T. Ayuse

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

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

Upper airway obstruction during sleep can trigger compensatory neuromuscular responses and/or prolong inspiration in order to maintain adequate minute ventilation. The aim of this study was to investigate the strength of these compensatory responses during upper airway obstruction during propofol anesthesia. We assessed respiratory timing and upper airway responses to decreases in nasal pressure in nine propofol anesthetized normal subjects under condition of decreased (passive) and increased (active) neuromuscular activity. Critical closing pressure (PCRIT) and upstream resistance (RUS) were derived from pressure-flow relationships generated from each condition. The inspiratory duty cycle (IDC), maximum inspiratory flow (V1max) and respiratory rate (f) were determined at two levels of mean inspiratory airflow (VI; mild airflow limitation with VI > or = 150 ml s-1; severe airflow limitation with VI < 150 ml s-1). Compared to the passive condition, PCRIT decreased significantly (5.3 +/- 3.8 cm H2O, p < 0.05) and RUS increased (7.4 cm H2O ml-1 s, p < 0.05) in the active condition. The IDC increased progressively and comparably as decreased in both the passive and active conditions (p < 0.05). These findings imply that distinct compensatory mechanisms govern the modulation of respiratory pattern and pharyngeal patency during periods of airway obstruction under propofol anesthesia.

Effect of Mandibular Position on Upper Airway Collapsibility and Resistance

It has been proposed that advancement of the mandible is a useful method for decreasing upper airway collapsibility. We carried out this study to test the hypothesis that mandibular advancement induces changes in upper airway patency during midazolam sedation. To explore its effect, we examined upper airway pressure-flow relationships in each of 4 conditions of mouth position in normal, healthy subjects (n = 9). In the neutral position, Pcrit (i.e., critical closing pressure, an index of upper airway collapsibility) was −4.2 cm H2O, and upstream resistance (Rua) was 21.2 cm H2O/L/sec. In the centric occlusal position, Pcrit was −7.1 cm H2O, and Rua was 16.6 cm H2O/L/sec. In the incisor position, Pcrit was significantly reduced to −10.7 cm H2O, and Rua was significantly reduced to 14.0 cm H2O/L/sec. Mandibular advancement significantly decreased Pcrit to −13.3 cm H2O, but did not significantly influence Rua (22.1 cm H2O/L/sec). We conclude that the mandibular incisors’ position improved airway patency and decreased resistance during midazolam sedation.

The Effect of Gender on Compensatory Neuromuscular Response to Upper Airway Obstruction in Normal Subjects Under Midazolam General Anesthesia

BACKGROUND: Upper airway patency may be compromised during sleep and anesthesia by either anatomical alterations (mechanical properties) or disturbances in the neural control (compensatory neuromuscular responses). The pathophysiology of upper airway obstruction during anesthesia may differ between men and women. Recently, we reported that the upper airway mechanical properties were comparable with those found during natural nonrapid eye movement sleep, as evaluated by measurements of passive critical closing pressure (PCRIT) and upstream resistance (RUS) during midazolam sedation. In this study, we compared the effects of gender on compensatory neuromuscular responses to upper airway obstruction during midazolam general anesthesia. METHOD: Thirty-two subjects (14 men and 18 women) were studied. We constructed pressure-flow relationships to evaluate PCRIT and RUS during midazolam anesthesia. The midazolam anesthesia was induced with an initial dose of midazolam (0.07–0.08 mg/kg bolus) and maintained by midazolam infusion (0.3–0.4 &mgr;g · kg−1 · min−1), and the level of anesthesia was assessed by Ramsay score (Level 5) and Observer’s Assessment of Alertness/Sedation score (Level 2). Polysomnographic and hemodynamic variables were monitored while nasal pressure (via mask), inspiratory air flow (via pneumotachograph), and genioglossal electromyograph (EMGGG) were recorded. PCRIT was obtained in both the passive condition, under conditions of decreased EMGGG (passive PCRIT), and in an active condition, whereas EMGGG was increased (active PCRIT). The difference between the active PCRIT and passive PCRIT (&Dgr;PCRIT P − A) was calculated in each subject to determine the compensatory neuromuscular response. RESULTS: The difference between the active PCRIT and passive PCRIT (&Dgr;PCRIT A − P) was significantly greater in women than in men (4.6 ± 2.8 cm H2O and 2.2 ± 1.7 cm H2O, respectively; P < 0.01), suggesting greater compensatory neuromuscular response to upper airway obstruction independent of arousal. CONCLUSION: We demonstrate that the arousal-independent compensatory neuromuscular responses to upper airway obstruction during midazolam anesthesia were partially maintained in women, and that gender may be a major determinant of the strength of compensatory responses during anesthesia.

Anaphylactoid-like Reaction to Midazolam During Oral and Maxillofacial Surgery

We experienced a case of life-threatening hypotension and bronchoconstriction associated with edema in a patient undergoing resection of a tumor of the right mandible following intravenous midazolam for induction of general anesthesia. We decided to postpone surgery for further examination of a possible drug-induced allergic reaction, and we rescheduled surgery for 1 week later. After administering H1 and H2 histamine antagonists, we administered a slow induction with sevoflurane in nitrous oxide and oxygen plus intravenous atropine sulfate after performing a test dose injection. We safely induced and maintained anesthesia with nitrous oxide, oxygen, and sevoflurane.

Tactile sensory and pain thresholds in the face and tongue of subjects asymptomatic for oro-facial pain and headache

The aim of this study was to examine the tactile sensory and pain thresholds in the face, tongue, hand and finger of subjects asymptomatic for pain. Sixteen healthy volunteers (eight men and eight women, mean age 35·7 years, range 27-41) participated. Using Semmes-Weinstein monofilaments, the tactile detection threshold (TDT) and the filament-prick pain detection threshold (FPT) were measured at five sites: on the cheek skin (CS), tongue tip (TT), palm side of the thenar skin (TS), dorsum of the hand (DH) and the finger tip (FT). The difference between the tactile sensory and pain threshold (FPT-TDT) was also calculated. Both for the TDT and FPT, TT and DH had the lowest and highest values, respectively. As for the FPT-TDT, there were no significant differences among the measurement sites. As the difference between FPT and TDT (FPT-TDT) is known to be an important consideration in interpreting QST (quantitative sensory testing) data and can be altered by neuropathology, taking the FPT-TDT as a new parameter in addition to the TDT and FPT separately would be useful for case-control studies on oro-facial pain patients with trigeminal neuralgia, atypical facial pain/atypical odontalgia and burning mouth syndrome/glossodynia.

Predictors of obstructive sleep apnoea-hypopnea severity and oral appliance therapy efficacy by using lateral cephalometric analysis.

Obstructive sleep apnoea-hypopnea (OSAH) is a common disorder characterised by repetitive complete or partial closure of the upper airway during sleep, which results in sleep fragmentation and oxygen desaturation. There is growing interest in the use of oral appliances (OAs) to treat OSAH. The purpose of this study was to clarify the cephalometric factors that are associated with OSAH severity and that predict the outcome of OA therapy. Two hundred nine patients with OSAH were recruited and analysed retrospectively. They had a polysomnographically documented apnoea-hypopnea index (AHI) of more than five respiratory events per hour. Lateral skull radiographs were used for cephalometric analysis. Only 67 of the 209 recruited patients underwent a second polysomnography (PSG) to evaluate the efficacy of OA therapy. In all recruited patients, the angle formed by the subspinal point (A) to the nasion (N) to the supramental point (B) (i.e. ANB angle) and the distance between the mandibular plane and hyoid bone (MP-H) were predictive factors of OSAH severity. In only 67 patients underwent PSG with an OA, the mean rate of decrease in the AHI was 47·8 ± 29·1%. OA therapy effectively treated OSAH in some patients with a very severe form of OSAH. However, patients who had a high position of the hyoid bone had a poor response to OA therapy. This study suggested that cephalometric analysis is useful for predicting OSAH severity and OA therapy efficacy.

The mandible advancement may alter the coordination between breathing and the non‐nutritive swallowing reflex

The coordination between nasal breathing and non-nutritive swallowing serves as a protective reflex against potentially asphyxiating material, i.e. saliva and secretions, entering the respiratory tract. Although this protective reflex is influenced by positional changes in the head and body, the effect of mandible position on this reflex is not fully understood. We examined the effect of mandible advancement associated with mouth opening on the coordination between nasal breathing and non-nutritive swallowing induced by continuous infusion of distilled water into the pharyngeal cavity. The combination of mandible advancement and mouth opening increased the duration of swallowing apnoea and submental electromyographic burst duration. When the mandible was advanced with the mouth open, the duration of swallowing apnoea increased significantly compared with the centric position (0.79 +/- 0.23 vs. 0.64 +/- 0.12 s, P < 0.05, n = 12), and the duration of submental electromyographic activity increased significantly (2.11 +/- 0.63 vs. 1.46 +/- 0.25 s, P < 0.05, n = 12). Mandible advancement with mouth opening altered the respiratory phase resetting during swallowing and the timing of swallow in relation to respiratory cycle phase. We conclude that mandible re-positioning may strongly influence the coordination between nasal breathing and non-nutritive swallowing by altering respiratory parameters and by inhibiting movement of the tongue-jaw complex.