Influence of respiratory drive on upper airway resistance in normal men

1989 ◽  
Vol 66 (3) ◽  
pp. 1242-1249 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules ◽  
J. La Forge
Keyword(s):  
Airway Resistance ◽  
Upper Airway ◽  
Base Line ◽  
Respiratory Drive ◽  
Upper Airway Resistance ◽  
Co2 Rebreathing ◽  
Bias Flow ◽  
Measured Flow ◽  
The Mean ◽  
Normal Men

The variations in nasal and pharyngeal resistance induced by changes in the central inspiratory drive were studied in 10 normal men. To calculate resistances we measured upper airway pressures with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other in the posterior nasopharynx, and we measured flow with a Fleisch no. 3 pneumotachograph connected to a tightly fitting mask. Both resistances were obtained continuously during CO2 rebreathing (Read's method) and during the 2 min after a 1-min voluntary maximal hyperventilation. The inspiratory drive was estimated by measurements of inspiratory pressure generated at 0.1 s after the onset of inspiration (P0.1) and by the mean inspiratory flow (VT/TI). In each subject both resistances decreased during CO2 rebreathing; these decreases were correlated with the increase in P0.1. During the posthyperventilation period, ventilation fell below base line in seven subjects; this was accompanied by an increase in both nasal and pharyngeal resistances. These resistances increased exponentially as VT/TI decreased. Parallel changes in nasal and pharyngeal resistances were seen during CO2 stimulus and during the period after the hyperventilation. We conclude that 1) the indexes quantifying the inspiratory drive reflect the activation of nasopharyngeal dilator muscles (as assessed by the changes in upper airway resistance) and 2) both nasal and pharyngeal resistances are similarly influenced by changes in the respiratory drive.

Effects of respiratory drive on upper airways in sleep apnea patients and normal subjects

1989 ◽  
Vol 67 (3) ◽  
pp. 973-979 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules ◽  
J. La Forge
Keyword(s):  
Sleep Apnea ◽  
Airway Resistance ◽  
Upper Airway ◽  
Normal Subjects ◽  
Base Line ◽  
Respiratory Drive ◽  
Upper Airway Resistance ◽  
Co2 Rebreathing ◽  
Airway Pressures ◽  
Line Level

We compared the changes in nasal and pharyngeal resistance induced by modifications in the central respiratory drive in 8 patients with sleep apnea syndrome (SAS) with the results of 10 normal men. Upper airway pressures were measured with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other above the uvula. Nasal and pharyngeal resistances were calculated at isoflow. During CO2 rebreathing and during the 2 min after maximal voluntary hyperventilation, we continuously recorded upper airway pressures, airflow, end-tidal CO2, and the mean inspiratory flow (VT/TI); inspiratory pressure generated at 0.1 s after the onset of inspiration (P0.1) was measured every 15–20 s. In both groups upper airway resistance decreased as P0.1 increased during CO2 rebreathing. When P0.1 increased by 500%, pharyngeal resistance decreased to 17.8 +/- 3.1% of base-line values in SAS patients and to 34.9 +/- 3.4% in normal subjects (mean +/- SE). During the posthyperventilation period the VT/TI fell below the base-line level in seven SAS patients and in seven normal subjects. The decrease in VT/TI was accompanied by an increase in upper airway resistance. When the VT/TI decreased by 30% of its base-line level, pharyngeal resistance increased to 319.1 +/- 50.9% in SAS and 138.5 +/- 4.7% in normal subjects (P less than 0.05). We conclude that 1) in SAS patients, as in normal subjects, the activation of upper airway dilators is reflected by indexes that quantify the central inspiratory drive and 2) the pharyngeal patency is more sensitive to the decrease of the central respiratory drive in SAS patients than in normal subjects.

Influence of passive changes of lung volume on upper airways

1990 ◽  
Vol 68 (5) ◽  
pp. 2159-2164 ◽  
Author(s):  
F. Series ◽  
Y. Cormier ◽  
M. Desmeules
Keyword(s):  
Lung Volume ◽  
Airway Resistance ◽  
Upper Airway ◽  
Normal Subjects ◽  
Base Line ◽  
Nasal Resistance ◽  
Inspiratory Flow Rate ◽  
Upper Airways ◽  
Lung Volumes ◽  
Bias Flow

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.

scholarly journals Sciatic nerve stimulation and its effects on upper airway resistance in the anesthetized rabbit model relevant to sleep apnea

2018 ◽  
Vol 125 (3) ◽  
pp. 763-769 ◽  
Author(s):  
Matthew Schiefer ◽  
Jenniffer Gamble ◽  
Kingman P. Strohl
Keyword(s):  
Sleep Apnea ◽  
Sciatic Nerve ◽  
Nerve Stimulation ◽  
Airway Resistance ◽  
Rabbit Model ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Upper Airway Resistance ◽  
Ventilatory Drive ◽  
Sciatic Nerve Stimulation

Obstructive sleep apnea (OSA) is a disorder characterized by collapse of the velopharynx and/or oropharynx during sleep when drive to the upper airway is reduced. Here, we explore an indirect approach for activation of upper airway muscles that might affect airway dynamics, namely, unilateral electrical stimulation of the afferent fibers of the sciatic nerve, in an anesthetized rabbit model. A nerve cuff electrode was placed around the sciatic and hypoglossal nerves to deliver stimulus while airflow, air pressure, and alae nasi electromyogram (EMG) were monitored both before and after sciatic transection. Sciatic nerve stimulation increased respiratory effort, rate, and alae nasi EMG, which persisted for seconds after stimulation; however, upper airway resistance was unchanged. Hypoglossal stimulation reduced resistance without altering drive. Although sciatic nerve stimulation is not ideal for treating OSA, it remains a target for altering respiratory drive. NEW & NOTEWORTHY Previously, sciatic nerve stimulation has been shown to activate upper airway and chest wall muscles. The supposition that resistance through the upper airway would be reduced with this afferent reflex was disproven. Findings were in contrast with the effect of hypoglossal nerve stimulation, which was shown to decrease resistance without changing muscle activation or ventilatory drive.

Breathing during wakefulness and NREM sleep in humans without an upper airway

1996 ◽  
Vol 81 (1) ◽  
pp. 274-281 ◽  
Author(s):  
M. J. Morrell ◽  
H. R. Harty ◽  
L. Adams ◽  
A. Guz
Keyword(s):  
Airway Resistance ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Rapid Eye Movement Sleep ◽  
Upper Airway Resistance ◽  
Control Subjects ◽  
The Mean ◽  
Tracheal Stoma ◽  
End Tidal ◽  
Related Increase

The increase in PCO2 that occurs during sleep may reflect an inadequate ventilatory compensation to an increase in upper airway resistance. To address this question in humans, we examined changes in breathing during wakefulness and non-rapid-eye-movement sleep in eight laryngectomized subjects who breathed through a tracheal stoma. In these subjects, any sleep-related increase in upper airway resistance could not affect ventilation. Healthy subjects breathing via an intact upper airway were studied as controls. The mean increase in end-tidal PCO2 from wakefulness to sleep was 2.7 +/- 2.6 (SD) Torr (P = 0.05) in laryngectomized subjects and 1.6 +/- 1.4 Torr (P = 0.02) in control subjects. During wakefulness, ventilation was lower in laryngectomized subjects compared with control subjects, although this difference was not statistically significant (6.8 +/- 1.9 vs. 7.4 +/- 1.2 l/min; P > 0.05). During sleep, the fall in ventilation was similar in the two groups (1.1 +/- 2.1 vs. 0.8 +/- 2.1 l/min; P > 0.05). Our observations are not consistent with the view that increases in upper airway resistance are obligatory for sleep-related CO2 retention in humans.

Changes in upper airway resistance during progressive normocapnic hypoxia in normal men

1991 ◽  
Vol 70 (2) ◽  
pp. 548-553 ◽  
Author(s):  
F. Maltais ◽  
L. Dinh ◽  
Y. Cormier ◽  
F. Series
Keyword(s):  
Functional Residual Capacity ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Baseline Period ◽  
Respiratory Drive ◽  
Nasal Resistance ◽  
Bias Flow ◽  
Residual Capacity ◽  
Mouth Occlusion Pressure ◽  
Normal Men

The effects of normocapnic progressive hypoxia on nasal and pharyngeal resistances were evaluated in nine normal men. To calculate resistances, upper airway pressures were measured with two low-bias flow catheters; one was placed at the tip of the epiglottis and the other in the posterior nasopharynx, and we measured flow with a Fleish no. 3 pneumotachograph connected to a tightly fitting mask. Both resistances were obtained during a baseline period and during progressive normocapnic hypoxia achieved by a rebreathing method. We collected the breath-by-breath values of upper airway resistances, minute ventilation, O2 and CO2 fractions, arterial O2 saturation (SaO2), and changes in functional residual capacity (inductance vest). The central respiratory drive was evaluated by the mouth occlusion pressure 0.1 s after the onset of inspiration (P0.1), and breath-by-breath P0.1 values were estimated by intrapolation from the linear relationship between P0.1 and SaO2. In each subject both resistances decreased during the hypoxic test. The slope of the decrease in resistance with decreasing SaO2 (%baseline/%SaO2) was steeper for pharyngeal resistance than for nasal resistance [2.67 +/- 0.29 and 1.61 +/- 0.25 (SE), respectively; P less than 0.05]. The slope of the decrease in resistance with increasing P0.1 (%baseline/cmH2O) was -0.24 +/- 0.05 for nasal resistance and -0.39 +/- 0.07 for pharyngeal resistance (P less than 0.05). Functional residual capacity progressively increased during the test, but the decrease in resistance was greater than expected from an isolated increase in lung volume. We conclude that nasal and pharyngeal resistances decrease during progressive normocapnic hypoxia.(ABSTRACT TRUNCATED AT 250 WORDS)

Novel method for evaluating the upper airway resistance using the ratio of neural respiratory drive to flow in OSA

2020 ◽  
Vol 73 ◽  
pp. 162-169
Author(s):  
Ning Zhang ◽  
Yuanming Luo ◽  
Liteng Yang ◽  
Zhigang Liu ◽  
Zhihui Qiu ◽  
...  
Keyword(s):  
Airway Resistance ◽  
Upper Airway ◽  
Respiratory Drive ◽  
Upper Airway Resistance ◽  
Novel Method

Responses to negative pressure surrounding the neck in anesthetized animals

1990 ◽  
Vol 68 (1) ◽  
pp. 154-160 ◽  
Author(s):  
A. D. Wolin ◽  
K. P. Strohl ◽  
B. N. Acree ◽  
J. M. Fouke
Keyword(s):  
Negative Pressure ◽  
Airway Resistance ◽  
Upper Airway ◽  
Transmural Pressure ◽  
Positive Pressure ◽  
Respiratory Drive ◽  
Airway Wall ◽  
Airway Patency ◽  
Upper Airway Resistance ◽  
Continuous Positive Pressure

Continuous positive pressure applied at the nose has been shown to cause a decrease in upper airway resistance. The present study was designed to determine whether a similar positive transmural pressure gradient, generated by applying a negative pressure at the body surface around the neck, altered upper airway patency. Studies were performed in nine spontaneously breathing anesthetized supine dogs. Airflow was measured with a pneumotachograph mounted on an airtight muzzle placed over the nose and mouth of each animal. Upper airway pressure was measured as the differential pressure between the extrathoracic trachea and the inside of the muzzle. Upper airway resistance was monitored as an index of airway patency. Negative pressure (-2 to -20 cmH2O) was applied around the neck by using a cuirass extending from the jaw to the thorax. In each animal, increasingly negative pressures were transmitted to the airway wall in a progressive, although not linear, fashion. Decreasing the pressure produced a progressive fall in upper airway resistance, without causing a significant change in respiratory drive or respiratory timing. At -5 cmH2O pressure, there occurred a significant fall in upper airway resistance, comparable with the response of a single, intravenous injection of sodium cyanide (0.5-3.0 mg), a respiratory stimulant that produces substantial increases in respiratory drive. We conclude that upper airway resistance is influenced by the transmural pressure across the airway wall and that such a gradient can be accomplished by making the extraluminal pressure more negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Upper airway resistance and geniohyoid muscle activity in normal men during wakefulness and sleep

1990 ◽  
Vol 69 (4) ◽  
pp. 1252-1261 ◽  
Author(s):  
D. A. Wiegand ◽  
B. Latz ◽  
C. W. Zwillich ◽  
L. Wiegand
Keyword(s):  
Eye Movement ◽  
Rem Sleep ◽  
Muscle Activity ◽  
Airway Resistance ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Supraglottic Airway ◽  
Rapid Eye Movement ◽  
Upper Airway Resistance ◽  
Normal Men

Sleep-related reduction in geniohyoid muscular support may lead to increased airway resistance in normal subjects. To test this hypothesis, we studied seven normal men throughout a single night of sleep. We recorded inspiratory supraglottic airway resistance, geniohyoid muscle electromyographic (EMGgh) activity, sleep staging, and ventilatory parameters in these subjects during supine nasal breathing. Mean inspiratory upper airway resistance was significantly (P less than 0.01) increased in these subjects during all stages of sleep compared with wakefulness, reaching highest levels during non-rapid-eye-movement (NREM) sleep [awake 2.5 +/- 0.6 (SE) cmH2O.l-1.s, stage 2 NREM sleep 24.1 +/- 11.1, stage 3/4 NREM sleep 30.2 +/- 12.3, rapid-eye-movement (REM) sleep 13.0 +/- 6.7]. Breath-by-breath linear correlation analyses of upper airway resistance and time-averaged EMGgh amplitude demonstrated a significant (P less than 0.05) negative correlation (r = -0.44 to -0.55) between these parameters in five of seven subjects when data from all states (wakefulness and sleep) were combined. However, we found no clear relationship between normalized upper airway resistance and EMGgh activity during individual states (wakefulness, stage 2 NREM sleep, stage 3/4 NREM sleep, and REM sleep) when data from all subjects were combined. The timing of EMGgh onset relative to the onset of inspiratory airflow did not change significantly during wakefulness, NREM sleep, and REM sleep. Inspiratory augmentation of geniohyoid activity generally preceded the start of inspiratory airflow. The time from onset of inspiratory airflow to peak inspiratory EMGgh activity was significantly increased during sleep compared with wakefulness (awake 0.81 +/- 0.04 s, NREM sleep 1.01 +/- 0.04, REM sleep 1.04 +/- 0.05; P less than 0.05). These data indicate that sleep-related changes in geniohyoid muscle activity may influence upper airway resistance in some subjects. However, the relationship between geniohyoid muscle activity and upper airway resistance was complex and varied among subjects, suggesting that other factors must also be considered to explain sleep influences on upper airway patency.

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