scholarly journals Effect of Head Elevation on Passive Upper Airway Collapsibility in Normal Subjects during Propofol Anesthesia

2011 ◽  
Vol 115 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Masato Kobayashi ◽  
Takao Ayuse ◽  
Yuko Hoshino ◽  
Shinji Kurata ◽  
Shunji Moromugi ◽  
...  

Background Head elevation can restore airway patency during anesthesia, although its effect may be offset by concomitant bite opening or accidental neck flexion. The aim of this study is to examine the effect of head elevation on the passive upper airway collapsibility during propofol anesthesia. Method Twenty male subjects were studied, randomized to one of two experimental groups: fixed-jaw or free-jaw. Propofol infusion was used for induction and to maintain blood at a constant target concentration between 1.5 and 2.0 μg/ml. Nasal mask pressure (PN) was intermittently reduced to evaluate the upper airway collapsibility (passive PCRIT) and upstream resistance (RUS) at each level of head elevation (0, 3, 6, and 9 cm). The authors measured the Frankfort plane (head flexion) and the mandible plane (jaw opening) angles at each level of head elevation. Analysis of variance was used to determine the effect of head elevation on PCRIT, head flexion, and jaw opening within each group. Results In both groups the Frankfort plane and mandible plane angles increased with head elevation (P < 0.05), although the mandible plane angle was smaller in the free-jaw group (i.e., increased jaw opening). In the fixed-jaw group, head elevation decreased upper airway collapsibility (PCRIT ~ -7 cm H₂O at greater than 6 cm elevation) compared with the baseline position (PCRIT ~ -3 cm H₂O at 0 cm elevation; P < 0.05). Conclusion : Elevating the head position by 6 cm while ensuring mouth closure (centric occlusion) produces substantial decreases in upper airway collapsibility and maintains upper airway patency during anesthesia.

2013 ◽  
Vol 115 (3) ◽  
pp. 337-345 ◽  
Author(s):  
David R. Hillman ◽  
Jennifer H. Walsh ◽  
Kathleen J. Maddison ◽  
Peter R. Platt ◽  
Alan R. Schwartz ◽  
...  

Increasing lung volume increases upper airway patency and decreases airway resistance and collapsibility. The role of diaphragm contraction in producing these changes remains unclear. This study was undertaken to determine the effect of selective diaphragm contraction, induced by phrenic nerve stimulation, on upper airway collapsibility and the extent to which any observed change was attributable to lung volume-related changes in pressure gradients or to diaphragm descent-related mediastinal traction. Continuous bilateral transcutaneous cervical phrenic nerve stimulation (30 Hz) was applied to nine supine, anesthetized human subjects during transient decreases in airway pressure to levels sufficient to produce flow limitation when unstimulated. Stimulation was applied at two intensities (low and high) and its effects on lung volume and airflow quantified relative to unstimulated conditions. Lung volume increased by 386 ± 269 ml (means ± SD) and 761 ± 556 ml during low and high stimulation, respectively ( P < 0.05 for the difference between these values), which was associated with peak inspiratory flow increases of 69 ± 57 and 137 ± 108 ml/s, respectively ( P < 0.05 for the difference). Stimulation-induced change in lung volume correlated with change in peak flow ( r = 0.65, P < 0.01). Diaphragm descent-related outward displacement of the abdominal wall produced no change in airflow unless accompanied by lung volume change. We conclude that phrenic nerve stimulation-induced diaphragm contraction increases lung volume and reduces airway collapsibility in a dose-dependent manner. The effect appears primarily mediated by changes in lung volume rather than mediastinal traction from diaphragm descent. The study provides a rationale for use of continuous phrenic stimulation to treat obstructive sleep apnea.


2004 ◽  
Vol 83 (9) ◽  
pp. 718-722 ◽  
Author(s):  
T. Ayuse ◽  
T. Inazawa ◽  
S. Kurata ◽  
I. Okayasu ◽  
E. Sakamoto ◽  
...  

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.


2006 ◽  
Vol 111 (5) ◽  
pp. 349-355 ◽  
Author(s):  
Wei Wang ◽  
Eric Verin ◽  
Frédéric Sériès

MB (mouth breathing) promotes the occurrence of sleep-disordered breathing even in non-apnoeic subjects. Considering that MO (mouth opening) contributes to an increase in UA (upper airway) collapsibility independently of MB, the aim of the present study was to assess the influence of breathing route on UA dynamics in the presence of MO. Bilateral anterior magnetic phrenic nerve stimulation was performed 2 s after expiratory onset in 12 healthy male subjects during wakefulness (age, 50±5 years; body mass index, 27.8±2.4 kg/m2) during MB through a mouthpiece and during exclusive NB (nasal breathing) with the same mouthpiece in place. Twitch-induced V̇I (instantaneous flow), Pph and Pes (pharyngeal and oesophageal pressures respectively) were recorded and the corresponding resistances were measured. A polynomial regression model, V̇I=k1Pd+k2Pd2, was used to characterize flow–pressure relationship and to determine the Pd value at which UA collapses. There was no difference in UA dynamic properties between NB and MB when UA collapse occurred above the pharyngeal catheter. For twitches where UA collapse occurred lower in the UA, pharyngeal resistance decreased from NB to MB (2.0±0.3 and 1.5±0.2 cmH2O·l−1·s respectively; P=0.02; values are means±S.D.), whereas closing pressure increased (−25.7±10.1 and −18.0±3.0 cmH2O respectively; P=0.04). We conclude that (i) in the presence of MO the dynamic properties of the proximal UA free of phasic activity do not differ between NB and MB, and (ii) MB decreases the upstream resistance and increases collapsibility of the distal UA.


1989 ◽  
Vol 66 (4) ◽  
pp. 1800-1808 ◽  
Author(s):  
L. Wiegand ◽  
C. W. Zwillich ◽  
D. P. White

Upper airway resistance (UAR) increases in normal subjects during the transition from wakefulness to sleep. To examine the influence of sleep on upper airway collapsibility, inspiratory UAR (epiglottis to nares) and genioglossus electromyogram (EMG) were measured in six healthy men before and during inspiratory resistive loading. UAR increased significantly (P less than 0.05) from wakefulness to non-rapid-eye-movement (NREM) sleep [3.1 +/- 0.4 to 11.7 +/- 3.5 (SE) cmH2O.1–1.s]. Resistive load application during wakefulness produced small increments in UAR. However, during NREM sleep, UAR increased dramatically with loading in four subjects although two subjects demonstrated little change. This increment in UAR from wakefulness to sleep correlated closely with the rise in UAR during loading while asleep (e.g., load 12: r = 0.90, P less than 0.05), indicating consistent upper airway behavior during sleep. On the other hand, no measurement of upper airway behavior during wakefulness was predictive of events during sleep. Although the influence of sleep on the EMG was difficult to assess, peak inspiratory genioglossus EMG clearly increased (P less than 0.05) after load application during NREM sleep. Finally, minute ventilation fell significantly from wakefulness values during NREM sleep, with the largest decrement in sleeping minute ventilation occurring in those subjects having the greatest awake-to-sleep increment in UAR (r = -0.88, P less than 0.05). We conclude that there is marked variability among normal men in upper airway collapsibility during sleep.


2005 ◽  
Vol 84 (6) ◽  
pp. 554-558 ◽  
Author(s):  
T. Inazawa ◽  
T. Ayuse ◽  
S. Kurata ◽  
I. Okayasu ◽  
E. Sakamoto ◽  
...  

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.


SLEEP ◽  
2011 ◽  
Vol 34 (6) ◽  
pp. 717-724 ◽  
Author(s):  
Helena Larramona Carrera ◽  
Joseph M. McDonough ◽  
Paul R. Gallagher ◽  
Swaroop Pinto ◽  
John Samuel ◽  
...  

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