Effect of airway impedance on CO2 retention and respiratory muscle activity during NREM sleep

We hypothesized that a sleep-induced increase in mechanical impedance contributes to CO2 retention and respiratory muscle recruitment during non-rapid-eye-movement (NREM) sleep. The effect NREM sleep on respiratory muscle activity and CO2 retention was measured in healthy subjects who increased maximum total pulmonary resistance (RLmax, 1-81 cmH2O.l-1.s) from awake to NREM sleep. We determined the effects of this sleep-induced increase in airway impedance by steady-state inhalation of a reduced-density gas mixture (79% He-21% O2, He-O2). Both arterialized blood PCO2 (PaCO2) and end-tidal PCO2 (PETCO2) were measured. Inspiratory (EMGinsp) and expiratory (EMGexp) respiratory muscle electromyogram activity was measured. NREM sleep caused 1) RLmax to increase (7 +/- 3 vs. 39 +/- 28 cmH2O.l-1.s), 2) PaCO2 and/or PETCO2 to increase in all subjects (40 +/- 2 vs. 44 +/- 3 Torr), and 3) EMGinsp to increase in 8 of 9 subjects and EMGexp to increase in 9 of 17 subjects. Compared with steady-state air breathing during NREM sleep, steady-state He-O2 breathing 1) reduced RLmax by 38%, 2) decreased PaCO2 and PETCO2 by 2 Torr, and 3) decreased both EMGinsp (-20%) and EMGexp (-54%). We concluded that the sleep-induced increase in upper airway resistance accompanied by the absence of immediate load compensation is an important determinant of CO2 retention, which, in turn, may cause augmentation of inspiratory and expiratory muscle activity above waking levels during NREM sleep.

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Load compensation and respiratory muscle function during sleep

Journal of Applied Physiology ◽

10.1152/jappl.1992.72.4.1221 ◽

1992 ◽

Vol 72 (4) ◽

pp. 1221-1234 ◽

Cited By ~ 40

Author(s):

K. G. Henke ◽

M. S. Badr ◽

J. B. Skatrud ◽

J. A. Dempsey

Keyword(s):

Eye Movement ◽

Chest Wall ◽

Muscle Activity ◽

Respiratory Muscle ◽

Airway Resistance ◽

Upper Airway ◽

Rapid Eye Movement Sleep ◽

Compensatory Mechanisms ◽

Ventilatory Control ◽

Load Compensation

The sleeping state places unique demands on the ventilatory control system. The sleep-induced increase in airway resistance, the loss of consciousness, and the need to maintain the sleeping state without frequent arousals require the presence of complex compensatory mechanisms. The increase in upper airway resistance during sleep represents the major effect of sleep on ventilatory control. This occurs because of a loss of muscle activity, which narrows the airway and also makes it more susceptible to collapse in response to the intraluminal pressure generated by other inspiratory muscles. The magnitude and timing of the drive to upper airway vs. other inspiratory pump muscles determine the level of resistance and can lead to inspiratory flow limitation and complete upper airway occlusion. The fall in ventilation with this mechanical load is not prevented, as it is in the awake state, because of the absence of immediate compensatory responses during sleep. However, during sleep, compensatory mechanisms are activated that tend to return ventilation toward control levels if the load is maintained. Upper airway protective reflexes, intrinsic properties of the chest wall, muscle length-compensating reflexes, and most importantly chemoresponsiveness of both upper airway and inspiratory pump muscles are all present during sleep to minimize the adverse effect of loading on ventilation. In non-rapid-eye-movement sleep, the high mechanical impedance combined with incomplete load compensation causes an increase in arterial PCO2 and augmented respiratory muscle activity. Phasic rapid-eye-movement sleep, however, interferes further with effective load compensation, primarily by its selective inhibitory effects on the phasic activation of postural muscles of the chest wall. The level and pattern of ventilation during sleep in health and disease states represent a compromise toward the ideal goal, which is to achieve maximum load compensation and meet the demand for chemical homeostasis while maintaining sleep state.

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Effects of continuous positive airway pressure on upper airway and respiratory muscle activity

Journal of Applied Physiology ◽

10.1152/jappl.1987.62.5.2026 ◽

1987 ◽

Vol 62 (5) ◽

pp. 2026-2030 ◽

Cited By ~ 35

Author(s):

C. G. Alex ◽

R. M. Aronson ◽

E. Onal ◽

M. Lopata

Keyword(s):

Continuous Positive Airway Pressure ◽

Respiratory System ◽

Muscle Activity ◽

Airway Pressure ◽

Respiratory Muscle ◽

Positive Airway Pressure ◽

Upper Airway ◽

Afferent Input ◽

Residual Capacity ◽

Respiratory Muscle Activity

To study the effects of continuous positive airway pressure (CPAP) on lung volume, and upper airway and respiratory muscle activity, we quantitated the CPAP-induced changes in diaphragmatic and genioglossal electromyograms, esophageal and transdiaphragmatic pressures (Pes and Pdi), and functional residual capacity (FRC) in six normal awake subjects in the supine position. CPAP resulted in increased FRC, increased peak and rate of rise of diaphragmatic activity (EMGdi and EMGdi/TI), decreased peak genioglossal activity (EMGge), decreased inspiratory time and inspiratory duty cycle (P less than 0.001 for all comparisons). Inspiratory changes in Pes and Pdi, as well as Pes/EMGdi and Pdi/EMGdi also decreased (P less than 0.001 for all comparisons), but mean inspiratory airflow for a given Pes increased (P less than 0.001) on CPAP. The increase in mean inspiratory airflow for a given Pes despite the decrease in upper airway muscle activity suggests that CPAP mechanically splints the upper airway. The changes in EMGge and EMGdi after CPAP application most likely reflect the effects of CPAP and the associated changes in respiratory system mechanics on the afferent input from receptors distributed throughout the intact respiratory system.

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Effect of sleep-induced increases in upper airway resistance on respiratory muscle activity

Journal of Applied Physiology ◽

10.1152/jappl.1991.70.1.158 ◽

1991 ◽

Vol 70 (1) ◽

pp. 158-168 ◽

Cited By ~ 37

Author(s):

K. G. Henke ◽

J. A. Dempsey ◽

M. S. Badr ◽

J. M. Kowitz ◽

J. B. Skatrud

Keyword(s):

Muscle Activity ◽

Respiratory Muscle ◽

Peak Flow ◽

Nrem Sleep ◽

Emg Activity ◽

Electromyographic Activity ◽

Stage 2 Sleep ◽

Expiratory Muscles ◽

Resistive Loads ◽

Respiratory Muscle Activity

To investigate the response of inspiratory and expiratory muscles to naturally occurring inspiratory resistive loads in the absence of conscious control, five male "snorers" were studied during non-rapid-eye-movement (NREM) sleep with and without continuous positive airway pressure (CPAP). Diaphragm (EMGdi) and scalene (EMGsc) electromyographic activity were monitored with surface electrodes and abdominal EMG activity (EMGab) with wire electrodes. Subjects were studied in the following conditions: 1) awake, 2) stage 2 sleep, 3) stage 3/4 sleep, 4) CPAP during stage 3/4 sleep, 5) CPAP plus end-tidal CO2 pressure (PETCO2) isocapnic to stage 2 sleep, and 6) CPAP plus PETCO2 isocapnic to stage 3/4 sleep. Inspired pulmonary resistance (RL) at peak flow rate and PETCO2 increased in all stages of sleep. Activity of EMGdi, EMGsc, and EMGab increased significantly in stage 3/4 sleep. CPAP reduced RL at peak flow, increased tidal volume and expired ventilation, and reduced PETCO2. EMGdi and EMGsc were reduced, and EMGab was silenced. During CPAP, with CO2 added to make PETCO2 isocapnic to stage 3/4 sleep, EMGsc and EMGab increased, but EMGdi was augmented in only one-half of the trials. EMG activity in this condition, however, was only 75% (EMGsc) and 43% (EMGab) of the activity observed during eupneic breathing in stage 3/4 sleep when PETCO2 was equal but RL was much higher. We conclude that during NREM sleep 1) inspiratory and expiratory muscles respond to internal inspiratory resistive loads and the associated dynamic airway narrowing and turbulent flow developed throughout inspiration, 2) some of the augmentation of respiratory muscle activity is also due to the hypercapnia that accompanies loading, and 3) the abdominal muscles are the most sensitive to load and CO2 and the diaphragm is the least sensitive.

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Dynamics of respiratory drive and pressure during NREM sleep in patients with occlusive apneas

Journal of Applied Physiology ◽

10.1152/jappl.1985.58.6.1971 ◽

1985 ◽

Vol 58 (6) ◽

pp. 1971-1974 ◽

Cited By ~ 12

Author(s):

E. Onal ◽

J. A. Leech ◽

M. Lopata

Keyword(s):

Muscle Activity ◽

Upper Airway ◽

Nrem Sleep ◽

Esophageal Pressure ◽

Base Line ◽

Respiratory Drive ◽

Nocturnal Sleep ◽

Muscle Groups ◽

Proportional Decrease ◽

Respiratory Muscle Activity

To study the dynamics of respiratory drive and pressure in patients with occlusive apneas, diaphragmatic electromyogram (EMGdi), esophageal pressure (Pes), and genioglossal electromyogram (EMGge) were monitored during nocturnal sleep in five patients. Both EMGs were analyzed as peak moving time average, and Pes was quantitated as the peak inspiratory change from base line. During the ventilatory phase both EMGs decreased proportionally. The decrease in Pes was less than the decrease observed in EMGdi, and Pes generated for a given EMGdi increased during the preapneic phase in spite of the proportional decrease in EMGdi and EMGge during this period. We conclude that negative inspiratory pressures which lead to the passive collapse of oropharyngeal walls are dependent on both respiratory and upper airway muscle activity and that occlusive apneas of non-rapid-eye-movement (NREM) sleep do occur in spite of proportional changes observed in the activity of both muscle groups. The preapneic increase in negative inspiratory pressures generated for a given respiratory muscle activity is most likely due to the decrease in upper airway muscle activity that is associated with an increase in oropharyngeal resistance.

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Effect of mechanical loading on expiratory and inspiratory muscle activity during NREM sleep

Journal of Applied Physiology ◽

10.1152/jappl.1990.68.3.1195 ◽

1990 ◽

Vol 68 (3) ◽

pp. 1195-1202 ◽

Cited By ~ 33

Author(s):

M. S. Badr ◽

J. B. Skatrud ◽

J. A. Dempsey ◽

R. L. Begle

Keyword(s):

Steady State ◽

Minute Ventilation ◽

Nrem Sleep ◽

Abdominal Muscles ◽

Compensatory Response ◽

Load Compensation ◽

Resistive Loading ◽

Chemical Stimuli ◽

End Tidal ◽

End Tidal Co2

We investigated the effect of acute and sustained inspiratory resistive loading (IRL) on the activity of expiratory abdominal muscles (EMGab) and the diaphragm (EMGdi) and on ventilation during wakefulness and non-rapid-eye-movement (NREM) sleep in healthy subjects. EMGdi and EMGab were measured with esophageal and transcutaneous electrodes, respectively. During wakefulness, EMGdi increased in response to acute loading (18 cmH2O.l-1.s) (+23%); this was accompanied by preservation of tidal volume (VT) and minute ventilation (VE). During NREM sleep, no augmentation was noted in EMGdi or EMGab. Inspiratory time (TI) was prolonged (+5%), but this was not sufficient to prevent a decrease in both VT and VE (-21 and -20%, respectively). During sustained loading (12 cmH2O.l-1 s) in NREM sleep, control breaths (C) were compared with the steady-state loaded breaths (SS) defined by breaths 41-50. Steady-state IRL was associated with augmentation of EMGdi (12%) and EMGab (50%). VT returned to control levels, expiratory time shortened, and breathing frequency increased. The net result was the increase in VE above control levels (+5%, P less than 0.01). No change was noted in end-tidal CO2 or O2. We concluded that 1) wakefulness is a prerequisite for immediate load compensation (in its absence, TI prolongation is the only compensatory response) and 2) during sustained IRL, the augmentation of EMGdi and EMGab can lead to complete ventilatory recovery without measurable changes in chemical stimuli.

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Upper airway muscle responsiveness to rising Pco 2 during NREM sleep

Journal of Applied Physiology ◽

10.1152/jappl.2000.89.4.1275 ◽

2000 ◽

Vol 89 (4) ◽

pp. 1275-1282 ◽

Cited By ~ 41

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.

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Sequence of respiratory muscle activity during varied vocal attack

Speech Monographs ◽

10.1080/03637756509375451 ◽

1965 ◽

Vol 32 (2) ◽

pp. 185-191 ◽

Cited By ~ 11

Author(s):

Michael S. Hoshiko ◽

Kenneth W. Berger

Keyword(s):

Muscle Activity ◽

Respiratory Muscle ◽

Respiratory Muscle Activity

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Phasic Genioglossus and Palatoglossus Muscle Activity during Recovery from Sevoflurane Anesthesia

Anesthesiology ◽

10.1097/aln.0b013e318295a27b ◽

2013 ◽

Vol 119 (3) ◽

pp. 562-568 ◽

Cited By ~ 2

Author(s):

Ilavajady Srinivasan ◽

Samuel Strantzas ◽

Mark W. Crawford

Keyword(s):

Muscle Activity ◽

Upper Airway ◽

Dependent Manner ◽

Sevoflurane Anesthesia ◽

Phasic Activity ◽

Similar Dose ◽

Inhalational Anesthetic ◽

Recovery From Anesthesia ◽

End Tidal ◽

Dose Dependent

Abstract Background: Inhalational anesthetic effects on upper airway muscle activity in children are largely unknown. The authors tested the hypothesis that phasic inspiratory genioglossus and palatoglossus activity increases during recovery from sevoflurane anesthesia in a dose-dependent manner in children. Methods: Sixteen children, aged 2.0 to 6.9 yr, scheduled for elective urological surgery were studied. Electromyogram recordings were acquired using intramuscular needle electrodes during spontaneous ventilation. After a 15-min period of equilibration, electromyogram activity was recorded over 30 s at each of three end-tidal concentrations, 1.5, 1.0, and 0.5 minimum alveolar concentration (MAC), administered in sequence. Results: Phasic genioglossus activity was noted in four children at 1.5 MAC, five at 1.0 MAC, and six children at 0.5 MAC sevoflurane. Phasic palatoglossus activity was noted in 4 children at 1.5 MAC, 6 at 1.0 MAC, and 10 children at 0.5 MAC sevoflurane. Both the proportion of children exhibiting phasic activity, and the magnitude of phasic activity increased during recovery from anesthesia. For the genioglossus, decreasing the depth of sevoflurane anesthesia from 1.5 to 1.0 MAC increased phasic activity by approximately 35% and a further decrease to 0.5 MAC more than doubled activity (median [range] at 1.5 and 0.5 MAC: 2.7 μV [0 to 4.0 μV] and 8.6 μV [3.2 to 17.6], respectively; P = 0.029). A similar dose-related increase was recorded at the palatoglossus (P = 0.0002). Conclusions: Genioglossus and palatoglossus activity increases during recovery from sevoflurane anesthesia in a dose-dependent manner over the clinical range of sevoflurane concentrations in children.

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