationship
At each level of nasal pressure, breaths were evaluated for the presence of inspiratory airflow limitation, as previously described (Schwartz et al., 1988, 1989; Boudewyns et al., 2000). Maximal inspiratory airflow (VImax) was measured in the last 3 flow-limited inspirations at each level of nasal pressure, as previously described (Schwartz et al., 1998a). We used pressure-flow data from these breaths to define the nasal pressure vs. VImax relationship, and least-squares linear regression to define the critical pressure (nasal pressure at zero flow) and upstream resistance (the inverse of the slope of this relationship). As reported previously (Gold and Schwartz, 1996), the pressure-flow relationship was fitted by the following equation: VImax = (Pn - Pcrit) / Rua, where Rua is the resistance of the portion of the airway upstream to the site of collapse.

We also evaluated the upper-airway opening pressure (minimally effective CPAP, eCPAP), which was defined as the minimal level of nasal continuous positive airway pressure required to prevent inspiratory airflow limitation (Issa and Sullivan, 1984; Condos et al., 1994; Hosselet et al., 2001).

Statistical Analysis
We studied the effects of mouth opening for each outcome variable (Pcrit, Rua, eCPAP) using ANOVA for repeated measures, with a post hoc protected Fisher’s test (Stat view 5.0). A value of p < 0.05 was considered significant. Pcrit and Rua values are reported as mean ± SD.


   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Moderate Sedation
Measurement of Pcrit under sedation was performed in 13 men ages 22.1 ± 1.9 yrs, mean body weights 66.0 ± 6.7 kg, mean height 1.71 ± 0.03 m, and BMI 22.6 ± 2.5 kg/m2. The average total amount of midazolam administered was 4.4 ± 1.2 mg (0.068 ± 0.011 mg/kg) over the 42.5 ± 4.5 min required for the experimental protocol to be completed. The value of SpO2 was stable 97.8 ± 0.7% to 96.2 ± 1.0% during sedation. The average value from the BIS monitor after the induction of sedation decreased from 94.7 ± 1.4 to 76.8 ± 4.9.

Effect of Mouth-opening on Upper-airway Function
From the flow-limited respiratory cycles of each experiment, we generated pressure-flow relationships to assess Pcrit and upper-airway resistance (Rua) in closed mouths, in mouths opened moderately, and in mouths opened maximally (Fig. 3Go). In this subject, mouth-opening from the closed to moderately then maximally opened conditions was associated with a progressive increase in Pcrit (see right shift in x-intercept). In contrast, Rua increased only in the maximally open compared with moderately open and closed-mouth conditions, as reflected by a decrease in the slope of the pressure-flow relationship. Analysis of the pooled data demonstrated that maximal mouth-opening increased Pcrit to –3.6 ± 2.9 cm H2O from –8.7 ± 2.8 (p = 0.002) in the closed and –7.2 ± 4.1 (p = 0.038) in the moderately open conditions. In contrast, upper-airway resistance was similar in all 3 conditions (18.4 ± 6.6 vs. 17.7 ± 7.6 vs. 21.5 ± 11.6 cm H2O/L/sec). Moreover, in the maximal mouth open condition at atmospheric pressure, all individuals developed upper-airway obstruction, as reflected by the presence of inspiratory airflow limitation. In contrast, upper-airway obstruction was not observed in the other 2 conditions at atmospheric nasal pressure. A mean nasal pressure of 4.3 ± 2.7 cm H2O was effective in eliminating upper-airway obstruction in the maximal mouth open condition.



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  		Figure 3. A representative example of the nasal pressure (Pn) vs. inspiratory flow (VImax) relationship in one subject. Nasal resistance (Rua) was defined as the reciprocal of the slope of the relationship between VImax and Pn, and Pcrit as the x intercept of the regression line as illustrated. In the mouth-closed condition (open circle), Pcrit was –9.4 cm H2O and Rua was 15.8 cm H2O/L/sec. In the moderate mouth-open condition (black circle), Pcrit was –7.0 cm H2O and Rua was 17.0 cm H2O/L/sec, while in the maximal mouth-open condition (open square), Pcrit was –4.0 cm H2O and Rua was 34.6 cm H2O/L/sec.

 

   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
The aim of the present study was to investigate the influence of mouth-opening on upper-airway patency (Pcrit and Rua) during midazolam sedation. There were two major findings: First, maximal mouth-opening led to substantial increases in critical pressure but did not change the upstream resistance. Second, the minimally effective CPAP pressure increased with mouth-opening, indicating that mouth-opening induced inspiratory airflow limitation (at atmospheric nasal pressure) that could be eliminated by an increase in nasal pressure. These findings indicate that mouth-opening increased pharyngeal collapsibility without altering breathing resistance during midazolam sedation, and that this effect can be overcome by the application of nasal CPAP. These findings have implications for dental surgery under sedation as well as for our understanding of OSA pathogenesis, diagnosis, and management.

Effect of Midazolam Sedation on Upper-airway Patency
Current evidence supports the concept that neuromuscular tone influences critical pressure measurements. When we compared our measurements of critical closing pressures during sedation with those during sleep, deep sedation/general anesthesia, and complete neuromuscular blockade, we found that the critical pressure was –8.7 ± 2.8 cm H2O in subjects with their mouths closed, which was slightly higher than that previously reported (Rowley et al., 2001) (–10.4 ± 3.1 cm H2O) in subjects sleeping normally during non-REM sleep. Moreover, our baseline critical pressures (mouth-closed condition) were comparable with those of a recent study (Litman et al., 2002) which documented values of –8.2 ± 4.3 cm H2O that were obtained when the investigators lowered the nasal pressure under midazolam sedation. Nevertheless, our critical pressures under sedation were much more negative than those reported from subjects under general anesthesia and paralysis (Isono et al., 1997; Eastwood et al., 2002a), which markedly decreases or eliminates neuromuscular mechanisms involved in the maintenance of airway patency. Thus, our critical pressure measurements, obtained from subjects under midazolam sedation, suggest that upper-airway neuromuscular mechanisms remain intact during moderate midazolam sedation and are comparable with those obtained during stable non-REM sleep.

Effects of Mouth-opening on Upper-airway Function
We found that mouth-opening increased the critical pressure without changing upstream resistance, a finding consistent with those previously reported during sleep (Meurice et al., 1996). Isolated elevations in critical pressure indicate that mouth-opening increased the collapsibility of the velo- or oropharynx (Eastwood et al., 2002b) without altering the airway patency farther upstream toward the nose. Although the mechanism for elevations in critical pressure is not clear, there are three possible explanations for our finding. First, this increase in Pcrit may be due to a reduction in the efficiency of phasic upper-airway dilator muscles. When the mouth is closed under physiological conditions, the neural activity in muscles in both the mandible and the hyoid bone may act to stabilize the upper airway. When the mouth is opened, however, reductions in the lengths of these muscles might reduce their contractile efficiency (Suratt and Hollowell, 1990) and the tongue-protrusion force generated by these muscles (Hollowell and Suratt, 1991), thereby destabilizing the pharynx. Second, mouth-opening might have narrowed the pharyngeal lumen, since downward movement of the mandible is associated with posterior displacement and reductions in the retroglossal airspace (Kuna and Remmers, 1985). Third, posterior displacement of the mandible may lead to compression of the pharyngeal lumen by soft tissues surrounding the airway (Watanabe et al., 2002). Thus, both anatomic and neuromuscular mechanisms might account for observed increases in upper-airway collapsibility when the mouth is opened during midazolam sedation.

Our findings have significant implications for therapy and clinical care. We found that mouth-opening led to progressive increases in upper-airway collapsibility, which increased the degree of upper-airway obstruction during sedation. To avoid the development of airway obstruction, therefore, one must take precautions to maintain upper-airway patency during procedures requiring a subject to have an open mouth under sedation. Our findings emphasize the importance of recognizing that upper-airway obstruction can develop during dental procedures performed on subjects under sedation, and that the use of a chin lift, mandible advancement maneuver, and/or nasal CPAP might be required to alleviate the obstruction caused during mouth-opening.


   ACKNOWLEDGMENTS
 
This study was supported by a Grant-in-Aid for Scientific Research (no. 11470441) (to K.O.) from the Japanese Ministry of Education, Science, Sports and Culture, and by NIH grants HL50381 and HL37379.

Received October 29, 2003; Last revision March 24, 2004; Accepted June 29, 2004


   REFERENCES
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS & METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Boudewyns A, Punjabi N, Van de Heyning PH, De Backer WA, O’Donnell CP, Schneider H, et al. (2000). Abbreviated method for assessing upper airway function in obstructive sleep apnea. Chest 118:1031–1041.[Abstract/Free Full Text]

Chernik DA, Gillings D, Laine H, Hendler J, Silver JM, Davidson AB, et al. (1990). Validity and reliability of the Observer’s Assessment of Alertness/Sedation Scale: study with intravenous midazolam. J Clin Psychopharmacol 10:244–251.[ISI][Medline]

Condos R, Norman RG, Krishnasamy I, Peduzzi N, Goldring RM, Rapoport DM (1994). Flow limitation as a noninvasive assessment of residual upper-airway resistance during continuous positive airway pressure therapy of obstructive sleep apnea. Am J Resp Crit Care Med 150:475–480.[Abstract]

Eastwood PR, Szollosi I, Platt PR, Hillman DR (2002a). Comparison of upper airway collapse during general anaesthesia and sleep. Lancet 359:1207–1209.[ISI][Medline]

Eastwood PR, Szollosi I, Platt PR, Hillman DR (2002b). Collapsibility of the upper airway during anesthesia with Isoflurane. Anesthesiology 97:786–793.[ISI][Medline]

Gold AR, Schwartz AR (1996). The pharyngeal critical pressure. The whys and hows of using nasal continuous positive airway pressure diagnostically. Chest 110:1077–1088.[Free Full Text]

Hollowell DE, Suratt PM (1991). Mandible position and activation of submental and masseter muscles during sleep. J Appl Physiol 71:2267–2273.[Abstract/Free Full Text]

Hosselet JJ, Ayappa I, Norman RG, Kreiger AC, Rapoport DM (2001). Classification of sleep-disordered breathing. Am J Resp Crit Care Med 163:398–405.[Abstract/Free Full Text]

Isono S, Tanaka A, Tagaito Y, Sho Y, Nishino T (1997). Pharyngeal patency in response to advancement of the mandible in obese anesthetized persons [see comments]. Anesthesiology 87:1055–1062.[ISI][Medline]

Issa FG, Sullivan CE (1984). Upper airway closing pressures in obstructive sleep apnea. J Appl Physiol 57:520–527.[Abstract/Free Full Text]

Kuna ST, Remmers JE (1985). Neural and anatomic factors related to upper airway occlusion during sleep. Med Clin North Am 69:1221–1242.[ISI][Medline]

Litman RS, Hayes JL, Basco MG, Schwartz AR, Bailey PL, Ward DS (2002). Use of dynamic negative airway pressure (DNAP) to assess sedative-induced upper airway obstruction. Anesthesiology 96:342–345.[Medline]

Meurice JC, Marc I, Carrier G, Series F (1996). Effects of mouth opening on upper airway collapsibility in normal sleeping subjects. Am J Resp Crit Care Med 153:255–259.[Abstract]

Morikawa S, Safar P, DeCarlo J (1961). Influence of head-jaw position on airway patency. Anesthesiology 22:265–270.[ISI][Medline]

Rowley JA, Zhou X, Vergine I, Shkoukani MA, Badr MS (2001). Influence of gender on upper airway mechanics: upper airway resistance and Pcrit. J Appl Physiol 91:2248–2254.[Abstract/Free Full Text]

Schwartz AR, Smith PL, Wise RA, Gold AR, Permutt S (1988). Induction of upper airway occlusion in sleeping individuals with subatmospheric nasal pressure. J Appl Physiol 64:535–542.[Abstract/Free Full Text]

Schwartz AR, Smith PL, Wise RA, Bankman I, Permutt S (1989). Effect of positive nasal pressure on upper airway pressure-flow relationships. J Appl Physiol 66:1626–1634.[Abstract/Free Full Text]

Schwartz AR, Eisele DW, Smith PL (1998a). Pharyngeal airway obstruction in obstructive sleep apnea: pathophysiology and clinical implications. Otolaryngol Clin North Am 31:911–918.[Medline]

Schwartz AR, O’Donnell CP, Baron J, Schubert N, Alam D, Samadi SD, et al. (1998b). The hypotonic upper airway in obstructive sleep apnea: role of structures and neuromuscular activity. Am J Resp Crit Care Med 157:1051–1057.[Abstract/Free Full Text]

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Verin E, Series F, Locher C, Straus C, Zelter M, Derenne JP, et al. (2002). Effects of neck flexion and mouth opening on inspiratory flow dynamics in awake humans. J Appl Physiol 92:84–92.[Abstract/Free Full Text]

Watanabe T, Isono S, Tanaka A, Tanzawa H, Nishino T (2002). Contribution of body habitus and craniofacial characteristics to segmental closing pressures of the passive pharynx in patients with sleep-disordered breathing. Am J Resp Crit Care Med 165:260–265.[Abstract/Free Full Text]




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