Mechanisms contributing to the response of upper-airway muscles to changes in airway pressure

2015 ◽  
Vol 118 (10) ◽  
pp. 1221-1228 ◽  
Author(s):  
Jayne C. Carberry ◽  
Hanna Hensen ◽  
Lauren P. Fisher ◽  
Julian P. Saboisky ◽  
Jane E. Butler ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Airway Pressure ◽  
Upper Airway ◽  
Nasal Breathing ◽  
Quiet Breathing ◽  
Surface Receptors ◽  
Reflex Responses ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Pressure Changes

This study assessed the effects of inhaled lignocaine to reduce upper airway surface mechanoreceptor activity on 1) basal genioglossus and tensor palatini EMG, 2) genioglossus reflex responses to large pulses (∼10 cmH2O) of negative airway pressure, and 3) upper airway collapsibility in 15 awake individuals. Genioglossus and tensor palatini muscle EMG and airway pressures were recorded during quiet nasal breathing and during brief pulses (250 ms) of negative upper-airway pressure. Lignocaine reduced peak inspiratory (5.6 ± 1.5 vs. 3.8 ± 1.1% maximum; mean ± SE, P < 0.01) and tonic (2.8 ± 0.8 vs. 2.1 ± 0.7% maximum; P < 0.05) genioglossus EMG during quiet breathing but had no effect on tensor palatini EMG (5.0 ± 0.8 vs. 5.0 ± 0.5% maximum; P = 0.97). Genioglossus reflex excitation to negative pressure pulses decreased after anesthesia (60.9 ± 20.7 vs. 23.6 ± 5.2 μV; P < 0.05), but not when expressed as a percentage of the immediate prestimulus baseline. Reflex excitation was closely related to the change in baseline EMG following lignocaine ( r2 = 0.98). A short-latency genioglossus reflex to rapid increases from negative to atmospheric pressure was also observed. The upper airway collapsibility index (%difference) between nadir choanal and epiglottic pressure increased after lignocaine (17.8 ± 3.7 vs. 28.8 ± 7.5%; P < 0.05). These findings indicate that surface receptors modulate genioglossus but not tensor palatini activity during quiet breathing. However, removal of input from surface mechanoreceptors has minimal effect on genioglossus reflex responses to large (∼10 cmH2O), sudden changes in airway pressure. Changes in pressure rather than negative pressure per se can elicit genioglossus reflex responses. These findings challenge previous views and have important implications for upper airway muscle control.

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.

scholarly journals A secondary reflex suppression phase is present in genioglossus but not tensor palatini in response to negative upper airway pressure

2010 ◽  
Vol 108 (6) ◽  
pp. 1619-1624 ◽  
Author(s):  
Danny J. Eckert ◽  
Julian P. Saboisky ◽  
Amy S. Jordan ◽  
David P. White ◽  
Atul Malhotra
Keyword(s):  
Negative Pressure ◽  
Airway Pressure ◽  
Respiratory Muscles ◽  
Upper Airway ◽  
Reflex Responses ◽  
Suppression Phase ◽  
Tonic Muscle ◽  
State Dependent ◽  
Pressure Peak ◽  
Inhibitory Components

On the basis of recent reports, the genioglossus (GG) negative-pressure reflex consists initially of excitation followed by a secondary state-dependent suppression phase. The mechanistic origin and functional role of GG suppression is unknown but has been hypothesized to arise from transient inhibition of respiratory active neurons as a protective reflex to prevent aspiration, as observed in other respiratory muscles (e.g., diaphragm) during airway occlusion. Unlike GG, tensor palatini (TP) is a tonic muscle with minimal respiratory phasic activation during relaxed breathing, although both muscles are important in preserving pharyngeal patency. This study aimed to compare GG vs. TP reflex responses to the same negative-pressure stimulus. We hypothesized that reflex suppression would be present in GG, but not TP. Intramuscular GG and TP EMGs were recorded in 12 awake, healthy subjects (6 female). Reflex responses were generated via 250-ms pulses of negative upper airway pressure (approximately −16 cmH2O mask pressure) delivered in early inspiration. GG and TP demonstrated reflex activation in response to negative pressure (peak latency 31 ± 4 vs. 31 ± 6 ms and peak amplitude 318 ± 55 vs. 314 ± 26% baseline, respectively). A secondary suppression phase was present in 8 of 12 subjects for GG (nadir latency 54 ± 7 ms, nadir amplitude 64 ± 6% baseline), but not in any subject for TP. These data provide further support for the presence of excitatory and inhibitory components of GG (phasic muscle) in response to brief upper airway negative-pressure pulses. Conversely, no reflex suppression below baseline was present in TP (tonic muscle) in response to the same stimuli. These differential responses support the hypothesis that GG reflex suppression may be mediated via inhibition of respiratory-related premotor input.

Influences of the breathing route on upper airway dynamics properties in normal awake subjects with constant mouth opening

2006 ◽  
Vol 111 (5) ◽  
pp. 349-355 ◽  
Author(s):  
Wei Wang ◽  
Eric Verin ◽  
Frédéric Sériès
Keyword(s):  
Polynomial Regression ◽  
Dynamic Properties ◽  
Mouth Opening ◽  
Upper Airway ◽  
Nasal Breathing ◽  
Airway Collapsibility ◽  
Flow Pressure ◽  
Upper Airway Collapsibility ◽  
Male Subjects ◽  
Closing Pressure

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.

Effects of continuous negative airway pressure-related lung deflation on upper airway collapsibility

1993 ◽  
Vol 75 (3) ◽  
pp. 1222-1225 ◽  
Author(s):  
F. Series ◽  
I. Marc
Keyword(s):  
Lung Volume ◽  
Airway Pressure ◽  
Linear Regression Analysis ◽  
Upper Airway ◽  
Flow Limitation ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Lung Deflation ◽  
The Relationship ◽  
Negative Airway Pressure

Continuous negative airway pressure (CNAP) causes a decrease in lung volume, which is known to increase upper airway resistance by itself. We studied how this lung volume change could modify upper airway collapsibility with five normal awake subjects. In a first trial, pressure in a nasal mask (Pm) was progressively decreased in 3- to 5-cmH2O steps (CNAP). In a second trial, changes in lung volumes resulting from CNAP were prevented by applying simultaneously an equivalent level of negative extrathoracic pressure into a poncho-type respirator [isovolumetric CNAP (CNAPisovol)]. For each trial, we examined the relationship between the maximal inspiratory airflow of each flow-limited inspiratory cycle and the corresponding Pm by least-squares linear regression analysis and determined the critical pressure. We also determined the Pm threshold corresponding to the first Pm value below which flow limitation occurred. Flow limitation was observed in each subject with CNAP but in only two subjects with CNAPisovol. In these two subjects, the Pm threshold values were -20 and -9 cmH2O with CNAP and -39 and -16 cmH2O with CNAPisovol, respectively. Critical pressures for the same two subjects were -161 and -96 cmH2O with CNAP and -202 and -197 cmH2O with CNAPisovol, respectively. We conclude that CNAP-induced decreases in lung volume increase upper airway collapsibility.

Influence of upper airway size on volume exhaled under negative pressure during evaluation of upper airway collapsibility

2011 ◽  
Vol 16 (2) ◽  
pp. 399-404 ◽  
Author(s):  
Luigi Taranto Montemurro ◽  
Michela Bettinzoli ◽  
Luciano Corda ◽  
Stefania Redolfi ◽  
Mauro Novali ◽  
...  
Keyword(s):  
Negative Pressure ◽  
Upper Airway ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility
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