Superior pharyngeal constrictor activation in obstructive sleep apnea.

Respiratory-related superior pharyngeal constrictor (SPC) muscle activity was determined in 18 obstructive sleep apnea (OSA) patients during wakefulness and sleep. Hooked-wire electrodes were implanted into the SPC muscle via a nasopharyngoscope. During quiet breathing in wakefulness, phasic expiratory SPC-muscle activity was consistently present in six subjects and intermittently present in 12 subjects, particularly following a swallow. The SPC muscle showed two patterns of activation during spontaneous obstructive apneic episodes in non-rapid-eye-movement (NREM) sleep: (1) activation during airway reopening, with or without waning phasic or tonic activation in the first half of the ensuing apnea (n = 13); and (2) absence of activation during apneas or arousals (n = 5). Activation on airway reopening following spontaneous apneas usually occurred on inspiration. When the apneic episodes were eliminated by application of nasal continuous positive airway pressure (CPAP), SPC-muscle activity was absent in NREM sleep in 16 subjects, but phasic expiratory activity persisted in two subjects. Sudden withdrawal of nasal CPAP in NREM sleep induced airway closure without a change in SPC-muscle activity. Arousal prior to or immediately after reapplication of nasal CPAP was associated with SPC-muscle activation during inspiration or expiration, and airway reopening. The results in OSA subjects indicate that SPC-muscle activation is similar to that of pharyngeal dilator muscles during spontaneous and induced apneas, and is not necessary to induce upper-airway closure during NREM sleep in OSA subjects.

Respiratory-related pharyngeal constrictor muscle activity in normal human adults.

Electromyographic activity of the superior, middle, and inferior pharyngeal constrictor (PC) muscles was examined in 10 normal adult humans during wakefulness and sleep. Wire electrodes were inserted close to the midline of the posterior pharyngeal wall at the level of the soft palate (superior PC), tip of the epiglottis (middle PC), and corniculate tubercle (inferior PC). In general, the three PC muscles exhibited similar patterns of activation. The PCs were activated during swallows, repetitive "pa" sounds, changes in head position, and the last portions of slow inspiratory and expiratory vital capacity maneuvers. Respiratory-related PC activity was infrequent during quiet breathing during wakefulness; variable and inconsistent phasic activation in expiration in one or more of the PCs was present in seven of the 10 subjects, particularly after a swallow. Progressive hyperoxic hypercapnia and progressive isocapnic hypoxia were associated with recruitment of phasic PC activity, which was predominantly expiratory; however, variable discharge patterns were observed within a given muscle and a given subject. When phasic PC activity was present, preactivation during late inspiration was frequently observed. PC activity was absent in NREM sleep and exhibited sporadic, nonrespiratory-related bursts of activity during REM sleep. Passively induced hypocapnic hyperventilation in NREM sleep was not associated with PC activation. The results indicate that the PCs have very similar patterns of activation and exhibit phasic expiratory activity during relatively high ventilatory output states in wakefulness.

Cricothyroid muscle activity during sleep in normal adult humans.

Previous investigators reported that cricothyroid (CT) muscle usually exhibits phasic inspiratory activity in normal adult humans during wakefulness. The purpose of this study was to determine respiratory-related CT activity in normal adult humans during sleep. Nighttime polysomnograms were performed in 16 subjects. Hooked-wire electrodes were percutaneously implanted in CT with 21-gauge needle-catheter unit that allowed artifact-free monopolar recordings during electrode placement. During wakefulness, CT was usually phasically active on inspiration, with tonic activity throughout the respiratory cycle. Phasic inspiratory activity was present throughout sleep in all subjects, even those without respiratory-related CT activity during wakefulness. Compared with non-rapid-eye-movement (NREM) sleep, phasic CT activity uniformly increased in rapid-eye-movement (REM) sleep. No differences were apparent in height of phasic CT activity between phasic and tonic REM sleep. Application of nasal continuous positive pressure in stage 3/4 NREM sleep was associated with a decrease in phasic CT activity. Passively induced hypocapnia with positive-pressure ventilation via a nose mask in stage 3/4 NREM sleep was associated with a disappearance of phasic CT activity. Cessation of positive-pressure ventilation under hypocapnic conditions frequently resulted in apnea. Phasic CT activity remained absent during apnea but reappeared coincident with or soon after resumption of spontaneous respiration. In summary, CT's phasic inspiratory activity and respiratory-related response to various stimuli during sleep were very similar to those of posterior cricoarytenoid muscle, the principal vocal cord abductor.

Effect of hypercapnia and hypoxia on arytenoideus muscle activity in normal adult humans.

The electrical activity of the arytenoideus muscle, a vocal cord adductor, was measured in 14 normal adult humans during progressive isocapnic hypoxia and progressive hyperoxic hypercapnia. Electromyograms of the arytenoideus were obtained with intramuscular hooked-wire electrodes implanted by means of a fiber-optic nasopharyngoscope. Correct placement of the electrodes was confirmed by discharge patterns during voluntary maneuvers. In three of the subjects, respiratory-related arytenoideus activity was not present during quiet breathing or chemical stimulation. During quiet breathing in the 11 other subjects, the arytenoideus exhibited phasic activity during expiration and usually tonic activity throughout the respiratory cycle. Phasic and tonic arytenoideus activity decreased under hypoxic and hypercapnic conditions. At higher levels of chemical stimulation in many subjects, short abrupt bursts of activity were frequently present at the transitions between inspiration and expiration. To determine the mechanical effect of the latter electromyographic findings, arytenoideus activity and fiber-optic images of the glottic aperture were simultaneously recorded in nine additional normal adult human subjects during progressive hyperoxic hypercapnia. The short abrupt bursts of arytenoideus activity were usually associated with a decrease in glottic aperture, although no change and an increase in glottic aperture were observed in individual subjects. The results suggest that the arytenoideus muscle may have an important role in the control of ventilation in normal human subjects.

Laryngeal response to passively induced hypocapnia during NREM sleep in normal adult humans.

Passively induced hypocapnia in animals activates vocal cord adductor muscles and decreases the glottic aperture. The purpose of this study was to determine if passively induced hypocapnia has similar effects in normal adult humans in stage 3/4 non-rapid-eye-movement (NREM) sleep. Hypocapnia was induced by hyperventilating the subjects with a positive-pressure ventilator via a nose mask. At hypocapnic levels below the CO2 apneic threshold, abrupt cessation of mechanical ventilation was followed by an apnea. In protocol 1, intramuscular electromyographic recordings of intrinsic laryngeal muscles were obtained in nine subjects. Activity of the posterior cricoarytenoid muscle, a vocal cord abductor, disappeared during passive hyperventilation. The muscle remained electrically silent during an apnea, but phasic inspiratory activity reappeared with the first respiratory effort. The thyroarytenoid and arytenoideus muscles, both vocal cord adductors, were electrically silent during spontaneous breathing in NREM sleep. Hypocapnia was frequently associated with activation of both adductor muscles. Once activated, the adductor muscles remained tonically active during an ensuring apnea. In protocol 2, a fiber-optic scope was advanced transnasally into the hypopharynx to determine glottic aperture size during passively induced hypocapnic apnea. In the seven subjects who achieved stable NREM sleep, the glottic aperture during an apnea was smaller than at any time throughout the respiratory cycle during spontaneous breathing just before positive-pressure ventilation. The results suggest that the decrease in glottic aperture observed during an induced hypocapnic apnea is due to suppression of the posterior cricoarytenoid muscle and/or activation of vocal cord adductor muscles.

Hypercarbic periodic breathing during sleep in a child with a central nervous system tumor.

A 4-yr-old girl with a ganglioglioma involving the cerebellum and pons presented with CO2 retention and arterial O2 desaturation during wakefulness and sleep. Despite the presence of a regular respiratory pattern during wakefulness, NREM sleep was associated with the appearance of a sustained periodic respiratory pattern characterized by clusters of usually two breaths separated by an 8 to 10-s expiratory pause. At sleep onset, this Biot's respiratory pattern appeared immediately after a sigh. Breathing frequency during NREM sleep became regular with administration of supplemental O2 and an attendant increase in end-tidal CO2. Shortly after withdrawal of supplemental O2 during NREM sleep, the periodic pattern resumed and was again immediately preceded by a sigh. The observations during NREM sleep in this patient with a central nervous system abnormality indicate that Biot's type respiratory pattern may be reversed by administration of supplemental oxygen. The results in this patient suggest: (1) the presence of a very elevated CO2 apnea threshold, and (2) that the pons may play a role in determining the effect of hypercapnic hypoxia on respiratory pattern during sleep.

Posterior cricoarytenoid muscle activity during wakefulness and sleep in normal adults.

Six normal adults were studied 1) to compare respiratory-related posterior cricoarytenoid (PCA) muscle activity during wakefulness and sleep and 2) to determine the effect of upper airway occlusions during non-rapid-eye-movement (NREM) sleep on PCA activity. A new electromyographic technique was developed to implant hooked-wire electrodes into the PCA by using a nasopharyngoscope. A previously described technique was used to induce upper airway occlusions during NREM sleep (Kuna and Smickley, J. Appl. Physiol. 64: 347-353, 1988). The PCA exhibited phasic inspiratory activity during quiet breathing in wakefulness and sleep in all subjects. Discounting changes in tonic activity, peak amplitude of PCA inspiratory activity during stage 3-4 NREM sleep decreased to 77% of its value in wakefulness. Tonic activity throughout the respiratory cycle was present in all subjects during wakefulness but was absent during state 3-4 NREM sleep. In this sleep stage, PCA phasic activity abruptly terminated near the end of inspiration. During nasal airway occlusions in NREM sleep, PCA phasic activity did not increase significantly during the first or second occluded effort. The results, in combination with recent findings for vocal cord adductors in awake and sleeping adults, suggest that vocal cord position during quiet breathing in wakefulness is actively controlled by simultaneously acting antagonistic intrinsic laryngeal muscles. In contrast, the return of the vocal cords toward the midline during expiration in stage 3-4 NREM sleep appears to be a passive phenomenon.

Intramuscular and esophageal electrode recordings of posterior cricoarytenoid activity in normal subjects.

Six normal human subjects were studied to compare intramuscular and esophageal electrode recordings of posterior cricoarytenoid (PCA) muscle activity. A new electromyographic technique was developed to implant hooked wire electrodes into the PCA via a nasopharyngoscope. The esophageal electrode was similar to that used by other investigators to record PCA activity (P. C. Kosch et al. J. Appl. Physiol. 64: 1968-1978, 1988). Simultaneous recordings from the intramuscular and esophageal electrodes were obtained during wakefulness and sleep. Changes in esophageal electrode activity were compared with changes in intramuscular electrode activity under four conditions: 1) voluntary maneuvers, 2) differences in state, 3) nasal airway occlusion during non-rapid-eye-movement sleep, and 4) spontaneous variations in respiratory efforts during non-rapid-eye-movement or rapid-eye-movement sleep. Although similar results were obtained from the esophageal and intramuscular electrodes, differences were present between the two recordings during both wakefulness and sleep. The esophageal electrode recorded activity from surrounding muscles during voluntary maneuvers, vocalization, and quiet breathing in wakefulness. Discrepancies between the two electrode recordings during sleep occurred under conditions of increased and decreased respiratory motor output. The data suggest that the esophageal electrode may not give an accurate assessment of PCA activity during many conditions in wakefulness and sleep.