Decrease in lung volume-related feedback enhances laryngeal reflexes to negative pressure

1992 ◽  
Vol 73 (3) ◽  
pp. 832-836 ◽  
Author(s):  
S. Zhang ◽  
O. P. Mathew
Keyword(s):  
Lung Volume ◽  
Negative Pressure ◽  
Upper Airway ◽  
Pressure Change ◽  
Inspiratory Flow ◽  
Lower Airway ◽  
Excitatory Effect ◽  
Peak Inspiratory Flow ◽  
Inspiratory Muscles ◽  
Pressure Pulses

Negative pressure applied to the upper airway has an excitatory effect on the activity of upper airway muscles and an inhibitory effect on thoracic inspiratory muscles. The role of lung volume feedback in this response was investigated in 10 anesthetized spontaneously breathing adult rabbits. To alter lung volume feedback, the lower airway was exposed to SO2 (250 ppm for 15 min), thereby blocking slowly adapting receptors (SARs). Negative pressure pulses (5, 10, and 20 cmH2O, 300-ms duration) were applied to the functionally isolated upper airway before and after SAR blockade. Tracheal airflow and electromyogram (EMG) of the genioglossus and alae nasi were recorded. Peak EMG, peak inspiratory flow, tidal volume, and respiratory timing of control breaths (3 breaths immediately preceding test) and test breaths were determined. Analysis of variance was used to determine the significance of the effects. Negative pressure pulses increased peak EMG of genioglossus and alae nasi and inspiratory duration and decreased peak inspiratory flow. These effects were larger after SAR blockade. We conclude that a decrease in volume feedback from the lung augments the response to upper airway pressure change.

Time of application of negative pressure pulses and upper airway muscle activity

1989 ◽  
Vol 67 (1) ◽  
pp. 366-370 ◽  
Author(s):  
D. L. Woodall ◽  
J. A. Hokanson ◽  
O. P. Mathew
Keyword(s):  
Negative Pressure ◽  
Upper Airway ◽  
Inhibitory Effect ◽  
Important Variable ◽  
Breathing Cycle ◽  
Time Of Application ◽  
Inspiratory Muscles ◽  
Pressure Pulses ◽  
Posterior Cricoarytenoid ◽  
Upper Airway Muscles

Effect of upper airway pressure changes on thoracic inspiratory muscles has been shown to depend on the time of application during the breathing cycle. The present study was designed to investigate the importance of the time of application of upper airway negative pressure pulses on upper airway muscles. The upper airway was functionally isolated into a closed system in 24 anesthetized spontaneously breathing rabbits. Negative pressure pulses were applied in early (within the first 200 ms) and late (greater than or equal to 200 ms) inspiration, while electromyograms (EMG) of the diaphragm (Dia), genioglossus (GG), alae nasi (AN), and/or posterior cricoarytenoid (PCA) muscles were simultaneously monitored. When negative pressure pulse was applied in early inspiration, the increase in GG activity was greater [0.49 +/- 0.37 to 4.24 +/- 3.71 arbitrary units (AU)] than when negative pressure was applied in late inspiration (0.44 +/- 0.29 to 2.64 +/- 3.05 AU). Similarly, increased activation of AN (2.63 +/- 1.01 to 4.26 +/- 1.69 AU) and PCA (3.46 +/- 1.16 to 6.18 +/- 2.93 AU) was also observed with early inspiratory application of negative pressure pulses; minimal effects were seen in these muscles with late application. An inhibitory effect on respiratory timing consisting of a prolongation in inspiration (TI) and a decrease in peak Dia EMG/TI was observed as previously reported. These results indicate that the time of application of negative pressure during the breathing cycle is an important variable in determining the magnitude of the response of upper airway muscles.(ABSTRACT TRUNCATED AT 250 WORDS)

Interaction between upper airway negative pressure pulses and CO2 on breathing pattern

1988 ◽  
Vol 65 (1) ◽  
pp. 205-209 ◽  
Author(s):  
D. L. Woodall ◽  
O. P. Mathew
Keyword(s):  
Closed System ◽  
Negative Pressure ◽  
Breathing Pattern ◽  
Upper Airway ◽  
System A ◽  
Pressure Pulses ◽  
Inspiratory Activity ◽  
Resultant Increase ◽  
Breathing Room ◽  
Spontaneously Breathing

The interaction between CO2 and negative pressure pulses on breathing pattern was investigated in 10 anesthetized, spontaneously breathing rabbits. The upper airway was functionally isolated into a closed system. A servo-respirator triggered by the inspiratory activity of the diaphragm was used to apply pressure pulses of -15 cmH2O to the isolated upper airway in early inspiration while the animal was breathing room air, 100% O2, 6% CO2 in O2, or 9% CO2 in O2. The negative pressure pulses produced a reversible inhibition of inspiration in most trials with resultant increase in inspiratory duration (TI); no change was observed in peak diaphragmatic electromyogram (Dia EMG) or expiratory duration, whereas a decrease was seen in mean inspiratory drive (peak Dia EMG/TI). This prolongation of inspiratory duration and decrease in mean inspiratory drive with negative pressure pulses persisted at higher levels of CO2; the slopes of the test breaths were not significantly different from that of control breaths. These results suggest that upper airway negative pressure pulses are equally effective in altering the breathing pattern at all levels of CO2.

Collapsibility of the Upper Airway during Anesthesia with Isoflurane

2002 ◽  
Vol 97 (4) ◽  
pp. 786-793 ◽  
Author(s):  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
David R. Hillman
Keyword(s):  
Lung Volume ◽  
Critical Pressure ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Flow Limitation ◽  
Anesthetic Depth ◽  
Volume Collapse ◽  
End Tidal ◽  
Spontaneously Breathing

Background The unprotected upper airway tends to obstruct during general anesthesia, yet its mechanical properties have not been studied in detail during this condition. Methods To study its collapsibility, pressure-flow relationships of the upper airway were obtained at three levels of anesthesia (end-tidal isoflurane = 1.2%, 0.8%, and 0.4%) in 16 subjects while supine and spontaneously breathing on nasal continuous positive airway pressure. At each level of anesthesia, mask pressure was transiently reduced from a pressure sufficient to abolish inspiratory flow limitation (11.8 +/- 2.7 cm H(2)O) to pressures resulting in variable degrees of flow limitation. The relation between mask pressure and maximal inspiratory flow was determined, and the critical pressure at which the airway occluded was recorded. The site of collapse was determined from simultaneous measurements of nasopharyngeal, oropharyngeal, and hypopharyngeal and esophageal pressures. Results The airway remained hypotonic (minimal or absent intramuscular genioglossus electromyogram activity) throughout each study. During flow-limited breaths, inspiratory flow decreased linearly with decreasing mask pressure (r(2) = 0.86 +/- 0.17), consistent with Starling resistor behavior. At end-tidal isoflurane of 1.2%, critical pressure was 1.1 +/- 3.5 cm H O; at 0.4% it decreased to -0.2 +/- 3.6 cm H(2)O ( < 0.05), indicating decreased airway collapsibility. This decrease was associated with a decrease in end-expiratory esophageal pressure of 0.6 +/- 0.9 cm H(2)O ( < 0.05), suggesting an increased lung volume. Collapse occurred in the retropalatal region in 14 subjects and in the retrolingual region in 2 subjects, and did not change with anesthetic depth. Conclusions Isoflurane anesthesia is associated with decreased muscle activity and increased collapsibility of the upper airway. In this state it adopts the behavior of a Starling resistor. The decreased collapsibility observed with decreasing anesthetic depth was not a consequence of neuromuscular activity, which was unchanged. Rather, it may be related to increased lung volume and its effect on airway wall longitudinal tension. The predominant site of collapse is the soft palate.

Upper airway negative-pressure effects on respiratory activity of upper airway muscles

1984 ◽  
Vol 56 (2) ◽  
pp. 500-505 ◽  
Author(s):  
O. P. Mathew
Keyword(s):  
Negative Pressure ◽  
Respiratory Activity ◽  
Superior Laryngeal Nerve ◽  
Upper Airway ◽  
Pressure Change ◽  
Pressure Effects ◽  
Rapid Decline ◽  
Airway Patency ◽  
Inspiratory Activity ◽  
Upper Airway Muscles

Influence of upper airway negative-pressure change on the respiratory activity of various upper airway muscles was investigated in 13 anesthetized rabbits. Phasic inspiratory activity increased or appeared during virtually all negative-pressure trials in nasolabial, cricothyroid, and posterior cricoarytenoid muscles. No phasic inspiratory activity was seen in the sternothyroid (ST) and sternohyoid (SH) muscles before negative-pressure applications but appeared during 80% of trials in ST and 62% of trials in SH. During maintained negative pressure, a gradual decline in activity was often observed in the nasolabial and laryngeal muscles, whereas a rapid decline in activity was seen in the cervical strap muscles. Reflex effects of negative pressure was markedly reduced or abolished by sectioning the internal branch of the superior laryngeal nerve bilaterally. Reflex augmentation of upper airway muscle activity reported here may have functional significance in the maintenance of upper airway patency. It could prevent upper airway collapse when negative pressure swings in the upper airway increase or facilitate recovery when large negative pressure swings are produced by obstructed inspiratory efforts.

Upper airway obstruction assessment: Peak inspiratory flow and clinical COPD Questionnaire

2018 ◽  
Vol 43 (5) ◽  
pp. 1303-1311
Author(s):  
J. Sanchez-Guerrero ◽  
J. Guerlain ◽  
S. Samaha ◽  
A. Burgess ◽  
J. Lacau St Guily ◽  
...  
Keyword(s):  
Airway Obstruction ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Upper Airway Obstruction ◽  
Peak Inspiratory Flow

Cricothyroid muscle responses to increased chemical drive in awake normal humans

1991 ◽  
Vol 70 (5) ◽  
pp. 2233-2241 ◽  
Author(s):  
J. R. Wheatley ◽  
A. Brancatisano ◽  
L. A. Engel
Keyword(s):  
Lead Time ◽  
Upper Airway ◽  
Inspiratory Flow ◽  
Inspiratory Time ◽  
Cricothyroid Muscle ◽  
Inspiratory Muscles ◽  
Inspiratory Activity ◽  
Normal Humans ◽  
Muscle Responses ◽  
Muscle Ct

To examine the response of the cricothyroid muscle (CT) to increased chemical drive, we measured its electromyogram simultaneously with that of the alae nasi (AN) in seven normal awake subjects. During both progressive hyperoxic hypercapnia and hypoxia, peak integrated inspiratory activity (moving time average, MTA) of the CT and AN increased as a power function of mean inspiratory flow (ratio of tidal volume to inspiratory time, VT/TI), given by MTA = a(VT/TI)b + c (where a, b, and c are constants). The exponent b varied from 0.009 to 3.4 among subjects but was correlated between CT and AN both during hypercapnia (r = 0.86) and hypoxia (r = 0.81). The onset of inspiratory activity of the CT and AN preceded that of inspiratory flow. Expressed as a percentage of expiratory time, the CT lead time rose from 7% at rest to 20% during hyperpnea. The corresponding values for the AN were from 22 to 52% (both P less than 0.03). Thus the pattern of response of the CT and AN is similar and related to that of the inspiratory muscles in a curvilinear manner. The findings suggest that during chemical stimulation the electrical activity of the CT is analogous to that of the AN, an upper airway dilator.

Oxygen cost of breathing during fatiguing inspiratory resistive loads

1989 ◽  
Vol 66 (5) ◽  
pp. 2045-2055 ◽  
Author(s):  
F. D. McCool ◽  
G. E. Tzelepis ◽  
D. E. Leith ◽  
F. G. Hoppin
Keyword(s):  
Lung Volume ◽  
Normal Subjects ◽  
Esophageal Pressure ◽  
Inspiratory Flow ◽  
Energy Utilization ◽  
Whole Body ◽  
Inspiratory Flow Rate ◽  
Inspiratory Muscles ◽  
Inspiratory Resistance ◽  
Resistive Loads

When a subject breathes against an inspiratory resistance, the inspiratory pressure, the inspiratory flow, and the lung volume at which the breathing task takes place all interact to determine the length of time the task can be sustained (Tlim). We hypothesized that the mechanism actually limiting tasks in which these parameters were varied involved the rate of energy utilization by the inspiratory muscles. To test this hypothesis, we studied four experienced normal subjects during fatiguing breathing tasks performed over a range of pressures and flows and at two different lung volumes. We assessed energy utilization by measuring the increment in the rate of whole body O2 consumption due to the breathing task (VO2 resp). Power and mean esophageal pressure correlated with Tlim but depended also on lung volume and inspiratory flow rate. In contrast, VO2 resp closely correlated with Tlim, and this relationship was not systematically altered by inspiratory flow or lung volume. The shape of the VO2 resp vs. Tlim curve was approximately hyperbolic, with high rates of VO2 resp associated with short endurance times and lower rates of VO2 resp approaching an asymptotic value at high Tlim. These findings are consistent with a mechanism whereby a critical rate of energy utilization determines the endurance of the inspiratory pump, and that rate varies with pressure, flow, and lung volume.

Effects of negative upper airway pressure on pattern of breathing in sleeping infants

1989 ◽  
Vol 66 (4) ◽  
pp. 1599-1605 ◽  
Author(s):  
B. T. Thach ◽  
A. P. Menon ◽  
G. L. Schefft
Keyword(s):  
Tidal Volume ◽  
Airway Pressure ◽  
Upper Airway ◽  
Face Mask ◽  
Inhibitory Effect ◽  
Lower Airway ◽  
Quiet Sleep ◽  
Reflex Mechanism ◽  
Inspiratory Muscles ◽  
Reflex Latency

Negative upper airway (UAW) pressure inhibits diaphragm inspiratory activity in animals, but there is no direct evidence of this reflex in humans. Also, little is known regarding reflex latency or effects of varying time of stimulation during the breathing cycle. We studied effects of UAW negative pressure on inspiratory airflow and respiratory timing in seven tracheostomized infants during quiet sleep with a face mask and syringe used to produce UAW suction without changing lower airway pressure. Suction trials lasted 2–3 s. During UAW suction, mean and peak inspiratory airflow as well as tidal volume was markedly reduced (16–68%) regardless of whether stimulation occurred in inspiration or expiration. Reflex latency was 42 +/- 3 ms. When suction was applied during inspiration or late expiration, the inspiration and the following expiration were shortened. In contrast, suction applied during midexpiration prolonged expiration and tended to prolong inspiration. The changes in flow, tidal volume, and timing indicate a marked inhibitory effect of UAW suction on thoracic inspiratory muscles. Such a reflex mechanism may function in preventing pharyngeal collapse by inspiratory suction pressure.

Influence of upper airway negative pressure reflex on response to airway occlusion in sleeping infants

1989 ◽  
Vol 67 (2) ◽  
pp. 749-755 ◽  
Author(s):  
B. T. Thach ◽  
G. L. Schefft ◽  
D. L. Pickens ◽  
A. P. Menon
Keyword(s):  
Upper Airway ◽  
Inspiratory Pressure ◽  
Reflex Response ◽  
Lower Airway ◽  
Pressure Waveform ◽  
Inspiratory Time ◽  
Quiet Sleep ◽  
Airway Occlusion ◽  
Inspiratory Muscles ◽  
Airway Reflex

Artificially produced upper airway suction inhibits the diaphragm in animals and infants; however, the effects of spontaneously generated suction in humans are unknown. We studied nine tracheostomized infants because separation of the upper from the lower airway allowed us to channel suction created by an occluded inspiratory effort to both upper and lower airways (upper + lower airway occlusions) or to the lower airway only (lower airway occlusion). The tracheostomy airway was briefly occluded at end expiration during quiet sleep. In upper + lower airway occlusions, peak airway pressure of the first occluded breath was less negative and rate of pressure decrease slower than that of lower airway occlusions, indicating that upper airway suction inhibits thoracic inspiratory muscles. The threshold for this response was less than or equal to 4 cmH2O suction pressure. The effect on inspiratory time was variable. A decrease in slope of the inspiratory pressure waveform occurring at approximately 0.12 s after inspiration onset was more marked in upper + lower airway occlusions. We conclude that infants have an upper airway reflex response to inspiratory pressure that alters not only the peak and slope but also the shape of the inspiratory pressure waveform.

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