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 A frequent phenotype for paediatric sleep apnoea: short lingual frenulum

2016 ◽  
Vol 2 (3) ◽  
pp. 00043-2016 ◽  
Author(s):  
Christian Guilleminault ◽  
Shehlanoor Huseni ◽  
Lauren Lo
Keyword(s):  
Clinical Investigation ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Obstructive Sleep Apnoea Syndrome ◽  
Systematic Screening ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Oral Anatomy ◽  
Symptoms And Signs

A short lingual frenulum has been associated with difficulties in sucking, swallowing and speech. The oral dysfunction induced by a short lingual frenulum can lead to oral-facial dysmorphosis, which decreases the size of upper airway support. Such progressive change increases the risk of upper airway collapsibility during sleep.Clinical investigation of the oral cavity was conducted as a part of a clinical evaluation of children suspected of having sleep disordered breathing (SDB) based on complaints, symptoms and signs. Systematic polysomnographic evaluation followed the clinical examination. A retrospective analysis of 150 successively seen children suspected of having SDB was performed, in addition to a comparison of the findings between children with and without short lingual frenula.Among the children, two groups of obstructive sleep apnoea syndrome (OSAS) were found: 1) absence of adenotonsils enlargement and short frenula (n=63); and 2) normal frenula and enlarged adenotonsils (n=87). Children in the first group had significantly more abnormal oral anatomy findings, and a positive family of short frenulum and SDB was documented in at least one direct family member in 60 cases.A short lingual frenulum left untreated at birth is associated with OSAS at later age, and a systematic screening for the syndrome should be conducted when this anatomical abnormality is recognised.

scholarly journals Role of common hypnotics on the phenotypic causes of obstructive sleep apnoea: paradoxical effects of zolpidem

2017 ◽  
Vol 50 (6) ◽  
pp. 1701344 ◽  
Author(s):  
Jayne C. Carberry ◽  
Lauren P. Fisher ◽  
Ronald R. Grunstein ◽  
Simon C. Gandevia ◽  
David K. McKenzie ◽  
...  
Keyword(s):  
Obstructive Sleep Apnoea ◽  
Muscle Activity ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Double Blind ◽  
Genioglossus Muscle ◽  
Airway Narrowing ◽  
Arousal Threshold ◽  
Obstructive Sleep ◽  
Airway Collapsibility

Hypnotics are contraindicated in obstructive sleep apnoea (OSA) because of concerns of pharyngeal muscle relaxation and delayed arousal worsening hypoxaemia. However, human data are lacking. This study aimed to determine the effects of three common hypnotics on the respiratory arousal threshold, genioglossus muscle responsiveness and upper airway collapsibility during sleep.21 individuals with and without OSA (18–65 years) completed 84 detailed sleep studies after receiving temazepam (10 mg), zolpidem (10 mg), zopiclone (7.5 mg) and placebo on four occasions in a randomised, double-blind, placebo-controlled, crossover trial (ACTRN12612001004853).The arousal threshold increased with zolpidem and zopicloneversusplacebo (mean±sd−18.3±10 and −19.1±9versus−14.6±7 cmH2O; p=0.02 and p<0.001) but not with temazepam (−16.8±9 cmH2O; p=0.17). Genioglossus muscle activity during stable non-REM sleep and responsiveness during airway narrowing was not different with temazepam and zopicloneversusplacebo but, paradoxically, zolpidem increased median muscle responsiveness three-fold during airway narrowing (median −0.15 (interquartile range −1.01 to −0.04)versus−0.05 (−0.29 to −0.03)% maximum EMG per cmH2O epiglottic pressure; p=0.03). The upper airway critical closing pressure did not change with any of the hypnotics.These doses of common hypnotics have differential effects on the respiratory arousal threshold but do not reduce upper airway muscle activity or alter airway collapsibility during sleep. Rather, muscle activity increases during airway narrowing with zolpidem.

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

Morphine alters respiratory control but not other key obstructive sleep apnoea phenotypes: a randomised trial

2020 ◽  
Vol 55 (6) ◽  
pp. 1901344
Author(s):  
Rodrigo T. Martins ◽  
Jayne C. Carberry ◽  
David Wang ◽  
Luke Rowsell ◽  
Ronald R. Grunstein ◽  
...  
Keyword(s):  
Upper Airway ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Ventilatory Control ◽  
Pharyngeal Muscle ◽  
Arousal Threshold ◽  
Ventilatory Responses ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Accidental opioid-related deaths are increasing. These often occur during sleep. Opioids such as morphine may worsen obstructive sleep apnoea (OSA). Thus, people with OSA may be at greater risk of harm from morphine. Possible mechanisms include respiratory depression and reductions in drive to the pharyngeal muscles to increase upper airway collapsibility. However, the effects of morphine on the four key phenotypic causes of OSA (upper airway collapsibility (pharyngeal critical closure pressure; Pcrit), pharyngeal muscle responsiveness, respiratory arousal threshold and ventilatory control (loop gain) during sleep) are unknown.21 males with OSA (apnoea–hypopnoea index range 7–67 events·h−1) were studied on two nights (1-week washout) according to a double-blind, randomised, cross-over design (ACTRN12613000858796). Participants received 40 mg of MS-Contin on one visit and placebo on the other. Brief reductions in continuous positive airway pressure (CPAP) from the therapeutic level were delivered to induce airflow limitation during non-rapid eye movement (REM) sleep to quantify the four phenotypic traits. Carbon dioxide was delivered via nasal mask on therapeutic CPAP to quantify hypercapnic ventilatory responses during non-REM sleep.Compared to placebo, 40 mg of morphine did not change Pcrit (−0.1±2.4 versus −0.4±2.2 cmH2O, p=0.58), genioglossus muscle responsiveness (−2.2 (−0.87 to −5.4) versus −1.2 (−0.3 to −3.5) μV·cmH2O−1, p=0.22) or arousal threshold (−16.7±6.8 versus −15.4±6.0 cmH2O, p=0.41), but did reduce loop gain (−10.1±2.6 versus −4.4±2.1, p=0.04) and hypercapnic ventilatory responses (7.3±1.2 versus 6.1±1.5 L·min−1, p=0.006).Concordant with recent clinical findings, 40 mg of MS-Contin does not systematically impair airway collapsibility, pharyngeal muscle responsiveness or the arousal threshold in moderately severe OSA patients. However, consistent with blunted chemosensitivity, ventilatory control is altered.

scholarly journals O023 Impact of weight loss of OSA pathophysiology

2021 ◽  
Vol 2 (Supplement_1) ◽  
pp. A10-A11
Author(s):  
A Wong ◽  
S Landry ◽  
K Yang ◽  
S Joosten ◽  
L Thomson ◽  
...  
Keyword(s):  
Weight Loss ◽  
Upper Airway ◽  
Sleep Apnoea ◽  
Loop Gain ◽  
Arousal Threshold ◽  
Post Surgery ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
The Impact

Abstract Introduction Obesity is a major risk factor for developing obstructive sleep apnoea (OSA), however, the underlying mechanisms are not fully understood. We aimed to assess the impact of weight loss on all OSA endotypes (i.e. upper airway collapsibility, muscle compensation, respiratory arousal threshold, and loop gain). Methods We analysed data from 40 OSA patients (collated from 3 centres) who underwent bariatric surgery. Demographics and clinical polysomnograms (PSG) were performed at baseline and at between 6–18 months post-surgery. OSA endotypes were measured during sleep using non-invasive endotyping methods (derived from clinical PSG). Results Participants lost 28±14 kg and had a post-surgery reduction in the AHI of 19.6 (Interquartile range[IQR] -9.8 to -35.4) events/hr [from baseline 39.9 (24.3 to 65.6) events/hr to 17.0 (9.9 to 33.3) events/hr]. Following surgical weight loss, there was significant improvement in collapsibility (∆6.2 [IQR -1.4 to 13]%Veupnoea, p&lt;0.0001), as well as significant reduction in loop gain and arousal threshold (∆-0.06 [-0.17 to 0.009], p&lt;0.001 and ∆-13.7 [-24.8 to -1.8]%Veupnoea, p&lt;0.001 respectively). There was no significant change in muscle compensation. Conclusion Our findings suggest that weight loss improves upper airway collapsibility and reduces loop gain and the arousal threshold, providing novel insights about the mechanisms by which obesity causes OSA. Further analysis is underway to determine whether knowledge of the baseline OSA endotypes (in isolation and/or in combination) can predict which individuals will have a response to weight loss alone.

scholarly journals Upper Airway Collapsibility During REM Sleep in Children with the Obstructive Sleep Apnea Syndrome

SLEEP ◽  
2009 ◽  
Vol 32 (9) ◽  
pp. 1173-1181 ◽  
Author(s):  
Jingtao Huang ◽  
Laurie R. Karamessinis ◽  
Michelle E. Pepe ◽  
Stephen M. Glinka ◽  
John M. Samuel ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Obstructive Sleep Apnea Syndrome ◽  
Rem Sleep ◽  
Sleep Apnea Syndrome ◽  
Upper Airway ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Apnea Syndrome ◽  
Upper Airway Collapsibility

scholarly journals An assessment of a simple clinical technique to estimate pharyngeal collapsibility in people with obstructive sleep apnea

SLEEP ◽  
2020 ◽  
Vol 43 (10) ◽  
Author(s):  
Amal M Osman ◽  
Benjamin K Tong ◽  
Shane A Landry ◽  
Bradley A Edwards ◽  
Simon A Joosten ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Characteristic Curve ◽  
Upper Airway ◽  
Clinical Intervention ◽  
Apnea Hypopnea Index ◽  
Cpap Titration ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

Abstract Study Objectives Quantification of upper airway collapsibility in obstructive sleep apnea (OSA) could help inform targeted therapy decisions. However, current techniques are clinically impractical. The primary aim of this study was to assess if a simple, novel technique could be implemented as part of a continuous positive airway pressure (CPAP) titration study to assess pharyngeal collapsibility. Methods A total of 35 participants (15 female) with OSA (mean ± SD apnea–hypopnea index = 35 ± 19 events/h) were studied. Participants first completed a simple clinical intervention during a routine CPAP titration, where CPAP was transiently turned off from the therapeutic pressure for ≤5 breaths/efforts on ≥5 occasions during stable non-rapid eye movement (non-REM) sleep for quantitative assessment of airflow responses (%peak inspiratory flow [PIF] from preceding 5 breaths). Participants then underwent an overnight physiology study to determine the pharyngeal critical closing pressure (Pcrit) and repeat transient drops to zero CPAP to assess airflow response reproducibility. Results Mean PIF of breaths 3–5 during zero CPAP on the simple clinical intervention versus the physiology night were similar (34 ± 29% vs. 28 ± 30% on therapeutic CPAP, p = 0.2; range 0%–90% vs. 0%–95%). Pcrit was −1.0 ± 2.5 cmH2O (range −6 to 5 cmH2O). Mean PIF during zero CPAP on the simple clinical intervention and the physiology night correlated with Pcrit (r = −0.7 and −0.9, respectively, p &lt; 0.0001). Receiver operating characteristic curve analysis indicated significant diagnostic utility for the simple intervention to predict Pcrit &lt; −2 and &lt; 0 cmH2O (AUC = 0.81 and 0.92), respectively. Conclusions A simple CPAP intervention can successfully discriminate between patients with and without mild to moderately collapsible pharyngeal airways. This scalable approach may help select individuals most likely to respond to non-CPAP therapies.

scholarly journals Upper airway collapsibility measured using a simple wakefulness test closely relates to the pharyngeal critical closing pressure during sleep in obstructive sleep apnea

SLEEP ◽  
2019 ◽  
Vol 42 (7) ◽  
Author(s):  
Amal M Osman ◽  
Jayne C Carberry ◽  
Peter G R Burke ◽  
Barbara Toson ◽  
Ronald R Grunstein ◽  
...  
Keyword(s):  
Obstructive Sleep Apnea ◽  
Sleep Apnea ◽  
Airway Pressure ◽  
Pressure Sensors ◽  
Upper Airway ◽  
Apnea Hypopnea Index ◽  
Pharyngeal Airway ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility

AbstractStudy ObjectivesA collapsible or crowded pharyngeal airway is the main cause of obstructive sleep apnea (OSA). However, quantification of airway collapsibility during sleep (Pcrit) is not clinically feasible. The primary aim of this study was to compare upper airway collapsibility using a simple wakefulness test with Pcrit during sleep.MethodsParticipants with OSA were instrumented with a nasal mask, pneumotachograph and two pressure sensors, one at the choanae (PCHO), the other just above the epiglottis (PEPI). Approximately 60 brief (250 ms) pulses of negative airway pressure (~ –12 cmH2O at the mask) were delivered in early inspiration during wakefulness to measure the upper airway collapsibility index (UACI). Transient reductions in the continuous positive airway pressure (CPAP) holding pressure were then performed during sleep to determine Pcrit. In a subset of participants, the optimal number of replicate trials required to calculate the UACI was assessed.ResultsThe UACI (39 ± 24 mean ± SD; range = 0%–87%) and Pcrit (–0.11 ± 2.5; range: –4 to +5 cmH2O) were quantified in 34 middle-aged people (9 female) with varying OSA severity (apnea–hypopnea index range = 5–92 events/h). The UACI at a mask pressure of approximately –12 cmH2O positively correlated with Pcrit (r = 0.8; p < 0.001) and could be quantified reliably with as few as 10 replicate trials. The UACI performed well at discriminating individuals with subatmospheric Pcrit values [receiver operating characteristic curve analysis area under the curve = 0.9 (0.8–1), p < 0.001].ConclusionsThese findings indicate that a simple wakefulness test may be useful to estimate the extent of upper airway anatomical impairment during sleep in people with OSA to direct targeted non-CPAP therapies for OSA.

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