scholarly journals Upper Airway Collapsibility (Pcrit) and Pharyngeal Dilator Muscle Activity are Sleep Stage Dependent

SLEEP ◽  
2016 ◽  
Vol 39 (3) ◽  
pp. 511-521 ◽  
Author(s):  
Jayne C. Carberry ◽  
Amy S. Jordan ◽  
David P. White ◽  
Andrew Wellman ◽  
Danny J. Eckert
Keyword(s):  
Muscle Activity ◽  
Sleep Stage ◽  
Upper Airway ◽  
Dilator Muscle ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

scholarly journals Desipramine improves upper airway collapsibility and reduces OSA severity in patients with minimal muscle compensation

2016 ◽  
Vol 48 (5) ◽  
pp. 1340-1350 ◽  
Author(s):  
Luigi Taranto-Montemurro ◽  
Scott A. Sands ◽  
Bradley A. Edwards ◽  
Ali Azarbarzin ◽  
Melania Marques ◽  
...  
Keyword(s):  
Crossover Trial ◽  
Positive Airway Pressure ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Double Blind ◽  
Healthy Humans ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

We recently demonstrated that desipramine reduces the sleep-related loss of upper airway dilator muscle activity and reduces pharyngeal collapsibility in healthy humans without obstructive sleep apnoea (OSA). The aim of the present physiological study was to determine the effects of desipramine on upper airway collapsibility and apnoea–hypopnea index (AHI) in OSA patients.A placebo-controlled, double-blind, randomised crossover trial in 14 OSA patients was performed. Participants received treatment or placebo in randomised order before sleep. Pharyngeal collapsibility (critical collapsing pressure of the upper airway (Pcrit)) and ventilation under both passive (V′0,passive) and active (V′0,active) upper airway muscle conditions were evaluated with continuous positive airway pressure (CPAP) manipulation. AHI was quantified off CPAP.Desipramine reduced activePcrit(median (interquartile range) −5.2 (4.3) cmH2O on desipramineversus−1.9 (2.7) cmH2O on placebo; p=0.049) but not passivePcrit(−2.2 (3.4)versus−0.7 (2.1) cmH2O; p=0.135). A greater reduction in AHI occurred in those with minimal muscle compensation (defined asV′0,active−V′0,passive) on placebo (r=0.71, p=0.009). The reduction in AHI was driven by the improvement in muscle compensation (r=0.72, p=0.009).In OSA patients, noradrenergic stimulation with desipramine improves pharyngeal collapsibility and may be an effective treatment in patients with minimal upper airway muscle compensation.

scholarly journals Variability of human upper airway collapsibility during sleep and the influence of body posture and sleep stage

2011 ◽  
Vol 20 (4) ◽  
pp. 533-537 ◽  
Author(s):  
JEREMY S. L. ONG ◽  
GABBY TOUYZ ◽  
SUE TANNER ◽  
DAVID R. HILLMAN ◽  
PETER R. EASTWOOD ◽  
...  
Keyword(s):  
Sleep Stage ◽  
Upper Airway ◽  
Body Posture ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Reduced genioglossal activity with upper airway anesthesia in awake patients with OSA

2000 ◽  
Vol 88 (4) ◽  
pp. 1346-1354 ◽  
Author(s):  
Robert B. Fogel ◽  
Atul Malhotra ◽  
Steven A. Shea ◽  
Jill K. Edwards ◽  
David P. White
Keyword(s):  
Muscle Activity ◽  
Upper Airway ◽  
Significant Rise ◽  
Tidal Breathing ◽  
Airflow Resistance ◽  
Dilator Muscle ◽  
Obstructive Sleep ◽  
Airway Mechanics ◽  
Airway Collapsibility ◽  
Negative Airway Pressure

We examined whether topical upper airway anesthesia leads to a reduction in genioglossal (GG) electromyogram (EMG) in patients with obstructive sleep apnea (OSA). Airway mechanics were also evaluated. In 13 patients with OSA, we monitored GG EMG during tidal breathing and during the application of pulses of negative airway pressure (−10 to −12 cmH2O). Airflow resistance and airway collapsibility were determined. All measurements were performed with and without topical anesthesia (lidocaine). Anesthesia led to a significant fall in the peak GG EMG response to negative pressure from 36.1 ± 4.7 to 24.8 ± 5.3% (SE) of maximum ( P < 0.01). This was associated with a fall in phasic and tonic EMG during tidal breathing (phasic from 24.4 ± 4.1 to 16.4 ± 3.4% of maximum and tonic from 10.9 ± 1.6 to 8.0 ± 1.3% of maximum, P < 0.01). A significant rise in pharyngeal airflow resistance was also observed. Our results demonstrate that topical receptor mechanisms in the nasopharynx importantly influence dilator muscle activity and are likely important in driving the augmented dilator muscle activity seen in the apnea patient.

Are respiratory events and/or arousals during each sleep stage different by upper airway collapsibility?

2015 ◽  
Author(s):  
Hideaki Nakayama ◽  
Mika Kobayashi ◽  
Mariko Yanagihara ◽  
Eiki Ito ◽  
Satoru Tsuiki ◽  
...  
Keyword(s):  
Sleep Stage ◽  
Upper Airway ◽  
Respiratory Events ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

scholarly journals Upper airway collapsibility, dilator muscle activation and resistance in sleep apnoea

2007 ◽  
Vol 30 (2) ◽  
pp. 345-353 ◽  
Author(s):  
R. Pierce ◽  
D. White ◽  
A. Malhotra ◽  
J. K. Edwards ◽  
D. Kleverlaan ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Dilator Muscle ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

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 ◽  
...  
Keyword(s):  
Upper Airway ◽  
Normal Subjects ◽  
Target Concentration ◽  
Airway Patency ◽  
Head Elevation ◽  
Jaw Opening ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Head Flexion ◽  
Male Subjects

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 &lt; 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 &lt; 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.

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