Collapsibility of the human upper airway during normal sleep

1989 ◽  
Vol 66 (4) ◽  
pp. 1800-1808 ◽  
Author(s):  
L. Wiegand ◽  
C. W. Zwillich ◽  
D. P. White
Keyword(s):  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Load Application ◽  
Resistive Load ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Small Increments ◽  
Normal Men

Upper airway resistance (UAR) increases in normal subjects during the transition from wakefulness to sleep. To examine the influence of sleep on upper airway collapsibility, inspiratory UAR (epiglottis to nares) and genioglossus electromyogram (EMG) were measured in six healthy men before and during inspiratory resistive loading. UAR increased significantly (P less than 0.05) from wakefulness to non-rapid-eye-movement (NREM) sleep [3.1 +/- 0.4 to 11.7 +/- 3.5 (SE) cmH2O.1–1.s]. Resistive load application during wakefulness produced small increments in UAR. However, during NREM sleep, UAR increased dramatically with loading in four subjects although two subjects demonstrated little change. This increment in UAR from wakefulness to sleep correlated closely with the rise in UAR during loading while asleep (e.g., load 12: r = 0.90, P less than 0.05), indicating consistent upper airway behavior during sleep. On the other hand, no measurement of upper airway behavior during wakefulness was predictive of events during sleep. Although the influence of sleep on the EMG was difficult to assess, peak inspiratory genioglossus EMG clearly increased (P less than 0.05) after load application during NREM sleep. Finally, minute ventilation fell significantly from wakefulness values during NREM sleep, with the largest decrement in sleeping minute ventilation occurring in those subjects having the greatest awake-to-sleep increment in UAR (r = -0.88, P less than 0.05). We conclude that there is marked variability among normal men in upper airway collapsibility during sleep.

scholarly journals Effect of Head Elevation on Passive Upper Airway Collapsibility in Normal Subjects during Propofol Anesthesia

2011 ◽  
Vol 115 (2) ◽  
pp. 273-281 ◽  
Author(s):  
Masato Kobayashi ◽  
Takao Ayuse ◽  
Yuko Hoshino ◽  
Shinji Kurata ◽  
Shunji Moromugi ◽  
...  
Keyword(s):  
Upper Airway ◽  
Normal Subjects ◽  
Target Concentration ◽  
Airway Patency ◽  
Head Elevation ◽  
Jaw Opening ◽  
Airway Collapsibility ◽  
Upper Airway Collapsibility ◽  
Head Flexion ◽  
Male Subjects

Background Head elevation can restore airway patency during anesthesia, although its effect may be offset by concomitant bite opening or accidental neck flexion. The aim of this study is to examine the effect of head elevation on the passive upper airway collapsibility during propofol anesthesia. Method Twenty male subjects were studied, randomized to one of two experimental groups: fixed-jaw or free-jaw. Propofol infusion was used for induction and to maintain blood at a constant target concentration between 1.5 and 2.0 μg/ml. Nasal mask pressure (PN) was intermittently reduced to evaluate the upper airway collapsibility (passive PCRIT) and upstream resistance (RUS) at each level of head elevation (0, 3, 6, and 9 cm). The authors measured the Frankfort plane (head flexion) and the mandible plane (jaw opening) angles at each level of head elevation. Analysis of variance was used to determine the effect of head elevation on PCRIT, head flexion, and jaw opening within each group. Results In both groups the Frankfort plane and mandible plane angles increased with head elevation (P < 0.05), although the mandible plane angle was smaller in the free-jaw group (i.e., increased jaw opening). In the fixed-jaw group, head elevation decreased upper airway collapsibility (PCRIT ~ -7 cm H₂O at greater than 6 cm elevation) compared with the baseline position (PCRIT ~ -3 cm H₂O at 0 cm elevation; P < 0.05). Conclusion : Elevating the head position by 6 cm while ensuring mouth closure (centric occlusion) produces substantial decreases in upper airway collapsibility and maintains upper airway patency during anesthesia.

Effect of episodic hypoxia on upper airway mechanics in humans during NREM sleep

2002 ◽  
Vol 92 (6) ◽  
pp. 2565-2570 ◽  
Author(s):  
Mahdi Shkoukani ◽  
Mark A. Babcock ◽  
M. Safwan Badr
Keyword(s):  
Minute Ventilation ◽  
Recovery Period ◽  
Control Period ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Hypoxic Exposure ◽  
Airway Mechanics ◽  
Episodic Hypoxia ◽  
Long Term Facilitation

We hypothesized that long-term facilitation (LTF) is due to decreased upper airway resistance (Rua). We studied 11 normal subjects during stable non-rapid eye movement sleep. We induced brief isocapnic hypoxia (inspired O2fraction = 8%) (3 min) followed by 5 min of room air. This sequence was repeated 10 times. Measurements were obtained during control, hypoxia, and at 20 min of recovery (R20) for ventilation, timing, and Rua. In addition, nine subjects were studied in a sham study with no hypoxic exposure. During the episodic hypoxia study, inspiratory minute ventilation (V˙i) increased from 7.1 ± 1.8 l/min during the control period to 8.3 ± 1.8 l/min at R20 (117% of control; P < 0.05). Conversely, there was no change in diaphragmatic electromyogram (EMGdia) between control (16.1 ± 6.9 arbitrary units) and R20 (15.3 ± 4.9 arbitrary units) (95% of control; P > 0.05). In contrast, increasedV˙i was associated with decreased Rua from 10.7 ± 7.5 cmH2O · l−1 · s during control to 8.2 ± 4.4 cmH2O · l−1 · s at R20 (77% of control; P < 0.05). No change was noted in V˙i, Rua, or EMGdia during the recovery period relative to control during the sham study. We conclude the following: 1) increased V˙i in the recovery period is indicative of LTF, 2) the lack of increased EMGdia suggests lack of LTF to the diaphragm, 3) reduced Rua suggests LTF of upper airway dilators, and 4) increased V˙i in the recovery period is due to “unloading” of the upper airway by LTF of upper airway dilators.

Time of day affects the frequency and duration of breathing events and the critical closing pressure during NREM sleep in participants with sleep apnea

2015 ◽  
Vol 119 (6) ◽  
pp. 617-626 ◽  
Author(s):  
Mohamad El-Chami ◽  
David Shaheen ◽  
Blake Ivers ◽  
Ziauddin Syed ◽  
M. Safwan Badr ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Sleep Apnea ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Time Of Day ◽  
Obstructive Sleep ◽  
Airway Collapsibility ◽  
Critical Closing Pressure ◽  
Upper Airway Collapsibility ◽  
Closing Pressure

We investigated if the number and duration of breathing events coupled to upper airway collapsibility were affected by the time of day. Male participants with obstructive sleep apnea completed a constant routine protocol that consisted of sleep sessions in the evening (10 PM to 1 AM), morning (6 AM to 9 AM), and afternoon (2 PM to 5 PM). On one occasion the number and duration of breathing events was ascertained for each sleep session. On a second occasion the critical closing pressure that demarcated upper airway collapsibility was determined. The duration of breathing events was consistently greater in the morning compared with the evening and afternoon during N1 and N2, while an increase in event frequency was evident during N1. The critical closing pressure was increased in the morning (2.68 ± 0.98 cmH2O) compared with the evening (1.29 ± 0.91 cmH2O; P ≤ 0.02) and afternoon (1.25 ± 0.79; P ≤ 0.01). The increase in the critical closing pressure was correlated to the decrease in the baseline partial pressure of carbon dioxide in the morning compared with the afternoon and evening ( r = −0.73, P ≤ 0.005). Our findings indicate that time of day affects the duration and frequency of events, coupled with alterations in upper airway collapsibility. We propose that increases in airway collapsibility in the morning may be linked to an endogenous modulation of baseline carbon dioxide levels and chemoreflex sensitivity (12), which are independent of the consequences of sleep apnea.

Chemosensitivity and the ventilatory response to airflow obstruction during sleep

1989 ◽  
Vol 67 (4) ◽  
pp. 1630-1637 ◽  
Author(s):  
K. Gleeson ◽  
C. W. Zwillich ◽  
D. P. White
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Respiratory Rhythm ◽  
Airflow Obstruction ◽  
Nrem Sleep ◽  
Normal Subjects ◽  
Initial Increase ◽  
Base Line ◽  
Expiratory Time ◽  
Normal Men

There is an accumulating body of evidence which suggests that chemical control of breathing can play a role in destabilizing respiratory rhythm during sleep. We hypothesized that the sleeping ventilatory response to hypercapnia (HCVR) and/or hypoxia (HVR) would predict respiratory events following release of inspiratory airway obstruction (IAO) in normal men during non-rapid-eye-movement (NREM) sleep. We therefore measured HCVR, HVR, and ventilation for three breaths preceding and eight breaths following three totally obstructed inspirations in eight normal subjects during NREM sleep. After IAO, we generally observed transient hyperventilation that resulted in hypocapnia and prolonged expiratory time. We found the initial increase in inspiratory minute ventilation (VI) following IAO to be correlated with HCVR (r = 0.72, P less than 0.05) but not HVR. In addition, the maximum decrease in PCO2 below base line was also related to HCVR (r = 0.83, P less than 0.05). This decrement in PCO2 predicted the subsequent prolongation in expiratory time (TE, r = 0.83, P less than 0.05) that was frequently observed. HCVR tended to predict the prolongation of TE, at the nadir of CO2 (r = 0.69, P = 0.057). In conjunction with this hypocapnia and prolongation of TE, hypoventilation with falling VI was often observed followed by periodic hyper- and hypoventilation. These results suggest that high HCVR may result in ventilatory overshoot following IAO and may contribute to ventilatory instability during sleep.

Upper airway muscle responsiveness to rising Pco 2 during NREM sleep

2000 ◽  
Vol 89 (4) ◽  
pp. 1275-1282 ◽  
Author(s):  
Giora Pillar ◽  
Atul Malhotra ◽  
Robert B. Fogel ◽  
Josee Beauregard ◽  
David I. Slamowitz ◽  
...  
Keyword(s):  
Muscle Activation ◽  
Slow Wave Sleep ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Dilator Muscle ◽  
Pharyngeal Muscles ◽  
Stage 2 Sleep ◽  
Significant Change ◽  
End Tidal

Although pharyngeal muscles respond robustly to increasing Pco 2 during wakefulness, the effect of hypercapnia on upper airway muscle activation during sleep has not been carefully assessed. This may be important, because it has been hypothesized that CO2-driven muscle activation may importantly stabilize the upper airway during stages 3 and 4 sleep. To test this hypothesis, we measured ventilation, airway resistance, genioglossus (GG) and tensor palatini (TP) electromyogram (EMG), plus end-tidal Pco 2(Pet CO2 ) in 18 subjects during wakefulness, stage 2, and slow-wave sleep (SWS). Responses of ventilation and muscle EMG to administered CO2(Pet CO2 = 6 Torr above the eupneic level) were also assessed during SWS ( n = 9) or stage 2 sleep ( n = 7). Pet CO2 increased spontaneously by 0.8 ± 0.1 Torr from stage 2 to SWS (from 43.3 ± 0.6 to 44.1 ± 0.5 Torr, P < 0.05), with no significant change in GG or TP EMG. Despite a significant increase in minute ventilation with induced hypercapnia (from 8.3 ± 0.1 to 11.9 ± 0.3 l/min in stage 2 and 8.6 ± 0.4 to 12.7 ± 0.4 l/min in SWS, P < 0.05 for both), there was no significant change in the GG or TP EMG. These data indicate that supraphysiological levels of Pet CO2 (50.4 ± 1.6 Torr in stage 2, and 50.4 ± 0.9 Torr in SWS) are not a major independent stimulus to pharyngeal dilator muscle activation during either SWS or stage 2 sleep. Thus hypercapnia-induced pharyngeal dilator muscle activation alone is unlikely to explain the paucity of sleep-disordered breathing events during SWS.

Influence of prior ventilatory experience on the estimation of breathlessness during exercise

1990 ◽  
Vol 78 (2) ◽  
pp. 149-153 ◽  
Author(s):  
Rachel C. Wilson ◽  
P. W. Jones
Keyword(s):  
Exercise Test ◽  
Prior Experience ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Resistive Load ◽  
Inspiratory Time ◽  
Borg Scale ◽  
Exercise Tests ◽  
Loaded Breathing ◽  
Inspiratory Load

1. The intensity of breathlessness was measured during exercise in nine normal subjects using a modified Borg scale to examine the effect of prior experience of breathlessness on subsequent estimates of breathlessness. 2. Each subject performed four exercise tests, each of which consisted of two identical runs of workload incrementation (run 1 and run 2). An inspiratory resistive load of 3.8 cmH2O s−1 l−1 was applied during the appropriate run of the exercise test to examine the effect of (a) prior experience of ‘loaded’ breathing on breathlessness estimation during ‘unloaded’ breathing, and (b) prior experience of ‘unloaded’ breathing on breathlessness estimation during ‘loaded’ breathing. Run 1 was the conditioning run; run 2 was the run in which the effect of conditioning was measured. 3. There was a good correlation between breathlessness and minute ventilation during both unloaded’ breathing (median r = 0.93) and ‘loaded’ breathing (median r = 0.95). 4. The slope of the Borg score/minute ventilation relationship was greater during ‘loaded’ breathing than during ‘unloaded’ breathing (P < 0.01). There was no difference in mean Borg score between ‘unloaded’ and ‘loaded’ breathing. 5. After a period of ‘loaded’ breathing during run 1, estimated breathlessness was significantly reduced during ensuing ‘unloaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which ‘unloaded’ breathing was experienced throughout both run 1 and run 2. 6. After a period of ‘unloaded’ breathing in run 1, estimated breathlessness was significantly increased during ensuing ‘loaded’ breathing in run 2 (P < 0.01) compared with the exercise test in which the inspiratory load had already been experienced in run 1. 7. Changes in the pattern of breathing (inspiratory time, expiratory time, total breath duration, inspiration time/total breath duration ratio and tidal volume) were not consistent with the changes in breathlessness. 8. We suggest that perception of breathlessness may be influenced by a subject's immediate prior experience of an altered relationship between breathlessness and ventilation.

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