Upper airway closing pressures in snorers

1984 ◽  
Vol 57 (2) ◽  
pp. 528-535 ◽  
Author(s):  
F. G. Issa ◽  
C. E. Sullivan
Keyword(s):  
Eye Movement ◽  
Alcohol Intake ◽  
Upper Airway ◽  
Clinical Severity ◽  
Dependent Manner ◽  
Airway Closure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Group A ◽  
Group B

We studied 14 subjects who were selected to represent the broad range of severity of snoring: group A, four subjects who gave a history of snoring only when provoked by nasal obstruction or alcohol intake; group B, six subjects who typically snored for long periods each night; and group C, four subjects who snored heavily all night and who typically experienced a few episodes of obstructive apnea (mean apnea index 4 apneas/h). Low levels of nasal continuous positive airway pressure (CPAP) (range, 2.0–6.0 cmH2O; mean, 4.0 cmH2O) prevented snoring. Nasal occlusion caused upper airway closure during inspiratory efforts in all 14 subjects. There was a relationship between the clinical severity of snoring and the upper airway closing pressure (UACP). Upper airway closure occurred at greater suction pressures in group A than in group C but there was overlap between the three categories. The upper airway was consistently more collapsible in rapid-eye-movement sleep than in non-rapid-eye-movement sleep. There was little evidence of breath-by-breath improvement of upper airway stability during sustained asphyxia, the UACP remaining constant despite marked increases in drive to the diaphragm. In five subjects UACP was measured following alcohol intake. Alcohol reduced upper airway stability in all subjects in a dose-dependent manner.

An induced blood pressure rise does not alter upper airway resistance in sleeping humans

1998 ◽  
Vol 84 (1) ◽  
pp. 269-276 ◽  
Author(s):  
Christine R. Wilson ◽  
Shalini Manchanda ◽  
David Crabtree ◽  
James B. Skatrud ◽  
Jerome A. Dempsey
Keyword(s):  
Blood Pressure ◽  
Arterial Pressure ◽  
Eye Movement ◽  
Airway Resistance ◽  
Pressure Rise ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Upper Airway Resistance ◽  
Blood Pressure Rise

Wilson, Christine R., Shalini Manchanda, David Crabtree, James B. Skatrud, and Jerome A. Dempsey. An induced blood pressure rise does not alter upper airway resistance in sleeping humans. J. Appl. Physiol. 84(1): 269–276, 1998.—Sleep apnea is associated with episodic increases in systemic blood pressure. We investigated whether transient increases in arterial pressure altered upper airway resistance and/or breathing pattern in nine sleeping humans (snorers and nonsnorers). A pressure-tipped catheter was placed below the base of the tongue, and flow was measured from a nose or face mask. During non-rapid-eye-movement sleep, we injected 40- to 200-μg iv boluses of phenylephrine. Parasympathetic blockade was used if bradycardia was excessive. Mean arterial pressure (MAP) rose by 20 ± 5 (mean ± SD) mmHg (range 12–37 mmHg) within 12 s and remained elevated for 105 s. There were no significant changes in inspiratory or expiratory pharyngeal resistance (measured at peak flow, peak pressure, 0.2 l/s or by evaluating the dynamic pressure-flow relationship). At peak MAP, end-tidal CO2 pressure fell by 1.5 Torr and remained low for 20–25 s. At 26 s after peak MAP, tidal volume fell by 19%, consistent with hypocapnic ventilatory inhibition. We conclude that transient increases in MAP of a magnitude commonly observed during non-rapid-eye-movement sleep-disordered breathing do not increase upper airway resistance and, therefore, will not perpetuate subsequent obstructive events.

Influence of sleep on tensor palatini EMG and upper airway resistance in normal men

1991 ◽  
Vol 70 (6) ◽  
pp. 2574-2581 ◽  
Author(s):  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Airway Resistance ◽  
Sleep Stage ◽  
Upper Airway ◽  
Sleep Stages ◽  
Normal Male ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Narrowing ◽  
Upper Airway Resistance

We propose that a sleep-induced decrement in the activity of the tensor palatini (TP) muscle could induce airway narrowing in the area posterior to the soft palate and therefore lead to an increase in upper airway resistance in normal subjects. We investigated the TP to determine the influence of sleep on TP muscle activity and the relationship between changing TP activity and upper airway resistance over the entire night and during short sleep-awake transitions. Seven normal male subjects were studied on a single night with wire electrodes placed in both TP muscles. Sleep stage, inspiratory airflow, transpalatal pressure, and TP moving time average electromyogram (EMG) were continuously recorded. In addition, in two of the seven subjects the activity (EMG) of both the TP and the genioglossus muscle simultaneously was recorded throughout the night. Upper airway resistance increased progressively from wakefulness through the various non-rapid-eye-movement sleep stages, as has been previously described. The TP EMG did not commonly demonstrate phasic activity during wakefulness or sleep. However, the tonic EMG decreased progressively and significantly (P less than 0.05) from wakefulness through the non-rapid-eye-movement sleep stages [awake, 4.6 +/- 0.3 (SE) arbitrary units; stage 1, 2.6 +/- 0.3; stage 2, 1.7 +/- 0.5; stage 3/4, 1.5 +/- 0.8]. The mean correlation coefficient between TP EMG and upper airway resistance across all sleep states was (-0.46). This mean correlation improved over discrete sleep-awake transitions (-0.76). No sleep-induced decrement in the genioglossus activity was observed in the two subjects studied.(ABSTRACT TRUNCATED AT 250 WORDS)

Upper Airway Dilating Muscle Hyperactivity during Non-Rapid Eye Movement Sleep in English Bulldogs

1993 ◽  
Vol 148 (1) ◽  
pp. 185-194 ◽  
Author(s):  
Joan C. Hendricks ◽  
Basil J. Petrof ◽  
Karen Panckeri ◽  
Allan I. Pack
Keyword(s):  
Eye Movement ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep

Influence of sleep on response to negative airway pressure of tensor palatini muscle and retropalatal airway

1993 ◽  
Vol 75 (5) ◽  
pp. 2117-2124 ◽  
Author(s):  
J. R. Wheatley ◽  
D. J. Tangel ◽  
W. S. Mezzanotte ◽  
D. P. White
Keyword(s):  
Eye Movement ◽  
Negative Pressure ◽  
Upper Airway ◽  
Normal Subjects ◽  
Rapid Onset ◽  
Reflex Response ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Narrowing ◽  
Airway Collapse

Increased retropalatal airway resistance may be caused by a sleep-induced loss of palatal muscle activity and a diminished ability of these muscles to respond to the increasing intrapharyngeal negative pressure that develops during sleep. To investigate these possibilities, in six normal subjects, we determined the effect of non-rapid-eye-movement sleep on 1) the tensor palatini (TP) electromyogram (EMG) response to rapid-onset negative-pressure generations (NPG) in the upper airway and 2) the collapsibility of the retropalatal airway during these NPGs. During wakefulness, the change in TP EMG from basal to peak levels (during NPG) was 19.8 +/- 3.2 arbitrary units (P < 0.005). This was markedly reduced during sleep (3.6 +/- 1.5 arbitrary units; P < 0.001). The latency of the TP EMG response was 48.5 +/- 5.6 ms during wakefulness but was prolonged during sleep (105.0 +/- 12.2 ms; P < 0.02). The peak transpalatal pressure during NPG (a measure of airway collapse) was 2.1 +/- 0.7 cmH2O during wakefulness and increased to 5.3 +/- 0.8 cmH2O during sleep (P < 0.05). We conclude that the brisk reflex response of the TP muscle to negative pressure during wakefulness is markedly reduced during non-rapid-eye-movement sleep, in association with a more collapsible retropalatal airway. We speculate that the reduction in this TP reflex response contributes to retropalatal airway narrowing during sleep in normal subjects.

Effect of Sleep State and Position on the Incidence of Obstructive and Central Apnea in Infants

PEDIATRICS ◽  
1985 ◽  
Vol 75 (5) ◽  
pp. 832-835
Author(s):  
William C. Orr ◽  
Monte L. Stahl ◽  
James Duke ◽  
Mary Anne McCaffree ◽  
Paul Toubas ◽  
...  
Keyword(s):  
Eye Movement ◽  
Supine Position ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Central Apnea ◽  
Rapid Eye Movement Sleep ◽  
Sleep State ◽  
Sleeping Position ◽  
History Of ◽  
Spontaneous Occurrence

Sixty-four infants with a history of apnea were studied to determine the effects of sleeping position and sleep state (rapid eye movement [REM]) v (nonrapid eye movement [NREM]) on the occurrence of central and obstructive apneas. All-night polysomnographic studies were conducted on each infant, and the spontaneous occurrence of central and obstructive apneic events was determined in the prone, supine, and side positions. Sleeping position did not significantly affect the rate or duration of central or obstructive apneas. Furthermore, neither central nor obstructive apneic episodes were significantly altered by sleep state. These data suggest that, in spite of an ostensible predisposition to upper airway obstruction in the supine position and during rapid eye movement sleep, neither sleeping position nor sleep state appears to affect the rate of duration of apneic events.

scholarly journals Chronic recordings of hypoglossal nerve activity in a dog model of upper airway obstruction

1999 ◽  
Vol 87 (6) ◽  
pp. 2197-2206 ◽  
Author(s):  
Mesut Sahin ◽  
Dominique M. Durand ◽  
Musa A. Haxhiu
Keyword(s):  
Eye Movement ◽  
Hypoglossal Nerve ◽  
Upper Airway ◽  
Esophageal Pressure ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Inspiratory Time ◽  
Pharyngeal Airway ◽  
Baseline Noise ◽  
Cuff Electrodes

The activity of the hypoglossal nerve was recorded during pharyngeal loading in sleeping dogs with chronically implanted cuff electrodes. Three self-coiling spiral-cuff electrodes were implanted in two beagles for durations of 17, 7, and 6 mo. During quiet wakefulness and sleep, phasic hypoglossal activity was either very small or not observable above the baseline noise. Applying a perpendicular force on the submental region by using a mechanical device to narrow the pharyngeal airway passage increased the phasic hypoglossal activity, the phasic esophageal pressure, and the inspiratory time in the next breath during non-rapid-eye-movement sleep. The phasic hypoglossal activity sustained at the elevated level while the force was present and increased with increasing amounts of loading. The hypoglossal nerve was very active in rapid-eye-movement sleep, especially when the submental force was present. The data demonstrate the feasibility of chronic recordings of the hypoglossal nerve with cuff electrodes and show that hypoglossal activity has a fast and sustained response to the internal loading of the pharynx induced by applying a submental force during non-rapid-eye-movement sleep.

scholarly journals Pentobarbital Dose-dependently Increases Respiratory Genioglossus Muscle Activity while Impairing Diaphragmatic Function in Anesthetized Rats

2009 ◽  
Vol 110 (6) ◽  
pp. 1327-1334 ◽  
Author(s):  
Matthias Eikermann ◽  
Philipp Fassbender ◽  
Sebastian Zaremba ◽  
Amy S. Jordan ◽  
Carl Rosow ◽  
...  
Keyword(s):  
Eye Movement ◽  
Muscle Activity ◽  
Upper Airway ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Natural Sleep ◽  
Pentobarbital Anesthesia ◽  
Diaphragmatic Function ◽  
Dose Dependent Decrease ◽  
Dose Dependent

Background Anesthetics depress both ventilatory and upper airway dilator muscle activity and thus put the upper airway at risk for collapse. However, these effects are agent-dependent and may involve upper airway and diaphragm muscles to varying degrees. The authors assessed the effects of pentobarbital on upper airway dilator and respiratory pump muscle function in rats and compared these results with the effects of normal sleep. Methods Tracheostomized rats were given increasing doses of pentobarbital to produce deep sedation then light and deep anesthesia, and negative pressure airway stimuli were applied (n = 11). To compare the effects of pentobarbital with those of natural sleep, the authors chronically instrumented rats (n = 10) with genioglossus and neck electromyogram and electroencephalogram electrodes and compared genioglossus activity during wakefulness, sleep (rapid eye movement and non-rapid eye movement), and pentobarbital anesthesia. Results Pentobarbital caused a dose-dependent decrease in ventilation and in phasic diaphragmatic electromyogram by 11 +/- 0.1%, but it increased phasic genioglossus electromyogram by 23 +/- 0.2%. Natural non-rapid eye movement sleep and pentobarbital anesthesia (10 mg/kg intraperitoneally) decreased respiratory genioglossus electromyogram by 61 +/- 29% and 45 +/- 35%, respectively, and natural rapid eye movement sleep caused the greatest decrease in phasic genioglossus electromyogram (95 +/- 0.3%). Conclusions Pentobarbital in rats impairs respiratory genioglossus activity compared to the awake state, but the decrease is no greater than seen during natural sleep. During anesthesia, in the absence of pharyngeal airflow, phasic genioglossus activity is increased in a dose-dependent fashion.

Upper airway and respiratory muscle responses to continuous negative airway pressure

1989 ◽  
Vol 66 (3) ◽  
pp. 1373-1382 ◽  
Author(s):  
R. M. Aronson ◽  
E. Onal ◽  
D. W. Carley ◽  
M. Lopata
Keyword(s):  
Eye Movement ◽  
Airway Pressure ◽  
Minute Ventilation ◽  
Upper Airway ◽  
Normal Subjects ◽  
Rapid Eye Movement ◽  
Rapid Eye Movement Sleep ◽  
Airway Patency ◽  
Negative Airway Pressure ◽  
Muscle Responses

To determine upper airway and respiratory muscle responses to nasal continuous negative airway pressure (CNAP), we quantitated the changes in diaphragmatic and genioglossal electromyographic activity, inspiratory duration, tidal volume, minute ventilation, and end-expiratory lung volume (EEL) during CNAP in six normal subjects during wakefulness and five during sleep. During wakefulness, CNAP resulted in immediate increases in electromyographic diaphragmatic and genioglossal muscle activity, and inspiratory duration, preserved or increased tidal volume and minute ventilation, and decreased EEL. During non-rapid-eye-movement and rapid-eye-movement sleep, CNAP was associated with no immediate muscle or timing responses, incomplete or complete upper airway occlusion, and decreased EEL. Progressive diaphragmatic and genioglossal responses were observed during non-rapid-eye-movement sleep in association with arterial O2 desaturation, but airway patency was not reestablished until further increases occurred with arousal. These results indicate that normal subjects, while awake, can fully compensate for CNAP by increasing respiratory and upper airway muscle activities but are unable to do so during sleep in the absence of arousal. This sleep-induced failure of load compensation predisposes the airways to collapse under conditions which threaten airway patency during sleep. The abrupt electromyogram responses seen during wakefulness and arousal are indicative of the importance of state effects, whereas the gradual increases seen during sleep probably reflect responses to changing blood gas composition.

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