Upper airway anesthesia delays arousal from airway occlusion induced during human NREM sleep

1992 ◽  
Vol 73 (2) ◽  
pp. 642-648 ◽  
Author(s):  
R. C. Basner ◽  
J. Ringler ◽  
E. Garpestad ◽  
R. M. Schwartzstein ◽  
D. Sparrow ◽  
...  
Keyword(s):  
Upper Airway ◽  
Nrem Sleep ◽  
Face Mask ◽  
Airway Occlusion ◽  
Before And After ◽  
Arousal Response ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Stable Stage

Six healthy subjects (5 males and 1 female, 26–40 yr old) were studied during non-rapid-eye-movement (NREM) sleep to assess the role of upper airway (UA) afferents in the arousal response to induced airway occlusion. Subjects wore an airtight face mask attached to a low-resistance one-way valve. A valve in the inspiratory circuit allowed instantaneous inspiratory airway occlusion and release; the expiratory circuit remained unoccluded at all times. Each subject was studied during two nights. On one night, occlusions were created during stable stage 2 NREM sleep before and after application of 4% lidocaine to the oral and nasal mucosa. On the other night, the protocol was duplicated with saline (“sham anesthesia”) rather than lidocaine. The order of nights was randomized. Occlusions were sustained until electroencephalographic arousal. Three to 12 occlusions were performed in each subject for each of the four parts of the protocol (pre- and post-lidocaine, pre- and post-saline). The auditory threshold for arousal (1,500-Hz tone beginning at 30 dB) was also tested before and after UA lidocaine. For the group, arousal time after UA anesthesia was prolonged compared with preanesthesia arousal time (P less than 0.001); arousal time after sham anesthesia did not significantly increase from before sham anesthesia (P = 0.9). The increase in arousal time with UA anesthesia was greater than the increase with sham anesthesia (P less than 0.001). The auditory arousal threshold did not increase after UA anesthesia. Inspiratory mask pressure, arterial O2 saturation of hemoglobin, and end-tidal PCO2 during occlusions were similar before and after UA anesthesia.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of hypercapnia on the arousal response to airway occlusion during sleep in normal subjects

1993 ◽  
Vol 74 (5) ◽  
pp. 2269-2275 ◽  
Author(s):  
R. B. Berry ◽  
C. K. Mahutte ◽  
R. W. Light
Keyword(s):  
Normal Subjects ◽  
Rate Of Change ◽  
Supraglottic Airway ◽  
Airway Occlusion ◽  
Rate Of Increase ◽  
Acute Increase ◽  
Arousal Response ◽  
Normal Males ◽  
End Tidal ◽  
Arterial O2 Saturation

The effect of an acute increase in PCO2 on the arousal response to occlusion of a mask covering the nose with the mouth sealed during non-rapid-eye-movement sleep was studied in six normal males aged 28.3 +/- 8.3 (SD) yr. Baseline occlusions, while subjects breathed a room air-O2 mixture adjusted to produce an arterial O2 saturation of 98%, were alternated with hypercapnic occlusions in which a small amount of 100% CO2 was added to increase the preocclusion end-tidal PCO2 by 3.5 +/- 0.59 Torr above the baseline value. The maximum deflections in supraglottic airway pressure (Pmax) were measured on the initial occluded breath (PmaxI) and the final breath preceding arousal (PmaxF). In the hypercapnic occlusions, the time to arousal was shorter (23.7 +/- 13.9 vs. 35.2 +/- 15.9 s, P < 0.03) and PmaxI and rate of change in Pmax were higher. However, the PmaxF in the baseline (20.2 +/- 4.1 cmH2O) and hypercapnic occlusions (20.4 +/- 4.4 cmH2O) did not differ. We conclude that an increase in PCO2 before airway occlusion shortens the time to arousal by increasing the initial occluded inspiratory effort (suction pressure) and the rate of increase in effort but does not change the arousal threshold.

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.

Ventilatory dynamics during transient arousal from NREM sleep: implications for respiratory control stability

1996 ◽  
Vol 80 (5) ◽  
pp. 1475-1484 ◽  
Author(s):  
M. C. Khoo ◽  
S. S. Koh ◽  
J. J. Shin ◽  
P. R. Westbrook ◽  
R. B. Berry
Keyword(s):  
Respiratory Control ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Before And After ◽  
Stage 2 Sleep ◽  
Repeated Administrations ◽  
Time Courses ◽  
Control Stability ◽  
Airway Dynamics ◽  
Normal Adults

The polysomnographic and ventilatory patterns of nine normal adults were measured during non-rapid-eye-movement (NREM) stage 2 sleep before and after repeated administrations of a tone (40-72 dB) lasting 5 s. The ventilatory response to arousal (VRA) was determined in data sections showing electrocortical arousal following the start of the tone. Mean inspiratory flow and tidal volume increased significantly above control levels in the first seven breaths after the start of arousal, with peak increases (64.2% > control) occurring on the second breath. Breath-to-breath occlusion pressure 100 ms after the start of inspiration showed significant increases only on the second and third postarousal breaths, whereas upper airway resistance declined immediately and remained below control for > or = 7 consecutive breaths. These results suggest that the first breath and latter portion of the VRA are determined more by upper airway dynamics than by changes in the neural drive to breathe. Computer model simulations comparing different VRA time courses show that sustained periodic apnea is more likely to occur when the fall in the postarousal increase in ventilation is more abrupt.

Arterial chemoreceptor input to respiratory hypoglossal motoneurons

1990 ◽  
Vol 69 (2) ◽  
pp. 700-709 ◽  
Author(s):  
S. W. Mifflin
Keyword(s):  
Membrane Potential ◽  
Upper Airway ◽  
Excitatory Input ◽  
Airway Patency ◽  
Hypoglossal Motoneurons ◽  
End Tidal ◽  
Carotid Body Chemoreceptors ◽  
Excitatory Drive ◽  
Arterial Chemoreceptor

To better understand the role of the arterial chemoreceptors in the regulation of upper airway patency at the level of the oropharynx, intracellular recordings were obtained from inspiratory hypoglossal motoneurons (IHMs), and the responses to selective activation of the carotid body chemoreceptors were examined. In pentobarbital-anesthetized, vagotomized, paralyzed, and artificially ventilated cats, chemoreceptor activation enhanced the inspiratory depolarization of membrane potential in 32 of 36 IHMs. This was manifested as an increase in either the amplitude (n = 13) or duration (n = 3) or an increase in both amplitude and duration (n = 16) of the inspiratory membrane potential depolarization. The amplitude and duration of the inspiratory membrane potential depolarization increased 98 +/- 15% (n = 29) and 78 +/- 13% (n = 19), respectively. Similar patterns of enhanced activity (increased duration and/or amplitude of membrane depolarization) were observed in five expiratory hypoglossal motoneurons (EHMs) after chemoreceptor activation. In 16 of the 32 IHMs, chemoreceptor activation also evoked changes in IHM membrane potential during expiration: enhanced post-inspiratory discharge (n = 6), expiratory depolarization/discharge (n = 6), and tonic depolarization/discharge, which persisted for several respiratory cycles (n = 4). The arterial chemoreceptors provide a powerful excitatory input to IHMs during both inspiration and expiration. This excitatory drive to IHMs and EHMs will aid in the maintenance of upper airway patency throughout the respiratory cycle during increases in end-tidal CO2.

Possible mechanisms of periodic breathing during sleep

1988 ◽  
Vol 64 (3) ◽  
pp. 1000-1008 ◽  
Author(s):  
K. R. Chapman ◽  
E. N. Bruce ◽  
B. Gothe ◽  
N. S. Cherniack
Keyword(s):  
Control System ◽  
Respiratory Control ◽  
Periodic Breathing ◽  
Nrem Sleep ◽  
Loop Gain ◽  
Hypoxic Conditions ◽  
Spontaneous Oscillations ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Stage 1

To determine the effect of respiratory control system loop gain on periodic breathing during sleep, 10 volunteers were studied during stage 1-2 non-rapid-eye-movement (NREM) sleep while breathing room air (room air control), while hypoxic (hypoxia control), and while wearing a tight-fitting mask that augmented control system gain by mechanically increasing the effect of ventilation on arterial O2 saturation (SaO2) (hypoxia increased gain). Ventilatory responses to progressive hypoxia at two steady-state end-tidal PCO2 levels and to progressive hypercapnia at two levels of oxygenation were measured during wakefulness as indexes of controller gain. Under increased gain conditions, five male subjects developed periodic breathing with recurrent cycles of hyperventilation and apnea; the remaining subjects had nonperiodic patterns of hyperventilation. Periodic breathers had greater ventilatory response slopes to hypercapnia under either hyperoxic or hypoxic conditions than nonperiodic breathers (2.98 ± 0.72 vs. 1.50 ± 0.39 l.min-1.Torr-1; 4.39 ± 2.05 vs. 1.72 ± 0.86 l.min-1.Torr-1; for both, P less than 0.04) and greater ventilatory responsiveness to hypoxia at a PCO2 of 46.5 Torr (2.07 ± 0.91 vs. 0.87 ± 0.38 l.min-1.% fall in SaO2(-1); P less than 0.04). To assess whether spontaneous oscillations in ventilation contributed to periodic breathing, power spectrum analysis was used to detect significant cyclic patterns in ventilation during NREM sleep. Oscillations occurred more frequently in periodic breathers, and hypercapnic responses were higher in subjects with oscillations than those without. The results suggest that spontaneous oscillations in ventilation are common during sleep and can be converted to periodic breathing with apnea when loop gain is increased.

Respiratory timing during NREM sleep in patients with occlusive sleep apnea

1986 ◽  
Vol 61 (4) ◽  
pp. 1444-1448 ◽  
Author(s):  
E. Onal ◽  
M. Lopata
Keyword(s):  
Sleep Apnea ◽  
Eye Movement ◽  
Upper Airway ◽  
Nrem Sleep ◽  
Afferent Input ◽  
Curvilinear Relationship ◽  
Neural Drive ◽  
Airway Occlusion ◽  
Timing Mechanisms ◽  
The Right

To study respiratory timing mechanisms in patients with occlusive apnea, inspiratory and expiratory times (TI and TE) were calculated from the diaphragmatic electromyogram obtained in seven patients during non-rapid-eye-movement (NREM) sleep. Peak diaphragmatic activity (EMGdi) had a curvilinear relationship with TI during the ventilatory and occlusive phases such that TI shortened as EMGdi decreased during the ventilatory phase (r = 0.87, P less than 0.05) and it prolonged as EMGdi increased during the occlusive phase (r = 0.89, P less than 0.02). However, EMGdi vs. TI for the occlusive phase was shifted to the right of that for the ventilatory phase, reflecting the relatively longer TI during upper airway occlusion. TI also had a linear relationship with pleural pressure (r = 0.94, P less than 0.001) that remained unchanged during the ventilatory and occlusive phases such that it prolonged as negative inspiratory pressure increased. These results indicate that respiratory timing is continuously modified in patients with occlusive apnea as inspiratory neural drive fluctuates during NREM sleep and suggest that this modification is due to the net effects of changing inspiratory neural drive and afferent input predominantly from upper airway mechanoreceptors.

Increased chemoreceptor output and ventilatory response to sustained hypoxia

1989 ◽  
Vol 67 (3) ◽  
pp. 1157-1163 ◽  
Author(s):  
D. Georgopoulos ◽  
S. Walker ◽  
N. R. Anthonisen
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Base Line ◽  
Breathing Patterns ◽  
Peripheral Chemoreceptor ◽  
Depressant Action ◽  
Before And After ◽  
End Tidal ◽  
Arterial O2 Saturation ◽  
Sustained Hypoxia

In adult humans the ventilatory response to sustained hypoxia (VRSH) is biphasic, characterized by an initial brisk increase, due to peripheral chemoreceptor (PC) stimulation, followed by a decline attributed to central depressant action of hypoxia. To study the effects of selective stimulation of PC on the ventilatory response pattern to hypoxia, the VRSH was evaluated after pretreatment with almitrine (A), a PC stimulant. Eight subjects were pretreated with A (75 mg po) or placebo (P) on 2 days in a single-blind manner. Two hours after drug administration, they breathed, in succession, room air (10 min), O2 (5 min), room air (5 min), hypoxia [25 min, arterial O2 saturation (SaO2) = 80%], O2 (5 min), and room air (5 min). End-tidal CO2 was kept constant at the normoxic base-line values. Inspiratory minute ventilation (VI) and breathing patterns were measured over the last 2 min of each period and during minutes 3–5 of hypoxia, and nadirs in VI were assessed just before and after O2 exposure. Independent of the day, the VRSH was biphasic. With P and A pretreatment, early hypoxia increased VI 4.6 +/- 1 and 14.2 +/- 1 (SE) l/min, respectively, from values obtained during the preceding room-air period. On A day the hypoxic ventilatory decline was significantly larger than that on P day, and on both days the decline was a constant fraction of the acute hypoxic response.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of surface tension of mucosal lining liquid on upper airway mechanics in anesthetized humans

2003 ◽  
Vol 95 (1) ◽  
pp. 357-363 ◽  
Author(s):  
Jason P. Kirkness ◽  
Peter R. Eastwood ◽  
Irene Szollosi ◽  
Peter R. Platt ◽  
John R. Wheatley ◽  
...  
Keyword(s):  
Surface Tension ◽  
Human Subjects ◽  
Upper Airway ◽  
Exogenous Surfactant ◽  
Airway Mechanics ◽  
Before And After ◽  
Airway Opening ◽  
Mucosal Lining ◽  
Effect Of Surface

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.

Effect of testosterone on the apneic threshold in women during NREM sleep

2003 ◽  
Vol 94 (1) ◽  
pp. 101-107 ◽  
Author(s):  
X. S. Zhou ◽  
J. A. Rowley ◽  
F. Demirovic ◽  
M. P. Diamond ◽  
M. S. Badr
Keyword(s):  
Ventilatory Response ◽  
Minute Ventilation ◽  
Premenopausal Women ◽  
Nrem Sleep ◽  
Central Apnea ◽  
Rapid Eye Movement Sleep ◽  
A Value ◽  
Before And After ◽  
Testosterone Administration ◽  
End Tidal

The hypocapnic apneic threshold (AT) is lower in women relative to men. To test the hypothesis that the gender difference in AT was due to testosterone, we determined the AT during non-rapid eye movement sleep in eight healthy, nonsnoring, premenopausal women before and after 10–12 days of transdermal testosterone. Hypocapnia was induced via nasal mechanical ventilation (MV) for 3 min with tidal volumes ranging from 175 to 215% above eupneic tidal volume and respiratory frequency matched to eupneic frequency. Cessation of MV resulted in hypocapnic central apnea or hypopnea depending on the magnitude of hypocapnia. Nadir minute ventilation as a percentage of control (%V˙e) was plotted against the change in end-tidal CO2(Pet CO2 ); %V˙e was given a value of zero during central apnea. The AT was defined as the Pet CO2 at which the apnea closest to the last hypopnea occurred; hypocapnic ventilatory response (HPVR) was defined as the slope of the linear regression V˙e vs. Pet CO2 . Both the AT (39.5 ± 2.9 vs. 42.1 ± 3.0 Torr; P = 0.002) and HPVR (0.20 ± 0.05 vs. 0.33 ± 0.11%V˙e/Torr; P = 0.016) increased with testosterone administration. We conclude that testosterone administration increases AT in premenopausal women, suggesting that the increased breathing instability during sleep in men is related to the presence of testosterone.

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