Fluctuation inspiratory DAVID

in timing of upper airway and chest wall muscle activity in obstructive sleep apnea W. HUDGEL

AND

THERESA

HARASICK

Department of Medicine, Case Western Reserve University, Department and Critical Care Medicine, and Respiratory Sleep Disorders Laboratory, Cleveland Metropolitan General Hospital, Cleveland, Ohio 44109

HUDGEL, DAVID Mr., AND THERESA HARASICK. Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea. J. Appl. Physiol. 69(Z): 443450,1990.-An imbalance in the amplitude of electrical activity of the upper airway and chest wall inspiratory muscles is associated with both collapse and reopening of the upper airway in obstructive sleep apnea (OSA). The purpose of this study was to examine whether timing of the phasic activity of these inspiratory muscles also was associated with changes in upper airway caliber in OSA. We hypothesized that activation of upper airway muscle phasic electrical activity before activation of the chest wall pump muscles would help preserve upper airway patency. In contrast, we anticipated that the reversal of this pattern with delayed activation of upper airway inspiratory muscles would be associated with upper airway narrowing or collapse. Therefore the timing and amplitude of midline transmandibular and costal margin moving time average (MTA) electromyogram (EMG) signals were analyzed from 58 apnea cycles in stage 2 sleep in six OSA patients. In 86% of the postapnea breaths analyzed the upper airway MTA peak activity preceded the chest wall peak activity. In 86% of the obstructed respiratory efforts the upper airway MTA peak activity followed the chest wall peak activity. The onset of phasic electrical activity followed this same pattern. During inspiratory efforts when phasic inspiratory EMG amplitude did not change from preapnea to apnea, the timing changes noted above occurred. Even within breaths the relative timing of the upper airway and chest wall electrical activities was closely associated with changes in the pressure-flow relationship. We conclude that the relative timing of inspiratory activity of the upper airway and chest wall inspiratory muscles fluctuates during sleep in OSA. We speculate that the relative timing of upper airway and chest wall inspiratory muscle contraction contributes to the inspiratory caliber of the upper airway during sleep.

electromyogram;

pulmonary

mechanics

FLUCTUATIONS in the magnitude of the electrical activity of upper airway and chest wall inspiratory muscles exist during sleep in patients with obstructive sleep apnea (17). During the high-resistance preapneic breaths, there is a disproportionate breath-to-breath decrease in the magnitude of electromyographic (EMG) tonic and phasic activity of the inspiratory upper airway muscles relative to the activity of the diaphragm. Coexistent with the resolution of the apnea, there is a disproportionately large increase in the magnitude of the upper airway muscle electrical activity. Therefore, fluctuations in elec0161-7567/90

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of Pulmonary

Science

trical activity of the upper airway and chest wall inspiratory muscle groups appear to be important in determining the upper airway caliber in sleep apnea. Even in nonapneic subjects changes in upper airway caliber occur simultaneously with changes in the relative magnitude of the electrical activity of the upper airway muscles and diaphragm (6). In addition to the occurrence of differences in the magnitude of electrical activities of these two muscle groups, differences in timing of inspiratory activity also have been noted in previous studies. Van Lunteren et al. (22) and Strohl et al. (21) demonstrated that inspiratory activation of muscles surrounding the upper airway occurred earlier than activation of the diaphragm in animals and humans, respectively. Presumably this early activation of the upper airway muscles serves to stabilize the upper airway and, thereby, counterbalance the collapsing force exerted on the upper airway by chest wall inspiratory muscle contraction (1). Delay in upper airway inspiratory muscle contraction relative to that of the chest wall inspiratory muscles would likely predispose to upper airway narrowing or collapse during sleep. Therefore, we hypothesized that the electrical activity of the upper airway inspiratory muscles would precede that of the chest wall inspiratory muscles during the low-resistance postapnea breaths and would follow the chest wall activity during obstructive apneas. We also hypothesized that, in addition to the disproportionate fluctuations in the magnitude of the electrical activity between the upper airway and chest wall inspiratory muscles, fluctuations in the timing of inspiratory muscle activation also would be associated with upper airway collapse and reopening of the airway in obstructive sleep apnea. To address these hypotheses, we compared the relative timing as well as the magnitudes of the peak moving time average inspiratory phasic electrical activity of the upper airway and chest wall inspiratory muscles during obstructed and unobstructed respiratory efforts in stage 2 sleep of patients with obstructive sleep apnea. METHODS Subjects. Six male subjects with symptoms of heavy snoring and daytime hypersomnolence who had repetitive obstructive apneas, documented by nocturnal polysomnography, volunteered for this study. Subjects’ ages ranged from 30 to 64 yr [47 t 14 (SD) yr]. Body weight

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was 95 t 18 kg. Height was 173 t 11 cm. No patients were in heart failure or on medications. Inspirutory muscle electrical activity. Midline transmandibular (19) and chest wall surface EMG signals (13) were recorded. Grass cup electrodes, 1 cm in diameter, were placed in the midline near the apex of the chin and beneath and posterior to the mandible at the most anterior point where the submental muscles could be felt to contract during swallowing. In two patients fine-wire stainless steel electrodes also were inserted into the genioglossus muscle just posterior to the mandible in the floor of the mouth (19). Chest wall electrodes were placed in the right anterior axillary line in the sixth and seventh intercostal spaces. The EMG signals were amplified with a Disa preamplifier (model 15 C 01) with a band pass of 20 to 1,000 Hz and recorded on paper and magnetic tape. Data were entered into a PDP 11/23 computer from tape at a sampling rate of 500 Hz. First, the signals were passed through a band pass filter of 20-230 Hz. This filter eliminated the majority of electrical cardiac activity and high-frequency noise. A moving time average (MTA) signal with a time constant of 300 ms was obtained. To precisely identify peak activity within a single phasic inspiratory EMG burst, a low-pass filter, 0.5 Hz, was applied to the MTA. Each EMG signal was treated identically with these procedures. Airwuy pressure-flow measurements. A 30.cm piece of tubing (1‘5 mm ID) was used for hypopharyngeal pressure measurement, The distal end was sealed with nontoxic glue, and eight l7-gauge holes were placed along the distal 1 cm. The proximal end of the catheter was connected to a Validyne transducer (model MP45, t 100 cmHzO). Tubing of identical length was placed on the other port of the differential transducer. To prevent airway secretions from plugging the catheter, a bias flow of compressed air at 0.1 l/min was passed through the catheter. With the bias flow running, the pharyngeal catheter had a 90-100% decay time of 0.075 s. No decrease in peak-to-peak amplitude of a sine wave signal recorded from the pharyngeal catheter occurred below 1 Hz. The pharyngeal catheter, with its bias flow running, and pneumotachograph signals were brought into phase by adjustment of tubing length connecting the pneumotachograph and its differential pressure transducer [Validyne model MP 45 t 5 cmHnO (6,17)]. The phase angle between pressure signals and flow was 2” at 1 Hz and 6.5O at 3 Hz. The pneumotachograph detected inspiratory flow through tubing connected to a Hans Rudolph threeway valve (model 1400). The three-way valve was attached to a facemask that was sealed around the nose and mouth. The dead space of the mask and three-way valve varied because of face configuration. The resistance of this inspiratory circuit was 0.25 cmHsO g1-l. s at 1.0 l/ s flow. A Grass recorder (model 7) was used for recordings with the one-half frequency high filter set at 35 Hz for pressure and flow signals. Analysis. Sleep stages were determined by standard criteria (16). An obstructive apnea was present when inspiratory phasic chest wall electrical activity persisted without inspiratory airflow for 3 10 s. A hypopnea existed if peak flow was decreased at least 50% from that

TIMING

IN

SLEEP

APNEA

recorded in the prehypopnea breaths with continued chest wall phasic activity during inspiration. An apnea or hypopnea cycle consisted of an obstructed apnea or hypopnea and the breaths immediately before those following the last apnea. Upper airway resistance was calculated from the pressure-flow relationship at peak inspiratory pressure for each breath within the apnea or hypopnea cycle. Resistance at peak pressure was used so that resistance values could be related to peak MTA EMG data. The peak amplitudes of chest wall and chin MTA EMG signals were measured in millimeters deflection from a base line drawn at the lowest end-expiratory level of a segment of consecutive apneic cycles. Peak MTA amplitude occurred during phasic inspiratory activity of the muscles; however, the deflection measured was comprised of both tonic and phasic inspiratory EMG activity. Timing of upper airway and chest wall EMG signals was determined as follows. Analysis was made on apnea and hypopnea cycles: the postapneic and subsequent apneic ventilatory efforts. For each apnea or hypopnea cycle analyzed, three totally obstructed breaths or hypopneic breaths with the highest resistances and the three postapneic breaths with the lowest resistances were analyzed for timing. The time interval between the upper airway and chest wall EMG MTA peak activities was measured for each of these breaths. Values for each threebreath sample were averaged. The net change in time of the MTA peak activity from the postapneic (or hyperpneic) unobstructed to the next series of obstructed breaths was calculated for each apnea cycle. Average amplitudes of activity for each of these three-breath samples were also calculated in the same manner, and comparisons were made postapnea during the subsequent apnea. To obtain a qualitative assessment of the interaction between the relative changes in inspiratory muscle electrical timing and amplitude and the pressure-flow relationship, analysis was done comparing plots of upper airway vs. chest wall MTA electrical activity with plots of flow vs. pressure on several individual breaths of varying resistance. In this way, we were able to examine the relationship between changes in both timing and amplitude of the upper airway and chest wall EMG signals and the mechanical properties of the upper airway. RESULTS

Timing of phasic inspiratory muscle electrical activity. An example of the fluctuations in inspiratory muscle timing that were observed between the postapneic unobstructed and apneic breaths can be seen in raw EMG signals presented in Fig. 1. For the whole group the MTA peak activity of the upper airway EMG signal preceded the chest wall MTA peak activity in 50 of 58 (86%) of the postapnea unobstructed breaths within apnea cycles analyzed. The time interval between the two EMG peaks was 0.34 t 0.08 (SE) s. In the remaining 14% of these breaths one of two patterns existed. Either the peak activities of the two EMG signals occurred simultaneously or the chest wall MTA peak activity led the upper

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Fluctuation in timing of upper airway and chest wall inspiratory muscle activity in obstructive sleep apnea.

An imbalance in the amplitude of electrical activity of the upper airway and chest wall inspiratory muscles is associated with both collapse and reope...
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