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(Chest. 2001;120:390-396.)
© 2001 American College of Chest Physicians

Abdominal Muscle Activity in Sleep Apnea During Continuous Positive Airway Pressure Titration*

Frédéric Lofaso, MD, PhD; Marie Pia d’Ortho, MD, PhD; Redouane Fodil, PhD; Christophe Delclaux, MD, PhD; Alain Harf, MD, PhD and Anne Marie Lorino, PhD

* From the Service de Physiologie, Explorations Fonctionnelles, Institut National de la Santé et de la Recherche Médicale, Créteil, France.

Correspondence to: Frédéric Lofaso, MD, PhD, Service de Physiologie, Explorations Fonctionnelles, Hôpital Raymond Poincaré, 92380 Garches, France; e-mail: f.lofaso{at}rpc.ap-hop-paris.fr


   Abstract
TOP
 Abstract
Introduction
 Materials and Methods
 Results
 Discussion
 References
 
Study objectives: The aim of this study was to investigate whether presence of expiratory abdominal muscle activity (EAMA) in obstructive sleep apnea syndrome (OSAS) patients during nasal continuous positive airway pressure (nCPAP) is due to either nCPAP overprescription or nCPAP underprescription.

Design: Airflow, esophageal pressure (Pes), and gastric pressure (Pga) were routinely measured during polysomnography aimed at determining the optimal nCPAP level, and the magnitude of EAMA was evaluated in relation to the nCPAP level and to the conventional indexes of upper-airway obstruction used during nCPAP titration.

Patients: The study was performed 12 patients with OSAS.

Results: Six patients displayed sustained EAMA, ie, EAMA lasting > 3 min, and characterized by a decrease in abdominal diameter and a paradoxical rise in Pga during expiration. In all six patients, EAMA decreased gradually as nCPAP neared optimal levels, and then disappeared when the optimal nCPAP level was achieved. The decrease in EAMA as nCPAP increased was associated with an increase in minute ventilation, decreases in both inspiratory and expiratory resistance, a decrease in Pes swing, and the normalization of the inspiratory flow contour.

Conclusions: We conclude that the EAMA observed in some OSAS patients might be an indirect marker of upper-airway obstruction, and that the presence of EAMA during nCPAP titration might indicate a suboptimal nCPAP level rather than a deleterious effect of nCPAP.

Key Words: expiratory resistance • nCPAP • OSAS


   Introduction
TOP
 Abstract
 Introduction
Materials and Methods
 Results
 Discussion
 References
 
Nasal continuous positive airway pressure (nCPAP), which was introduced in 1981 by Sullivan et al,1 has considerably improved the treatment and prognosis of patients with obstructive sleep apnea syndrome (OSAS).1 In practice, the optimal nCPAP level is a trade-off between pressure-related side effects and efficacy in preventing upper-airway obstruction during sleep. This optimal level is generally determined during an overnight study. We noted that the overnight studies in some patients showed prolonged periods of expiratory abdominal muscle activity (EAMA). The mechanism of this EAMA was obscure, so that it was unclear whether the level of nCPAP needed to be increased or decreased. Indeed, EAMA can be due either to hyperinflation induced by nCPAP overprescription, as shown by studies2 3 4 5 6 in which high levels of nCPAP induced EAMA in healthy awake subjects, or to persistent airway obstruction resulting from nCPAP underprescription, as indicated by reports7 8 9 10 11 that increasing upper-airway resistance during sleep in snorers and patients with OSAS can induce expiratory activity. To determine whether EAMA was due to nCPAP overprescription or underprescription, we studied the level of EAMA in relation to the level of nCPAP and to conventional indexes of upper-airway obstruction used for nCPAP titration.


   Materials and Methods
TOP
 Abstract
 Introduction
 Materials and Methods
Results
 Discussion
 References
 
Patients
This study was approved by our institutional review board. Patients with OSAS scheduled for nCPAP titration during an overnight polysomnography study were included. All patients gave informed consent to their participation in the study.

The overnight polysomnography study included EEG (C4-A1, C3-A2), electro-oculography, chin electromyography, thoracic and abdominal movement assessment by uncalibrated inductive plethysmography (Respitrace; Ambulatory Monitoring; Ardsley, NY), and arterial pulse oximetry (Nellcor BS; Nellcor; Hayward, CA). During the study night, oronasal airflow was quantified using a tightly fitting nasal mask and a Fleisch No. 2 pneumotachograph (Fleisch; Lausanne, Switzerland) connected to a differential pressure transducer (Validyne MP 45 ± 5 cm H2O; Validyne Engineering; Northridge, CA). Nasal mask pressure was measured using a differential pressure transducer (Validyne MP 45 ± 35 cm H2O; Validyne Engineering). The mask and the pneumotachograph were maintained by a crosspiece, which also kept the patient in the supine position.

In addition, gastric pressure (Pga) and esophageal pressure (Pes) were measured using a probe equipped with two piezo-electric sensors (Gaeltec S7B/2; Gaeltec Ltd; Dunvegan, Isle of Skye, Scotland). We evaluated the frequency response of these piezo-electric sensors and observed that no change in signal amplitude or phase lag occurred up to frequencies as high as 10 Hz. The probe was inserted through a nostril and advanced until the distal sensor was in the stomach and the proximal sensor in the lower third of the esophagus. Appropriate placement of the esophageal sensor was verified with an occlusion test. Proper placement of the gastric transducer was verified based on the finding of Pga fluctuations when gentle pressure was applied to the subject’s stomach and on the absence on the Pga trace of the sharp Pes increase due to esophageal contraction when the subject was asked to drink water. All signals were recorded using a 14-channel paper recorder EEG (Nihon Kohden; Tokyo, Japan), digitized at 128 Hz, and sampled using an analog-to-digital system (MP100; Biopac Systems; Goleta, CA) for subsequent analysis.

nCPAP Titration Protocol
nCPAP was applied through a small, tightly fitting nasal mask. nCPAP was increased from the lowest value preventing rebreathing (4 cm H2O), in increments of 1 cmH2O, up to the level at which three conditions were fulfilled: (1) no apnea, hypopnea, or snoring; (2) no inspiratory flow limitation, ie, no plateau on the nasal inspiratory flow signal; and (3) Pes swing ({Delta}Pes) [{Delta}Pes amplitude not more than 1.5-fold the baseline value during wakefulness].12 The nCPAP level was decreased at the request of the patient on awakening. Each nCPAP step lasted at least 3 min. Generally, as previously described,13 the effective pressure was reached within 1 h of sleep onset, although adjustments were occasionally made later in the night.

Data Analysis
Sustained EAMA was evaluated as previously described with6 and without CPAP treatment14 15 16 based on Pga and abdominal cross-section area changes. On the Pga trace, we measured the decrease from the maximal end-expiratory level to the minimal value (gastric pressure increase during the expiratory phase [{Delta}Pga]). Figure 1 illustrates this measurement in a representative patient breathing at 10 cm H2O of nCPAP. In this patient, relaxation of the diaphragm during early expiration resulted in a fall in Pga and in a decrease in abdominal cross-sectional area. After this early expiratory phase, Pga increased until the end of the expiration, whereas abdominal cross-sectional area continued to decrease. From the end-expiratory value, Pga dropped ({Delta}Pga), whereas the abdominal cross-sectional area increased. This pattern clearly indicates EAMA, and we used the {Delta}Pga of the breathing cycle as an index of the direct mechanical effect of EAMA. We considered that EAMA was clinically significant when {Delta}Pga remained > 2 cm H2O for at least 3 min. Global respiratory effort was evaluated as the amplitude of the {Delta}Pes.



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  		Figure 1. Polygraph recording in a representative subject breathing at a 10 cm H2O nCPAP level (airway pressure [Paw]), showing changes in respiratory flow, Pes, Pga, thoracic movements (CW), and abdominal movements (AB). The {Delta}Pga is also indicated. I = inspiratory phase; E = expiratory phase.

 
Airway/lung resistance was evaluated for each breath according to the formula based on the technique of Mead and Whittenberger17 : R airway/lung = ([P0 - Pes] - [V/C])/, where is the instantaneous airflow, V is the instantaneous volume calculated as the time integral of , P0 is the Pes value at the beginning of inspiration, and C is the dynamic lung compliance calculated as the ratio of tidal volume over the Pes difference between the beginning and the end of inspiration. Mean values throughout inspiration and expiration were used as estimates of inspiratory and expiratory airway/lung resistance, respectively.

Inspiratory flow contour was analyzed qualitatively by two observers according to the criteria proposed by Montserrat et al.18 Disagreements in interpretation were resolved by consensus. A flow score was calculated and expressed as an integer variable varying from 1 (no limitation) to 3 (severe limitation).

Statistics
Data are given as means ± SDs. Comparisons between groups were performed using the Mann-Whitney test. Comparisons between the nCPAP level at which apneas disappeared and the optimal nCPAP level were performed using the Wilcoxon test. The level of significance was set at 5%.


   Results
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
Discussion
 References
 
From January to June 1999, 16 OSAS patients underwent nCPAP titration. Of these 16 patients, 2 patients declined to participate in the study and 2 other patients had a technical failure of Pes measurement. Compared to the 12 OSAS patients who were successfully investigated, these 4 patients had a similar mean apnea/hypopnea index (AHI) but were older (all 4 patients were > 60 years old).

Of the 12 patients studied, only 6 patients displayed sustained EAMA. These six patients did not differ from the 6 other patients in terms of age (57 ± 7 years vs 53 ± 11 years), body mass index (BMI; 31 ± 3 kg/m2 vs 32 ± 6 kg/m2), or AHI (56 ± 29 events per hour vs 51 ± 21 events per hour), respectively. Of the six patients with sustained EAMA, three patients had lung function testing evidence of airway or lung disease (Table 1 ) and three patients did not. In the six patients without sustained EAMA, no evidence of airway or lung disease was observed. In addition, when we analyzed the pattern of breathing of both of these populations during wakefulness and, more particularly, when we tried to detect belly breathing by calculating the Gilbert index, defined as the ratio of the Pga increase during inspiration to the transdiaphragmatic pressure,19 we observed no significant difference between the patients who presented with EAMA and those who did not (0.20 ± 0.03 vs 0.19 ± 0.04).


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  		Table 1. Characteristics of the Six Studied Patients With OSAS *

 
In the six patients who displayed sustained EAMA, apneas disappeared at nCPAP levels between 5 cm H2O and 10 cm H2O (Fig 2 ). At these nCPAP levels, sustained EAMA was present in all six patients, with {Delta}Pga values ranging from 2.2 to 10.5 cm H2O (mean ± SD, 6.1 ± 3.4 cm H2O; Fig 2 ). Interestingly, as shown in Figure 2 , {Delta}Pga decreased gradually in all six patients as the nCPAP level increased, and disappeared after an increase in nCPAP of 3 cm H2O in four patients and 4 cm H2O in two patients. An example of the {Delta}Pga decrease as nCPAP increased is presented in Figure 3 . The nCPAP level at which EAMA disappeared was equal to the effective nCPAP that abolished sustained high inspiratory effort in three patients and was lower than the effective nCPAP in the other three patients.



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  		Figure 2. Relationships between the {Delta}Pga and the minute ventilation (VE) increase to nCPAP level in the six patients with EAMA.

 


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  		Figure 3. Representative tracing of respiratory variables from a patient with OSAS during nCPAP titration, showing Pes (Peso), Pga, thoracic movements (CW), and abdominal movements (AB). Note the rapid decrease in {Delta}Pga after a small (1 cm H2O) increase in nCPAP, and the simultaneous decrease in Pes swing.

 
It is worth noting that the decrease observed in EAMA as nCPAP increased was associated with (1) a significant increase in minute ventilation (from 7.3 ± 2.1 to 10.3 ± 2.1 L/min, p < 0.03; Fig 2 ); (2) a significant decrease in both inspiratory resistance (from 74 ± 52 to 13 ± 5 cm H2O/L/s, p < 0.03) and expiratory resistance (from 80 ± 56 to 14 ± 3 cm H2O/L/s, p < 0.03; Fig 4 ); (3) a significant decrease in {Delta}Pes (from 43 ± 23 to 15 ± 3 cmH2O, p < 0.03); and (4) a significant decrease in flow score (from 2.7 ± 0.5 to 1.3 ± 0.5, p < 0.04; Fig 4 ).



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  		Figure 4. Relationships of {Delta}Pga to {Delta}Pes, inspiratory flow score, expiratory resistance, and inspiratory resistance.

 

   Discussion
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
References
 
Many physiologic abnormalities occur during sleep apnea; consequently, a choice has to be made among the various physiologic variables to be studied. As the clinical aim of nCPAP titration was to determine the pressure level that ensured upper-airway patency, we elected to study the physiologic parameters that are currently used as direct or indirect indexes of upper-airway obstruction, namely inspiratory resistance, expiratory resistance, flow contour, and {Delta}Pes.

Simultaneous analysis of these parameters allowed us to demonstrate that sustained EAMA was associated with upper-airway obstruction and gradually disappeared as nCPAP neared its optimal level, ie, as upper-airway obstruction was abolished. This strongly suggests that EAMA is also an indirect marker of upper-airway obstruction in patients with OSAS during nCPAP titration.

To our knowledge, this is the first study that investigates expiratory effort in sleeping OSAS patients during nCPAP titration, and demonstrates that sustained EAMA occurs in some of them as long as the optimal nCPAP level is not reached. As shown by the similar values of the Gilbert index19 in both groups of patients, the inspiratory breathing pattern during wakefulness, and more particularly the differences between abdominal and chest-wall excursions during waking inspiration, did not allow us to predict the presence of EAMA in OSAS patients during nCPAP titration.

We observed a gradual decrease in EAMA as the nCPAP level increased. It follows that the EAMA observed in our study has a different physiologic meaning from the EAMA during nCPAP reported in previous studies.2 3 4 5 6 Indeed, in these studies, high nCPAP levels were associated with lung hyperinflation,2 3 4 5 6 which the subjects tried to overcome by increasing the expiratory activity of their abdominal muscles.2 4 6

Interestingly, the EAMA observed in our study was consistently associated with an increase in airway resistance during both inspiration and expiration, and decreased gradually as airway resistance also decreased during nCPAP titration. Previous studies12 20 21 22 23 24 have demonstrated that upper-airway narrowing can occur in OSAS patients, snorers, and normal subjects, not only during inspiration but also during expiration. Models using collapsible tubes do not explain this increase in expiratory airway resistance during sleep. The effect of gravity on upper-airway structures,25 together with relaxation of pharyngeal dilator muscles such as the tensor palatini and the genioglossus,26 may conceivably promote local upper-airway narrowing during expiration. We recently developed a model consisting of a series of individualized mass-spring components, each with its own compliance designed to reflect local differences in anatomic and physiologic properties across pharyngeal regions. When we applied gravity and Bernoulli’s laws to this model, we observed upper-airway obstruction during inspiration associated with segmental narrowing of the upper airway.27 We also tested this model during expiration and observed that, in contrast to the Starling resistor model, it could also explain expiratory obstruction.24

EAMA has been observed during obstructive sleep apnea.9 10 11 28 Interestingly, these studies reported a progressive recruitment of abdominal muscles with the increase of inspiratory activity. Similarly we observed a decrease in expiratory activity with the decrease in inspiratory effort (Fig 4) . Furthermore, the decrease we observed in expiratory activity was associated with a decrease in expiratory resistance (Fig 4) . This is in accordance with the results obtained in snorers by Skatrud and Dempsey,7 who pointed out that the increase in expiratory resistance could contribute to the activation of abdominal muscles. In more recent studies, the same authors demonstrated that expiratory muscle activity is not only an immediate neuromechanical compensatory reflex in response to internal loading, but also a consequence of the diminution in minute ventilation, and thereby of the CO2 retention which may induce in turn an augmentation in inspiratory and expiratory muscle activity.8 29 Unfortunately, we did not measured end-tidal CO2. However, we clearly observed that the decrease in expiratory activity was associated with an increase in minute ventilation (Fig 2) . Thus, our study extends to a population of OSAS patients during nCPAP titration (previous findings7 8 29 ), namely that expiratory muscle activity is associated with abnormally high expiratory resistance values and/or reduced minute ventilation.

Interestingly, EAMA was absent in six patients. Our patients without EAMA were not different from those with EAMA in term of age, BMI, and OSAS severity. Nevertheless, the lack of expiratory activity in some snorers or patients with OSAS has also been previously observed.8 10 11 Wilcox et al10 suggested that the lack of EAMA during respiratory events might be indicative of a reduced ventilatory response to upper-airway obstruction. Similarly, Sanci et al11 suggested that expiratory activity should only occur when an inspiratory effort threshold is reached, and that this threshold, which might vary from one patient to another, should not be systematically reached during obstructive respiratory events. Consequently, one may assume that in our six patients without EAMA, the ventilatory response to either upper-airway obstruction or CO2 retention was reduced. This illustrates the fact that the lack of EAMA in OSAS patients during nCPAP titration is a necessary but not a sufficient condition to judge the effectiveness of the nCPAP level.

Since an expiratory increase of Pga can be considered as an accurate method to quantify expiratory activity of abdominal muscle,6 14 15 we used this simple but invasive method. However, as Pga is not routinely used during the CPAP titration, more simple methods might be used to detect such abnormalities routinely. Accordingly, the monitoring of the electrical activity of the abdominal muscles performed from surface electrodes, which has been proposed during the polysomnography of children9 28 and adult snorers,29 could be employed as a simple tool in the optimization of the nCPAP titration procedure.

In conclusion, EAMA observed in OSAS patients during carefully conducted nCPAP titration is not due to nCPAP-induced hyperinflation. Our study demonstrates that the EAMA can be observed at suboptimal nCPAP levels, and is associated with both a reduced minute ventilation and a residual increase in inspiratory and/or expiratory resistance. These results suggest that EAMA might be proposed as an indirect marker of upper-airway obstruction in OSAS during nCPAP titration, and that nCPAP has to be increased as long as expiratory muscle activity occurs.


   Footnotes
 
Abbreviations: AHI = apnea/hypopnea index; BMI = body mass index; {Delta}Pes = esophageal pressure swing; {Delta}Pga = gastric pressure increase during the expiratory phase; EAMA = expiratory abdominal muscle activity; nCPAP = nasal continuous positive airway pressure; OSAS = obstructive sleep apnea syndrome; Pes = esophageal pressure; Pga = gastric pressure

Received for publication August 11, 2000. Accepted for publication March 6, 2001.


   References
TOP
 Abstract
 Introduction
 Materials and Methods
 Results
 Discussion
 References
 

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