Influence of upper airway sensory receptors on respiratory muscle activation in humans

1987 ◽  
Vol 63 (1) ◽  
pp. 368-374 ◽  
Author(s):  
S. Redline ◽  
K. P. Strohl

We reasoned that neural information from upper airway (UA) sensory receptors could influence the relationship between UA and diaphragmatic neuromuscular responses to hypercapnia. In this study, the electromyographic (EMG) activities of the alae nasi (AN), genioglossus (GG), and chest wall (CW) or diaphragm (Di) to ventilatory loading were assessed in six laryngectomized, tracheostomized human subjects and in six subjects breathing with an intact UA before and after topical UA anesthesia. The EMG activities of the UA and thoracic muscles increased at similar rates with increasing hypercapnia in normal subjects, in subjects whose upper airways were anesthetized, and in laryngectomized subjects breathing with a cervical tracheostomy. Furthermore, in the laryngectomized subjects, respiratory muscle EMG activation increased with resistive inspiratory loading (15 cmH2O X l–1 X s) applied at the level of a cervical tracheostomy. At an average expired CO2 fraction of 7.0%, resistive loading resulted in a 93 +/- 26.3% (SE) increase in peak AN EMG activity, a 39 +/- 2.0% increase in peak GG EMG activity, and a 43.2 +/- 16.5% increase in peak CW (Di) EMG activity compared with control values. We conclude that the ventilatory responses of the UA and thoracic muscles to ventilatory loading are not substantially influenced by laryngectomy or UA anesthesia.

1996 ◽  
Vol 81 (1) ◽  
pp. 470-479 ◽  
Author(s):  
P. C. Deegan ◽  
P. Nolan ◽  
M. Carey ◽  
W. T. McNicholas

To determine upper airway (UA) and ventilatory responses to nasal continuous positive airway pressure (CPAP) and expiratory positive airway pressure (EPAP), we quantitated changes in alae nasi (AN) and genioglossus (GG) electromyographic (EMG) activity, ventilatory timing, and end-expiratory lung volume (EELV) at various levels of CPAP and EPAP in six normal subjects during wakefulness and in seven during sleep. The same measurements were also made before and after UA anesthesia in six normal subjects during wakefulness. During both wakefulness and sleep, CPAP application significantly increased EELV and decreased AN and GG EMG activities. In contrast, EPAP significantly increased EMG activities of both muscles while also increasing EELV during wakefulness. The EMG responses were less marked during sleep. Anesthesia of the UA abolished the EMG responses to CPAP but not to EPAP. These results suggest that, in normal subjects, CPAP application causes a reflex reduction in UA dilator muscle activity mediated by UA sensory receptors. In contrast, EPAP increases UA dilator muscle activity, with the response mediated by conscious influences or reflexes arising outside of the UA.


2009 ◽  
Vol 106 (3) ◽  
pp. 893-903 ◽  
Author(s):  
Z. Ghanim ◽  
J. C. Lamy ◽  
A. Lackmy ◽  
V. Achache ◽  
N. Roche ◽  
...  

The vestibular responses evoked by transmastoid galvanic stimulation (GS) in the rectified soleus electromyogram (EMG) in freely standing human subjects disappear when seated. However, a GS-induced facilitation of the soleus monosynaptic (H and tendon jerk) reflex has been described in few experiments in subjects lying prone or seated. This study addresses the issue of whether this reflex facilitation while seated is of vestibulospinal origin. GS-induced responses in the soleus (modulation of the rectified ongoing EMG and of the monosynaptic reflexes) were compared in the same normal subjects while freely standing and sitting with back and head support. The polarity-dependent biphasic responses in the free-standing position were replaced by a non-polarity-dependent twofold facilitation while seated. The effects of GS were hardly detectable in the rectified ongoing voluntary EMG activity, weak for the H reflex, but large and constant for the tendon jerk. They were subject to habituation. Anesthesia of the skin beneath the GS electrodes markedly reduced the reflex facilitation, while a similar, although weaker, facilitation of the tendon jerk was observed when GS was replaced with purely cutaneous stimulation, a tap to the tendon of the sternomastoid muscle, or an auditory click. The stimulation polarity independence of the GS-induced reflex facilitation argues strongly against a vestibular response. However, the vestibular afferent volley, insufficient to produce a vestibular reflex response while seated, could summate with the GS-induced tactile or proprioceptive volley to produce a startle-like response responsible for the reflex facilitation.


1990 ◽  
Vol 68 (3) ◽  
pp. 1041-1047 ◽  
Author(s):  
W. A. Carlo ◽  
J. M. DiFiore

Upper airway muscles and the diaphragm may have different quantitative responses to chemoreceptor stimulation. To compare the respiratory muscle responses to changes in CO2, 10 ventilator-dependent preterm infants (gestational age 28 +/- 1 wk, postnatal age 40 +/- 6 days, weight 1.4 +/- 0.1 kg) were passively hyperventilated to apnea and subsequently hypoventilated. Electromyograms from the genioglossus, alae nasi, posterior cricoarytenoid, and diaphragm were recorded from surface electrodes. Apneic CO2 thresholds of all upper airway muscles (genioglossus 46.8 +/- 4.3 Torr, alae nasi 42.4 +/- 3.6 Torr, posterior cricoarytenoid 41.6 +/- 3.2 Torr) were higher than those of the diaphragm (38.8 +/- 2.6 Torr, all P less than 0.05). Above their CO2 threshold levels, responses of all upper airway muscles appeared proportional to those of the diaphragm. We conclude that nonproportional responses of the respiratory muscles to hypercapnia may be the result of differences in their CO2 threshold. These differences in CO2 threshold may cause imbalance in respiratory muscle activation with changes in chemical drive, leading to upper airway instability and obstructive apnea.


2003 ◽  
Vol 95 (1) ◽  
pp. 97-103 ◽  
Author(s):  
Pierre-Hugues Fortier ◽  
Philippe Reix ◽  
Julie Arsenault ◽  
Dominique Dorion ◽  
Jean-Paul Praud

We tested the hypotheses that active upper airway closure during induced central apneas in nonsedated lambs 1) is complete and occurs at the laryngeal level and 2) is not due to stimulation of the superior laryngeal nerves (SLN). Five newborn lambs were surgically instrumented to record thyroarytenoid (TA) muscle (glottal constrictor) electromyographic (EMG) activity with supra- and subglottal pressures. Hypocapnic and nonhypocapnic central apneas were induced before and after SLN sectioning in the five lambs. A total of 174 apneas were induced, 116 before and 58 after sectioning of the internal branch of the SLN (iSLN). Continuous TA EMG activity was observed in 88% of apneas before iSLN section and in 87% of apneas after iSLN section. A transglottal pressure different from zero was observed in all apneas with TA EMG activity, with a mean subglottal pressure of 4.3 ± 0.8 cmH2O before and 4.7 ± 0.7 cmH2O after iSLN section. Supraglottal pressure was consistently atmospheric. Sectioning of both iSLNs had no effects on the results. We conclude that upper airway closure during induced central apneas in lambs is active, complete, and occurs at the glottal level only. Consequently, a positive subglottal pressure is maintained throughout the apnea. Finally, this complete active glottal closure is independent from laryngeal afferent innervation.


2011 ◽  
Vol 19 (6) ◽  
pp. 1369-1376 ◽  
Author(s):  
Andréa Lopes Barbosa ◽  
Maria Vera Lúcia Moreira Leitão Cardoso ◽  
Thays Bezerra Brasil ◽  
Carmen Gracinda Silvan Scochi

This study investigated which physiological parameters change when endotracheal and upper airway suctioning is performed immediately before, immediately after and five minutes after this procedure is performed in newborns hospitalized in a Neonatal Intensive Care Unit (NICU). This is a quantitative and longitudinal study, before and after type, performed in the NICU of a public institution in the city of Fortaleza, CE, Brazil. The sample was composed of 104 newborns using oxigenotherapy and who needed endotracheal and upper airway suctioning. The results showed significant alterations in respiratory and heart rates (p<0.05) in neonates using Oxyhood and nasal CPAP while the pulse significantly changed (p<0.05) in newborns placed in oxyhood, using nasal CPAP and Mechanical Ventilation; oxygen saturation was the only parameter that did not alter significantly. We propose that nurses develop non-pharmacological interventions to reduce potential alterations caused in newborns’ physiological parameters due to this procedure.


1993 ◽  
Vol 74 (6) ◽  
pp. 2694-2703 ◽  
Author(s):  
M. J. Wasicko ◽  
J. S. Erlichman ◽  
J. C. Leiter

We sought to determine if the upper airway response to an added inspiratory resistive load (IRL) during wakefulness could be used to predict the site of upper airway collapse in patients with obstructive sleep apnea (OSA). In 10 awake patients with OSA, we investigated the relationship between resistance in three segments of the upper airway (nasal, nasopharyngeal, and oropharyngeal) and three muscles known to influence these segments (alae nasi, tensor veli palatini, and genioglossus) while the patient breathed with or without a small IRL (2 cmH2O.l–1.s). During IRL, patients with OSA exhibited increased nasopharyngeal resistance and no significant increase in either the genioglossus or tensor veli palatini activities. Neither nasal resistance nor alae nasi EMG activity was affected by IRL. We contrasted this to the response of five normal subjects, in whom we found no change in the resistance of either segment of the airway and no change in the genioglossus EMG but a significant activation of the tensor palatini. In six patients with OSA, we used the waking data to predict the site of upper airway collapse during sleep and we had limited success. The most successful index (correct in 4 of 6 patients) incorporated the greatest relative change in segmental resistance during IRL at the lowest electromyographic activity. We conclude, in patients with OSA, IRL narrows the more collapsible segment of the upper airway, in part due to inadequate activation of upper airway muscles. However, it is difficult to predict the site of upper airway collapse based on the waking measurements where upper airway muscle activity masks the passive airway characteristics.


2003 ◽  
Vol 95 (1) ◽  
pp. 357-363 ◽  
Author(s):  
Jason P. Kirkness ◽  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
John R. Wheatley ◽  
...  

Upper airway (UA) patency may be influenced by surface tension (γ) operating within the (UAL). We examined the role of γ of UAL in the maintenance of UA patency in eight isoflurane-anesthetized supine human subjects breathing via a nasal mask connected to a pneumotachograph attached to a pressure delivery system. We evaluated 1) mask pressure at which the UA closed (Pcrit), 2) UA resistance upstream from the site of UA collapse (RUS), and 3) mask pressure at which the UA reopened (Po). A multiple pressure-transducer catheter was used to identify the site of airway closure (velopharyngeal in all subjects). UAL samples (0.2 μl) were collected, and the γ of UAL was determined by using the “pull-off force” technique. Studies were performed before and after the intrapharyngeal instillation of 5 ml of exogenous surfactant (Exosurf, Glaxo Smith Kline). The γ of UAL decreased from 61.9 ± 4.1 (control) to 50.3 ± 5.0 mN/m (surfactant; P < 0.02). Changes in Po, RUS, and Po - Pcrit (change = control - surfactant) were positively correlated with changes in γ ( r2 > 0.6; P < 0.02) but not with changes in Pcrit ( r2 = 0.4; P > 0.9). In addition, mean peak inspiratory airflow (no flow limitation) significantly increased ( P < 0.04) from 0.31 ± 0.06 (control) to 0.36 ± 0.06 l/s (surfactant). These findings suggest that γ of UAL exerts a force on the UA wall that hinders airway opening. Instillation of exogenous surfactant into the UA lowers the γ of UAL, thus increasing UA patency and augmenting reopening of the collapsed airway.


1989 ◽  
Vol 256 (1) ◽  
pp. R91-R97
Author(s):  
E. L. Coates ◽  
G. O. Ballam

The ventilatory response of the garter snake, Thamnophis sirtalis, to 2% CO2 delivered to the upper airways (UA) was measured before and after the olfactory or vomeronasal nerves were transected. The UA (nasal cavities and mouth) were isolated from the gas source inspired into the lungs by inserting an endotracheal T tube into the glottis. CO2 was administered to the UA via a head chamber. The primary ventilatory response to UA CO2 was a significant decrease in ventilatory frequency (f) and minute ventilation. The decrease in f was caused by a significant increase in the pause duration. Tidal volume, expiratory duration, and inspiratory duration were not altered with UA CO2. The f response to UA CO2 was abolished with olfactory nerve transection, whereas vomeronasal nerve transection significantly increased the magnitude of the f depression. These results indicate that CO2-sensitive receptors are located in the nasal epithelium and that the olfactory nerves must be intact for the UA CO2 f response to be observed. In addition, the vomeronasal system appears to modulate the ventilatory response to UA CO2.


1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules

The total upper airway resistances are modified during active changes in lung volume. We studied nine normal subjects to assess the influence of passive thoracopulmonary inflation and deflation on nasal and pharyngeal resistances. With the subjects lying in an iron lung, lung volumes were changed by application of an extrathoracic pressure (Pet) from 0 to 20 (+Pet) or -20 cmH2O (-Pet) in 5-cmH2O steps. Upper airway pressures were measured with two low-bias flow catheters, one at the tip of the epiglottis and the other in the posterior nasopharynx. Breath-by-breath resistance measurements were made at an inspiratory flow rate of 300 ml/s at each Pet step. Total upper airway, nasal, and pharyngeal resistances increased with +Pet [i.e., nasal resistance = 139.6 +/- 14.4% (SE) of base-line and pharyngeal resistances = 189.7 +/- 21.1% at 10 cmH2O of +Pet]. During -Pet there were no significant changes in nasal resistance, whereas pharyngeal resistance decreased significantly (pharyngeal resistance = 73.4 +/- 7.4% at -10 cmH2O). We conclude that upper airway resistance, particularly the pharyngeal resistance, is influenced by passive changes in lung volumes, especially pulmonary deflation.


1961 ◽  
Vol 16 (2) ◽  
pp. 326-330 ◽  
Author(s):  
Robert E. Hyatt ◽  
Roger E. Wilcox

Simultaneous extrathoracic and intrathoracic flow resistance was measured in 19 unanesthetized subjects during mouth breathing. Lateral intratracheal pressure was recorded from a needle introduced 2 cm below the larynx. The intratracheal-oral pressure gradient was recorded during various respiratory maneuvers. The pressure drop from esophagus to trachea was also recorded. The extrathoracic pressure-flow relationships were alinear. Large inter- and intrasubject variability in upper airway resistance was encountered. Some factors contributing to this variability were defined. The upper airway accounted for approximately 45% of the total airway resistance in nine normal and 20% in 10 emphysematous human subjects. Upper airway resistance decreased with increasing lung inflation in four normal subjects. The magnitude and potential variability of the upper airway resistance must be considered in evaluating maneuvers designed to alter intrathoracic flow resistance, especially in normal human beings. It appears that during mouth breathing the major component of the upper airway resistance is located in the larynx. Submitted on September 14, 1960


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