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Posture-Dependent Change of Tracheal Sounds at Standardized Flows in Patients With Obstructive Sleep Apnea
Posture-Dependent Change of Tracheal Sounds at Standardized Flows in Patients With Obstructive Sleep Apnea* Hans Pasterkamp, MD; Jiirgen Schafer, MD; and George R. Wodicka, PhD
Background: The ability of awake subjects with obstructive sleep apnea (OSA) to dilate their pharynx during inspiration may be defective. Airflow through a relatively more narrow pharyngeal passage should lead to increased flow turbulence and hence to louder respiratory sounds. We therefore studied the increase of tracheal sound intensity (TSI) in the supine position as an indicator of abnormal pharyngeal dynamics in patients with documented OSA. Subjects and methods: Sound was recorded with a contact sensor at the suprasternal notch in 7 patients with OSA (age, 52:±:8 years; body mass index, 29.0:±:3; apnea-hypopnea index, 58:±:17; means:±:SD), and in 8 control subjects, including obese subjects and snorers (age, 39:±:8 years; body mass index, 28.6:±:4). Subjects breathed through a pneumotachograph and aimed at target flows of 1.5 to 2 Us, first sitting, then supine. Flow and sound signals were digitized at a 10-KHz rate. Fourier analysis was applied to sounds within the target flow range and average power spectra were obtained. Spectral power was calculated for frequency bands 0.2 to 1, 1 to 2, and 2 to 3 KHz. Results: In the supine position, OSA patients had a significantly greater increase of inspiratory TSI than control subjects: 7.5:±:1.2 dB vs 1.7:±:3.4 dB (p
Abbreviations: AHI=apnea-hypopnea index; BMI=body mass index; OSA=obstructive sleep apnea; TSI=tracheal sound intensity
obstruction of the upper airways during sleep is a significant health problem that affects at least 4% of the male population during middle age. Women and children suffer less commonly from obstructive sleep apnea (OSA). The diagnosis of OSA is usually made after polygraphic monitoring during sleep. Investigations during wakefulness have shown some static and dynamic abnormalities of the upper airways in subjects with OSA, but only a minority of patients have gross anatomic anomalies. *From the De~1tme nt of Pediatrics and Child Health, University of Manitoba (Dr. Pasterkamp), Winnipeg, MB, Canada; the DepartmentofOtorhinolaJYI:lgoiogy, UniversityofUlm (Dr. Schafer), Germanx; and the School of Electrical and Computer Engjneering, Puraue Universi!)' (Dr. Wodicka), West Lafayette, Ina. Presented in part at tlie American Thoracic Society meeting, May 1995, Seattle. Supported by the Children's Hospital of Winnipeg Research Foundation (Dr. Pasterkamp). Manuscript received February 26, 1996; revision accepted June 18. Reprint requests: Dr. Pasterkamp, Pediatric Respirology, CN529, 840 Sherbrook Street, Winnipeg, Manitoba, Canada K3A lSl
Techniques for the dimensional and functional imaging of the upper airways include radiographic cephalometry, fluoroscopy, CT, MRI, nasopharyngoscopy, and airway acoustic reflectometry. 1 Each of these techniques has its merits and limitations, and only a few can be used in both upright and supine positions of the patient. However, postural effects on upper airway geometry are well recognized2•3 and may be more pronounced in OSA patients because their ability to dilate the pharynx during inspiration may be defective.4 We postulated that abnormal narrowing of the pharynx in the supine position would lead to increased flow turbulence and would thereby increase respiratory sound levels at the trachea. Thus, asimple acoustical measurement might detect increased airflow resistance which otherwise would require more invasive pharyngeal pressure manometry. Preliminary observations in our laboratory had provided support for CHEST/110 / 6/DECEMBER, 1996
1493
Table !-Subject Characteristics* Control Subjects
OSA Patients
Subject
Age, yr
BMl
AHI
6.TSI, dB
Subject
1 2 3 4 5 6 7 8 Mean SD
52 30 42 32 39 30 40 48 39.1 8.2
27.4 26.5 33.9 30.0 35.0 25.9 25.0 24.8 28.6 4.0
<5 <5 18 6 <5 <5 <5 <5 6.8 4.6
2.6 2.3 6.2 5.1 -3.7 -2.4 3.3 0.4 1.7 3.4
9 10 11 12 13 14 15
Age, yr
BMI
AHI
52 65 44 59 51 46 46
32.4 25.3 27.5 26.5 27.1 33.3 30.7
40 37 65 45 68 77 74
8.4 5.9 6.1 8.0 8.2 8.8 7.1
51.9 7.7
29.0 3.1
58.0 16.8
7.5 1.2
D.TSI , dB
*Control subjects 1 and 8 had been r efe rred to the Sleep Laboratory for the investigation of snoring. Control subjects 3 ;md 4 gave no history of snoring but had some s el ep apnea during monitming at home (see text for details). ATSI= change in TSI from sitting to supine position. Values are inspiratory measurements from 0.2 to 3.0 KHz.
the diagnostic potential of respiratory acoustical measurements by showing a greater increase of inspiratory tracheal sound intensity (TSI) in OSA patients than in normal subjects. 5 However, the control subjects in our first observation were significantly younger, not obese, and did not include snorers. The purpose of the present study was to extend our initial observations on posture-dependent changes in normal tracheal sounds with the inclusion of obese subjects and snorers among control subjects. Furthermore, we wanted to examine theoretically the generation of respiratory sounds in upper airways and their propagation to a tracheal recording site at the anterior part of the neck. MATERIALS AJ\0 METHODS
Patients with OSA, documented during polysomnography at the Sleep Laboratory, D epartment of Otorhinolaryngology at the University of Ulm, were asked to participate. Gross anatomic abnormality of the upper airways was a reason for exclusion from the study. Control subjects were recruited from volunteers among hospital staff who gave no history of OSA and also from patients who came to the Sleep Laboratory for investigation of snoring but had no evidence of OSA on polysomnography v,,;thin l week prior to the study. The hospital staff volunteers were tested for apnea events during sleep at home (Micro DigiTrapper-S; Synectics; Austin, Texas) within 1 month of the study. All pmticipants had to be free of respiratory tract infection 1 month before the study. The investigation followed the guidelines for the use of human subjects in research as outlined by the Medical Ethics Committee at the Univers ity of Ulm and all subjects gave their informed consent before participation. All recordings were obtained in a quiet but not soundproof room at the Department of Otorhinola1yngology, University of Ulm. A piezoelectric accelerometer (EMT25C; Siemens; Iselin, NJ) was attached with double-sided adhesive tape over the trachea in the midline between cricoid and suprasternal notch. The subj ects were seated comfortably and were asked to breathe through a calibrated pneumotachograph (ScreenMate; Jaeger; Boulder, Colo) while wearing a nose clip. They obse1ved the flow signal on a storage oscilloscope and were coached to reach t arget flows between 1.5 and 2.0 Us during both respiratory phases. Recordings of at least 30-s duration were obtained first in the sitting and then in the supine position for each subject and position. A neutral position of the neck
1494
was maintained throughout. No instructions were given regarding the position of the tongue. The sound signal was high-pass filtered (first order Butterworth filter, cutoff at 50 Hz) to reduce large-amplitude input from muscle and cardiovascular sounds at low frequencies. The sounds were then amplified and low-pass filtered to avoid aliasing (eighth order Butterworth filter, cutoff 2.5 KHz) before analog-to-digital conversion (12 bit AID; model2801; DataTranslation; Marlboro, Mass ) at a10,240 sample per second rate. Acoustic signals and airflow were simultaneously acquired using a personal computer. A customwritten computer program (R.A.L.E. ; Medi-Wave; Winnipeg, Canada) was used for data acquisition, storage, analysis, and display. 6 Samples of airflow were decimated to 320 data points per second. The sound signals were parsed into segments of 2,048 data points with a 50% overlap of points between successive segments. Each segment was windowed with a Hanning function before power spectral estimates were obtained by fast Fourier transfonnation. Auditmy verification on digital-to-analog playback was used to verifY signal quality. All segments v,,;th mtifacts were marked for exclusion from further automated analysis. Power spectra of respiratory sounds v,,;thin the target flow range from 1.5 to 2.0 Us were averaged for inspiration and eJ
RESULTS
We studied seven OSA patients and eight control subjects. The controls were younger on average (p
Table 2-Tracheal Sound Samples* Inspiration
Recording, (s) Control subjects OSA patients Average flow, Us Control subjects OSA patients
Expiration
Sitting
Supine
Sitting
Supine
6.05::!:1.97 6.67::'::1.33
6.29::'.:1.42 7.36::'.:2.64
3.73::'.:1.86 5.06::'.:1.80
4.43::!:2.41 4.09::!:2.09
1.68::'.:0.07 1.67::'.:0.08
1.67::'.:0.08 1.69::!:0.10
1.67::!:0.12 1.67::'.:0.10
1.68::'.:0.11 1.67::'.:0.14
*Recording=average length of analyzed sounds within target flow range (number of Fourier spectra divided b y10; see text for details). Values shown are means::!:SD.
4, Table 1) during sleep polygraphic monitoring at home subsequent to the sound recording. There were fewer samples within target flow range during expiration than during inspiration (p<0.05), but differences between the study groups were not significant (Table 2). Average flows in the upright and supine positions were not significantly different within subjects or between groups (Table 2). Tracheal sound spectra showed maximum signal-to-noise ratios greater than 40 dB and bandwidths exceeding 2 KHz at the higher frequencies. Peaks in the power spectra were similar during inspiration and expiration, but different between individuals. In the same individual, some but
not all spectral peaks changed with posture (Figs 1 and 2) .
At the same inspiratory flow, the increase in TSI from upright to supine position was greater in OSA patients than in control subjects (Table 1, Fig 3). The observed differences were statistically significant for all frequency bands: 7.5:±: 1.2 dB in OSA patients vs 1.7:±:3.4 dB in control subjects at low frequencies (p<0.001), 6.6:±:1.7 dB vs 1.3:±:3.9 dB at medium frequencies (p<0.005), and 12.2:±:3.2 dB vs 5.6:±:3.1 dB at high frequencies (p<0.001). Subjects 3 and 4 (AHI 18 and 6, respectively; Table 1) had the greatest increase of inspiratory TSI in the supine position
Subject #8 (control)
Subject #9 (OSA)
inspiration
60
inspiration
60 40 40 20 20
,-......
fg
'-"
,-......
0
•
--sitting ·-·····-·-- breath hold --supine
1-<
~0
~
fg
'-"
0
1-<
~
0
60
~
expiration
60
40
40
20
20
o~~~~~~~~~~~~~~~
500.0
l.Ok
1.5k
2.0k
2.5k
3.0k
Frequency (Hz) FIGURE l. Average tracheal sound spectra in a healthy male subject. Background noise spectra were obtained from sound during breath-holding. Note the peaks and troughs in the tracheal sound spectra, and the changes in the supine position (see text for details ).
500.0
l.Ok
1.5k
2.0k
2.5k
3.0k
Frequency (Hz) FIGURE 2. Average tracheal sound spectra in a patient with OSA. Note the significant increase in power across the entire frequency range in the supine position. CHEST I 11 0 I 6 I DECEMBER, 1996
1495
OSA
Controls 60 40
2t
2t
fg 0 ...._,
£!
inspiration upright •
0
1-<
~
supine
0
~
60
I!
40
£!
1!
20 expiration
0
0.2-1
1-2
~
*
f!
2!
20 r--.
~!
*
•
~t
!
! 2-3
*
*
1
0.2- 1 1 -2
2-3 kHz
Frequency bands FIGURE 3. Average tracheal sound power at low, medium, and high frequencies. Error bars indicate ±SD. Significant differences in postural effects between OSA subjects and control subjects are shown by asterisks (unpaired Student's t tests, p <0.05).
among control subjects: 6.2 and 5.1 dB over the entire frequency range (0.2 to 3KHz). Total expiratory sound intensity (0.2 to 3KHz) increased in both groups in the supine position: 7.1±1.6 dB in OSA patients vs 4.5±5.3 dB in control subjects. The difference was not significant between groups except at high frequencies: 13.5±3.7 dB in OSA patients vs 8.3±4.3 dB in control subjects (p<0.05). In patients and control subjects, there was a direct relation between AHI and the increase of inspiratory TSI within the 3 frequency bands in the supine position (r=0.755, 0.710, and 0.747 at low, medium, and high frequencies, respectively; p<0.01). The relation between AHI and expiratory tracheal sound changes was not significant. Age and BMI did not show a significant effect on posture-dependent tracheal sound changes in either respiratory phase. DISCUSSION
These findings confirm our earlier observations on posture-dependent changes of tracheal sounds in five OSA patients 5 whose conditions had been diagnosed at the Sleep Laboratory, St. Boniface General Hospital, Winnipeg (Director: Dr. M. Kryger). In those patients, we had found an average increase of the inspiratory 1496
tracheal sound power by 8.1 dB in the supine position, similar to the average increase of 7.5 dB observed at lower frequencies in the present study. The average change of inspiratory tracheal sounds in the five control subjects of our earlier investigation was minimal (-0.4 dB ), again similar to the +1.7-dB change observed now. This suggests that obesity per se does not explain an increased postural dependence of inspiratory tracheal sounds at standardized flows. However, the expiratory TSI increased more in the present control subjects than in the younger, nonobese, and nonsnoring individuals of the earlier study. The disproportionate increase of inspiratory TSI in supine patients with OSA is likely a reflection of increased flow turbulence in upper airways. Patients with OSA may have anatomic abnormalities, ie, a narrow pharynx,1 and also physiologic dysfunction, ie, a reduced ability to dilate the pharynx during inspiration.4 A combination of structural and functional abnormalities appears to exist in most of patients and in heavy snorers? Most imaging studies of the upper airways in OSA patients are done in either the upright (eg, lateral cephalometry) or the supine position (eg, CT, MRI). Fouke and StrohP used acoustic reflectometry in normal subjects to measure the cross-sectional area of the upper airways. They found a decrease of the pharyngeal cross-section in the supine position by 23% on average. These observations were recently confirmed by Pae et al2 who measured upper airway sizes in OSA patients and in control subjects using upright and supine cephalograms. Control subjects in their study had an average decrease of 29% in the oropharyngeal cross-sectional area while the reduction in OSA patients was 37%. Different effects of posture may be even more prominent if dynamic measurements are made. Stauffer and colleagues4 could not detect a difference in the cross-sectional pharyngeal area b etween OSA patients and control subjects using static CT imaging, but the dynamic measurement of inspiratory pharyngeal resistance uncovered significantly greater values in their awake OSA patients. If we extrapolate from these observations and assume that the upper airway size of our OSA patients was reduced more than that of the control subjects in the supine position, we may relate the acoustical findings to increased flow turbulence. To understand if narrowing of the pharynx could explain the observed magnitude of tracheal sound changes recorded below the glottis, we applied a theoretical model of the upper and central airways acoustic properties at low frequencies. 8 In this representation, the respiratory tract consists of cascaded tube sections with nonrigid walls,9 •10 extending from the mouth to the bronchi (Fig 4). The Clinical Investigations
vocal tract component consists of 3 such sections of equal 5.5-cm length representing the open mouth, glossophal)'IlX, and laryngophal)'IlX (with respective cross-sectional areas of 8, 2, and 8 cm29 ). The model trachea contains two 6-cm long sections of 2.5 cm2 cross-sectional area 11 below a g lottis of depth 0.3 em and area of 0.5 cm 2 . The composite effect of the branching bronchi is incorporated as 2 cascaded 5-cm-long sections with an area equal to that of the trachea12 and open at their distal end to the large air reservoir of the lungs. For the simulations, each section of respiratory tract was assumed to produce sound due to turbulent airflow through it. In general, turbulence noise is generated by the rapid flow of air through a constriction. An example for this mechanism is the variety of sounds made during speech. Although there exists an infinite number of possible geometric configurations of the constriction, it has been shown that many create the equivalent of a local dipole sound source. When integrated into each section of the respiratory tract model, such one-dimensional dipoles have radiated sound pressure magnitudes that are nearly frequency independent below 1 KHz and are of the following form:
Mouth Laryngopharynx
Tube
Vocal Folds
Trachea
Bronchi
Ps=KU3A-2.5 where K is a geometry-dependent constant, U is the volume velocity, and A is the cross-sectional area. This indicates a strong relationship between local sound production and the cross-sectional area of the constriction. A key determination of the simulations was the sensitivity of the sound power as measured with the accelerometer over the extrathoracic trachea to a constriction of the glossophal)'IlX occurring more than 6 em away, noting that the narrow and therefore soundproducing vocal folds lie inbetween. To match the clinical experimental situation as closely as possible, the acoustic propetties of the pneumotachograph and breathing tube (12 em total length) were incorporated . into the model as 2 additional tube sections attached to the mouth, and the acoustic mass of the accelerometer and the tissues overlying the extrathoracic trachea were included. 8 Results of the simulations indicate that with decreasing glossopharyngeal area, the predicted sound power (as would be measured with an accelerometer) over the extrathoracic trachea increases at the considered model frequencies up to 1 KHz. The exact relationship between these variables, however, is not as sensitive as the previously stated dependence might indicate because the constriction and measurement location are separated and other sound sources exist within the tract. For example, the strong area (A -25 ) dependence yields more than a 15-dB (multiplicative
Breathing
Lung
Volume
4. Schematic representation of the model respiratory tract used for simulations.
FIGU RE
factor of roughly 5.5) increase in the strength of the local sound pressure source in the glossophal)'IlX for a 50% decrease in this area, yet the model predicts slightly less than a 6-dB (factor of 2) increase over the extrathoracic trachea in this case. This predicted relationship is still quite significant in terms of sensitivity because it indicates a nearly inverse proportionality between glossopharyngeal area and tracheal sound power. Our simulations also suggest that the closer the sound measurement site is to the constriction, the higher the sensitivity to area changes. However, the inability to place a surface transducer more closely overlying the glossophal)'IlX may leave the proximal trachea as the site of practical choice. The most consistent changes in TSI occurred below 1 KHz and the model predictions were also limited to this range to facilitate the computational process. However, postural effects on tracheal sounds were also observed at higher frequencies. It should be noted that CHEST /11 0 /6/ DECEMBER, 1996
1497
the accelerometer (Siemens) decreases in sensitivity at frequencies above 1.2 KHz by approximately 12 dB per octave 13 and that the low-pass filter used for antialiasing further reduced sound power above 2.5 KHz. Our observations, therefore, underestimate the true level of tracheal sounds at medium, and particularly at highfrequencies, but indicate a tracheal sound bandwidth that is much broader than has traditionally been recognized. We have observed previously similar broadband tracheal sound spectra at standardized flows to change significantly during the course of upper airway infection and subglottic stenosis. 14 Narrowing of the glottis and proximal trachea has been observed in some patients with OSA,15 but it is unlikely that the posture effects in our patients were related to airway narrowing in those regions. Extension of the head could have enlarged the pharyngeal cross-section, 16 thereby affecting flow turbulence and sound generation, but we paid attention to keep the neck in a neutral position. Peaks and troughs in the tracheal sound spectra exhibited great intersubject variability while they were quite reproducible for a given individual. We have reported previously the dependence of tracheal sound characteristics on body height 13 and on the density of the respired gasP indicating an effect of airway resonances. Speech researchers have recognized subglottal resonances in voiceless aspiration sounds. 18 Conversely, one should consider that resonances in the vocal tract above the larynx may affect respiratory sounds at the trachea. This offers the potential to obtain more detailed information concerning the upper airway configuration from tracheal sound analysis, similar to the modeling of the vocal tract from voice sound analysis as applied in speech research.9 At present, asimple sound level meter in conjunction with a pneumotachograph may be enough to help identify subjects with abnormal upper airways by the postural dependence of their tracheal sounds. ACKNOWLEDGMENTS: Dr. Pasterkamp visited the Department of Otorhinolaryngology at the University of Ulm, Germany, and the School of Electrical and Computer Engineering, Purdue University, West Lafayette, Ind, during a sabbatical leave from July
1498
to December 1994. Secretarial suppmt for this article was provided by Patricia Macintosh. REFERENCES
1 Fleetham JA. Upper airway imaging in relation to obstructive sleep apnea. Clin Chest Med 1992; 13:399-416 2 Pae EK, Lowe AA, Sasaki K, et a!. A cephalometric and electromyographic study of upper airway structures in the upright and supine positions. Am J Orthod Dentofacial Orthop 1994; 106:52-9 3 Fouke JM, Strohl KP. Effect of position and lung volume on upper airway geometry. J Appl Physiol 1987; 63:375-80 4 Stauffer JL, Zwillich CW, Cadieux RJ, eta!. Pharyngeal size and resistance in obstructive sleep apnea. Am Rev Respir Dis 1987; 136:623-27 5 Pasterkamp H, Kryger M , Sanchez I, et a!. Position dependent changes of flow-standardized tracheal sounds in patients with obstructive sleep apnea [abstract]. Am Rev Respir Dis 1991; 143:A388 6 Pasterkamp H, Carson C, Daien D, et a!. Digital respirosonography-new images of lung sounds. Chest 1989; 96:1405-12 7 Schafer J, Sieron J, Pirsig W, et a!. Radiocephalometric findings and duration of snoring in habitual snming and obstructive apnea syndrome [in German]. Laryngorhinootologie 1989; 68:163-68 8 Wodicka GR, Stevens KN, Golub HL, et a!. A model of acoustic transmission in the respiratory system. IEEE Trans Biomed Eng 1989; 36:925-34 9 Flanagan JL. Speech analysis, synthesis and perception. New York: Springer Verlag, 1972 10 Ishizaka K, French JC, Flanagan JL. Direct determination of vocal tract wall impedance. IEEE Trans Acoust Speech Sign Proc 1975; 23:370-73 11 Weibel ER. Morphometry of the human lung. Berlin: Springer Verlag, 1963 12 Gupta V, Wilson TA, Beavers GS. A model for vocal cord excitation. J Acoust Soc Am 1973; 54:1607-17 13 Sanchez I, Pasterkamp H. Tracheal sound spectra depend on body height. Am Rev Respir Dis 1993; 148:1083-87 14 Pasterkamp H, Sanchez I. Tracheal sounds in upper airway obstruction. Chest 1992; 102:963-65 15 Rubinstein I, Bradley TD, Zamel N, eta!. Glottic and cervical tracheal narrowing in patients with obstructive sleep apnea. J Appl Physiol1989; 67:2427-31 16 Hellsing E. Changes in the pharyngeal airway in relation to extension of the head. Eur J Orthod 1989; 11:359-65 17 Pasterkamp H, Sanchez I. Effect of gas density on respiratory sounds. Am J Respir Crit Care Med 1996; 153:1087-92 18 Klatt DH, Klatt LC. Analysis, synthesis, and perception of voice quality variations among female and male talkers. J Acoust Soc Am 1990; 87:820-57
Clinical Investigations
Background: The ability of awake subjects with obstructive sleep apnea (OSA) to dilate their pharynx during inspiration may be defective. Airflow through a relatively more narrow pharyngeal passage should lead to increased flow turbulence and hence to louder respiratory sounds. We therefore studied the increase of tracheal sound intensity (TSI) in the supine position as an indicator of abnormal pharyngeal dynamics in patients with documented OSA. Subjects and methods: Sound was recorded with a contact sensor at the suprasternal notch in 7 patients with OSA (age, 52:±:8 years; body mass index, 29.0:±:3; apnea-hypopnea index, 58:±:17; means:±:SD), and in 8 control subjects, including obese subjects and snorers (age, 39:±:8 years; body mass index, 28.6:±:4). Subjects breathed through a pneumotachograph and aimed at target flows of 1.5 to 2 Us, first sitting, then supine. Flow and sound signals were digitized at a 10-KHz rate. Fourier analysis was applied to sounds within the target flow range and average power spectra were obtained. Spectral power was calculated for frequency bands 0.2 to 1, 1 to 2, and 2 to 3 KHz. Results: In the supine position, OSA patients had a significantly greater increase of inspiratory TSI than control subjects: 7.5:±:1.2 dB vs 1.7:±:3.4 dB (p
Abbreviations: AHI=apnea-hypopnea index; BMI=body mass index; OSA=obstructive sleep apnea; TSI=tracheal sound intensity
obstruction of the upper airways during sleep is a significant health problem that affects at least 4% of the male population during middle age. Women and children suffer less commonly from obstructive sleep apnea (OSA). The diagnosis of OSA is usually made after polygraphic monitoring during sleep. Investigations during wakefulness have shown some static and dynamic abnormalities of the upper airways in subjects with OSA, but only a minority of patients have gross anatomic anomalies. *From the De~1tme nt of Pediatrics and Child Health, University of Manitoba (Dr. Pasterkamp), Winnipeg, MB, Canada; the DepartmentofOtorhinolaJYI:lgoiogy, UniversityofUlm (Dr. Schafer), Germanx; and the School of Electrical and Computer Engjneering, Puraue Universi!)' (Dr. Wodicka), West Lafayette, Ina. Presented in part at tlie American Thoracic Society meeting, May 1995, Seattle. Supported by the Children's Hospital of Winnipeg Research Foundation (Dr. Pasterkamp). Manuscript received February 26, 1996; revision accepted June 18. Reprint requests: Dr. Pasterkamp, Pediatric Respirology, CN529, 840 Sherbrook Street, Winnipeg, Manitoba, Canada K3A lSl
Techniques for the dimensional and functional imaging of the upper airways include radiographic cephalometry, fluoroscopy, CT, MRI, nasopharyngoscopy, and airway acoustic reflectometry. 1 Each of these techniques has its merits and limitations, and only a few can be used in both upright and supine positions of the patient. However, postural effects on upper airway geometry are well recognized2•3 and may be more pronounced in OSA patients because their ability to dilate the pharynx during inspiration may be defective.4 We postulated that abnormal narrowing of the pharynx in the supine position would lead to increased flow turbulence and would thereby increase respiratory sound levels at the trachea. Thus, asimple acoustical measurement might detect increased airflow resistance which otherwise would require more invasive pharyngeal pressure manometry. Preliminary observations in our laboratory had provided support for CHEST/110 / 6/DECEMBER, 1996
1493
Table !-Subject Characteristics* Control Subjects
OSA Patients
Subject
Age, yr
BMl
AHI
6.TSI, dB
Subject
1 2 3 4 5 6 7 8 Mean SD
52 30 42 32 39 30 40 48 39.1 8.2
27.4 26.5 33.9 30.0 35.0 25.9 25.0 24.8 28.6 4.0
<5 <5 18 6 <5 <5 <5 <5 6.8 4.6
2.6 2.3 6.2 5.1 -3.7 -2.4 3.3 0.4 1.7 3.4
9 10 11 12 13 14 15
Age, yr
BMI
AHI
52 65 44 59 51 46 46
32.4 25.3 27.5 26.5 27.1 33.3 30.7
40 37 65 45 68 77 74
8.4 5.9 6.1 8.0 8.2 8.8 7.1
51.9 7.7
29.0 3.1
58.0 16.8
7.5 1.2
D.TSI , dB
*Control subjects 1 and 8 had been r efe rred to the Sleep Laboratory for the investigation of snoring. Control subjects 3 ;md 4 gave no history of snoring but had some s el ep apnea during monitming at home (see text for details). ATSI= change in TSI from sitting to supine position. Values are inspiratory measurements from 0.2 to 3.0 KHz.
the diagnostic potential of respiratory acoustical measurements by showing a greater increase of inspiratory tracheal sound intensity (TSI) in OSA patients than in normal subjects. 5 However, the control subjects in our first observation were significantly younger, not obese, and did not include snorers. The purpose of the present study was to extend our initial observations on posture-dependent changes in normal tracheal sounds with the inclusion of obese subjects and snorers among control subjects. Furthermore, we wanted to examine theoretically the generation of respiratory sounds in upper airways and their propagation to a tracheal recording site at the anterior part of the neck. MATERIALS AJ\0 METHODS
Patients with OSA, documented during polysomnography at the Sleep Laboratory, D epartment of Otorhinolaryngology at the University of Ulm, were asked to participate. Gross anatomic abnormality of the upper airways was a reason for exclusion from the study. Control subjects were recruited from volunteers among hospital staff who gave no history of OSA and also from patients who came to the Sleep Laboratory for investigation of snoring but had no evidence of OSA on polysomnography v,,;thin l week prior to the study. The hospital staff volunteers were tested for apnea events during sleep at home (Micro DigiTrapper-S; Synectics; Austin, Texas) within 1 month of the study. All pmticipants had to be free of respiratory tract infection 1 month before the study. The investigation followed the guidelines for the use of human subjects in research as outlined by the Medical Ethics Committee at the Univers ity of Ulm and all subjects gave their informed consent before participation. All recordings were obtained in a quiet but not soundproof room at the Department of Otorhinola1yngology, University of Ulm. A piezoelectric accelerometer (EMT25C; Siemens; Iselin, NJ) was attached with double-sided adhesive tape over the trachea in the midline between cricoid and suprasternal notch. The subj ects were seated comfortably and were asked to breathe through a calibrated pneumotachograph (ScreenMate; Jaeger; Boulder, Colo) while wearing a nose clip. They obse1ved the flow signal on a storage oscilloscope and were coached to reach t arget flows between 1.5 and 2.0 Us during both respiratory phases. Recordings of at least 30-s duration were obtained first in the sitting and then in the supine position for each subject and position. A neutral position of the neck
1494
was maintained throughout. No instructions were given regarding the position of the tongue. The sound signal was high-pass filtered (first order Butterworth filter, cutoff at 50 Hz) to reduce large-amplitude input from muscle and cardiovascular sounds at low frequencies. The sounds were then amplified and low-pass filtered to avoid aliasing (eighth order Butterworth filter, cutoff 2.5 KHz) before analog-to-digital conversion (12 bit AID; model2801; DataTranslation; Marlboro, Mass ) at a10,240 sample per second rate. Acoustic signals and airflow were simultaneously acquired using a personal computer. A customwritten computer program (R.A.L.E. ; Medi-Wave; Winnipeg, Canada) was used for data acquisition, storage, analysis, and display. 6 Samples of airflow were decimated to 320 data points per second. The sound signals were parsed into segments of 2,048 data points with a 50% overlap of points between successive segments. Each segment was windowed with a Hanning function before power spectral estimates were obtained by fast Fourier transfonnation. Auditmy verification on digital-to-analog playback was used to verifY signal quality. All segments v,,;th mtifacts were marked for exclusion from further automated analysis. Power spectra of respiratory sounds v,,;thin the target flow range from 1.5 to 2.0 Us were averaged for inspiration and eJ
RESULTS
We studied seven OSA patients and eight control subjects. The controls were younger on average (p
Table 2-Tracheal Sound Samples* Inspiration
Recording, (s) Control subjects OSA patients Average flow, Us Control subjects OSA patients
Expiration
Sitting
Supine
Sitting
Supine
6.05::!:1.97 6.67::'::1.33
6.29::'.:1.42 7.36::'.:2.64
3.73::'.:1.86 5.06::'.:1.80
4.43::!:2.41 4.09::!:2.09
1.68::'.:0.07 1.67::'.:0.08
1.67::'.:0.08 1.69::!:0.10
1.67::!:0.12 1.67::'.:0.10
1.68::'.:0.11 1.67::'.:0.14
*Recording=average length of analyzed sounds within target flow range (number of Fourier spectra divided b y10; see text for details). Values shown are means::!:SD.
4, Table 1) during sleep polygraphic monitoring at home subsequent to the sound recording. There were fewer samples within target flow range during expiration than during inspiration (p<0.05), but differences between the study groups were not significant (Table 2). Average flows in the upright and supine positions were not significantly different within subjects or between groups (Table 2). Tracheal sound spectra showed maximum signal-to-noise ratios greater than 40 dB and bandwidths exceeding 2 KHz at the higher frequencies. Peaks in the power spectra were similar during inspiration and expiration, but different between individuals. In the same individual, some but
not all spectral peaks changed with posture (Figs 1 and 2) .
At the same inspiratory flow, the increase in TSI from upright to supine position was greater in OSA patients than in control subjects (Table 1, Fig 3). The observed differences were statistically significant for all frequency bands: 7.5:±: 1.2 dB in OSA patients vs 1.7:±:3.4 dB in control subjects at low frequencies (p<0.001), 6.6:±:1.7 dB vs 1.3:±:3.9 dB at medium frequencies (p<0.005), and 12.2:±:3.2 dB vs 5.6:±:3.1 dB at high frequencies (p<0.001). Subjects 3 and 4 (AHI 18 and 6, respectively; Table 1) had the greatest increase of inspiratory TSI in the supine position
Subject #8 (control)
Subject #9 (OSA)
inspiration
60
inspiration
60 40 40 20 20
,-......
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'-"
,-......
0
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--sitting ·-·····-·-- breath hold --supine
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~
fg
'-"
0
1-<
~
0
60
~
expiration
60
40
40
20
20
o~~~~~~~~~~~~~~~
500.0
l.Ok
1.5k
2.0k
2.5k
3.0k
Frequency (Hz) FIGURE l. Average tracheal sound spectra in a healthy male subject. Background noise spectra were obtained from sound during breath-holding. Note the peaks and troughs in the tracheal sound spectra, and the changes in the supine position (see text for details ).
500.0
l.Ok
1.5k
2.0k
2.5k
3.0k
Frequency (Hz) FIGURE 2. Average tracheal sound spectra in a patient with OSA. Note the significant increase in power across the entire frequency range in the supine position. CHEST I 11 0 I 6 I DECEMBER, 1996
1495
OSA
Controls 60 40
2t
2t
fg 0 ...._,
£!
inspiration upright •
0
1-<
~
supine
0
~
60
I!
40
£!
1!
20 expiration
0
0.2-1
1-2
~
*
f!
2!
20 r--.
~!
*
•
~t
!
! 2-3
*
*
1
0.2- 1 1 -2
2-3 kHz
Frequency bands FIGURE 3. Average tracheal sound power at low, medium, and high frequencies. Error bars indicate ±SD. Significant differences in postural effects between OSA subjects and control subjects are shown by asterisks (unpaired Student's t tests, p <0.05).
among control subjects: 6.2 and 5.1 dB over the entire frequency range (0.2 to 3KHz). Total expiratory sound intensity (0.2 to 3KHz) increased in both groups in the supine position: 7.1±1.6 dB in OSA patients vs 4.5±5.3 dB in control subjects. The difference was not significant between groups except at high frequencies: 13.5±3.7 dB in OSA patients vs 8.3±4.3 dB in control subjects (p<0.05). In patients and control subjects, there was a direct relation between AHI and the increase of inspiratory TSI within the 3 frequency bands in the supine position (r=0.755, 0.710, and 0.747 at low, medium, and high frequencies, respectively; p<0.01). The relation between AHI and expiratory tracheal sound changes was not significant. Age and BMI did not show a significant effect on posture-dependent tracheal sound changes in either respiratory phase. DISCUSSION
These findings confirm our earlier observations on posture-dependent changes of tracheal sounds in five OSA patients 5 whose conditions had been diagnosed at the Sleep Laboratory, St. Boniface General Hospital, Winnipeg (Director: Dr. M. Kryger). In those patients, we had found an average increase of the inspiratory 1496
tracheal sound power by 8.1 dB in the supine position, similar to the average increase of 7.5 dB observed at lower frequencies in the present study. The average change of inspiratory tracheal sounds in the five control subjects of our earlier investigation was minimal (-0.4 dB ), again similar to the +1.7-dB change observed now. This suggests that obesity per se does not explain an increased postural dependence of inspiratory tracheal sounds at standardized flows. However, the expiratory TSI increased more in the present control subjects than in the younger, nonobese, and nonsnoring individuals of the earlier study. The disproportionate increase of inspiratory TSI in supine patients with OSA is likely a reflection of increased flow turbulence in upper airways. Patients with OSA may have anatomic abnormalities, ie, a narrow pharynx,1 and also physiologic dysfunction, ie, a reduced ability to dilate the pharynx during inspiration.4 A combination of structural and functional abnormalities appears to exist in most of patients and in heavy snorers? Most imaging studies of the upper airways in OSA patients are done in either the upright (eg, lateral cephalometry) or the supine position (eg, CT, MRI). Fouke and StrohP used acoustic reflectometry in normal subjects to measure the cross-sectional area of the upper airways. They found a decrease of the pharyngeal cross-section in the supine position by 23% on average. These observations were recently confirmed by Pae et al2 who measured upper airway sizes in OSA patients and in control subjects using upright and supine cephalograms. Control subjects in their study had an average decrease of 29% in the oropharyngeal cross-sectional area while the reduction in OSA patients was 37%. Different effects of posture may be even more prominent if dynamic measurements are made. Stauffer and colleagues4 could not detect a difference in the cross-sectional pharyngeal area b etween OSA patients and control subjects using static CT imaging, but the dynamic measurement of inspiratory pharyngeal resistance uncovered significantly greater values in their awake OSA patients. If we extrapolate from these observations and assume that the upper airway size of our OSA patients was reduced more than that of the control subjects in the supine position, we may relate the acoustical findings to increased flow turbulence. To understand if narrowing of the pharynx could explain the observed magnitude of tracheal sound changes recorded below the glottis, we applied a theoretical model of the upper and central airways acoustic properties at low frequencies. 8 In this representation, the respiratory tract consists of cascaded tube sections with nonrigid walls,9 •10 extending from the mouth to the bronchi (Fig 4). The Clinical Investigations
vocal tract component consists of 3 such sections of equal 5.5-cm length representing the open mouth, glossophal)'IlX, and laryngophal)'IlX (with respective cross-sectional areas of 8, 2, and 8 cm29 ). The model trachea contains two 6-cm long sections of 2.5 cm2 cross-sectional area 11 below a g lottis of depth 0.3 em and area of 0.5 cm 2 . The composite effect of the branching bronchi is incorporated as 2 cascaded 5-cm-long sections with an area equal to that of the trachea12 and open at their distal end to the large air reservoir of the lungs. For the simulations, each section of respiratory tract was assumed to produce sound due to turbulent airflow through it. In general, turbulence noise is generated by the rapid flow of air through a constriction. An example for this mechanism is the variety of sounds made during speech. Although there exists an infinite number of possible geometric configurations of the constriction, it has been shown that many create the equivalent of a local dipole sound source. When integrated into each section of the respiratory tract model, such one-dimensional dipoles have radiated sound pressure magnitudes that are nearly frequency independent below 1 KHz and are of the following form:
Mouth Laryngopharynx
Tube
Vocal Folds
Trachea
Bronchi
Ps=KU3A-2.5 where K is a geometry-dependent constant, U is the volume velocity, and A is the cross-sectional area. This indicates a strong relationship between local sound production and the cross-sectional area of the constriction. A key determination of the simulations was the sensitivity of the sound power as measured with the accelerometer over the extrathoracic trachea to a constriction of the glossophal)'IlX occurring more than 6 em away, noting that the narrow and therefore soundproducing vocal folds lie inbetween. To match the clinical experimental situation as closely as possible, the acoustic propetties of the pneumotachograph and breathing tube (12 em total length) were incorporated . into the model as 2 additional tube sections attached to the mouth, and the acoustic mass of the accelerometer and the tissues overlying the extrathoracic trachea were included. 8 Results of the simulations indicate that with decreasing glossopharyngeal area, the predicted sound power (as would be measured with an accelerometer) over the extrathoracic trachea increases at the considered model frequencies up to 1 KHz. The exact relationship between these variables, however, is not as sensitive as the previously stated dependence might indicate because the constriction and measurement location are separated and other sound sources exist within the tract. For example, the strong area (A -25 ) dependence yields more than a 15-dB (multiplicative
Breathing
Lung
Volume
4. Schematic representation of the model respiratory tract used for simulations.
FIGU RE
factor of roughly 5.5) increase in the strength of the local sound pressure source in the glossophal)'IlX for a 50% decrease in this area, yet the model predicts slightly less than a 6-dB (factor of 2) increase over the extrathoracic trachea in this case. This predicted relationship is still quite significant in terms of sensitivity because it indicates a nearly inverse proportionality between glossopharyngeal area and tracheal sound power. Our simulations also suggest that the closer the sound measurement site is to the constriction, the higher the sensitivity to area changes. However, the inability to place a surface transducer more closely overlying the glossophal)'IlX may leave the proximal trachea as the site of practical choice. The most consistent changes in TSI occurred below 1 KHz and the model predictions were also limited to this range to facilitate the computational process. However, postural effects on tracheal sounds were also observed at higher frequencies. It should be noted that CHEST /11 0 /6/ DECEMBER, 1996
1497
the accelerometer (Siemens) decreases in sensitivity at frequencies above 1.2 KHz by approximately 12 dB per octave 13 and that the low-pass filter used for antialiasing further reduced sound power above 2.5 KHz. Our observations, therefore, underestimate the true level of tracheal sounds at medium, and particularly at highfrequencies, but indicate a tracheal sound bandwidth that is much broader than has traditionally been recognized. We have observed previously similar broadband tracheal sound spectra at standardized flows to change significantly during the course of upper airway infection and subglottic stenosis. 14 Narrowing of the glottis and proximal trachea has been observed in some patients with OSA,15 but it is unlikely that the posture effects in our patients were related to airway narrowing in those regions. Extension of the head could have enlarged the pharyngeal cross-section, 16 thereby affecting flow turbulence and sound generation, but we paid attention to keep the neck in a neutral position. Peaks and troughs in the tracheal sound spectra exhibited great intersubject variability while they were quite reproducible for a given individual. We have reported previously the dependence of tracheal sound characteristics on body height 13 and on the density of the respired gasP indicating an effect of airway resonances. Speech researchers have recognized subglottal resonances in voiceless aspiration sounds. 18 Conversely, one should consider that resonances in the vocal tract above the larynx may affect respiratory sounds at the trachea. This offers the potential to obtain more detailed information concerning the upper airway configuration from tracheal sound analysis, similar to the modeling of the vocal tract from voice sound analysis as applied in speech research.9 At present, asimple sound level meter in conjunction with a pneumotachograph may be enough to help identify subjects with abnormal upper airways by the postural dependence of their tracheal sounds. ACKNOWLEDGMENTS: Dr. Pasterkamp visited the Department of Otorhinolaryngology at the University of Ulm, Germany, and the School of Electrical and Computer Engineering, Purdue University, West Lafayette, Ind, during a sabbatical leave from July
1498
to December 1994. Secretarial suppmt for this article was provided by Patricia Macintosh. REFERENCES
1 Fleetham JA. Upper airway imaging in relation to obstructive sleep apnea. Clin Chest Med 1992; 13:399-416 2 Pae EK, Lowe AA, Sasaki K, et a!. A cephalometric and electromyographic study of upper airway structures in the upright and supine positions. Am J Orthod Dentofacial Orthop 1994; 106:52-9 3 Fouke JM, Strohl KP. Effect of position and lung volume on upper airway geometry. J Appl Physiol 1987; 63:375-80 4 Stauffer JL, Zwillich CW, Cadieux RJ, eta!. Pharyngeal size and resistance in obstructive sleep apnea. Am Rev Respir Dis 1987; 136:623-27 5 Pasterkamp H, Kryger M , Sanchez I, et a!. Position dependent changes of flow-standardized tracheal sounds in patients with obstructive sleep apnea [abstract]. Am Rev Respir Dis 1991; 143:A388 6 Pasterkamp H, Carson C, Daien D, et a!. Digital respirosonography-new images of lung sounds. Chest 1989; 96:1405-12 7 Schafer J, Sieron J, Pirsig W, et a!. Radiocephalometric findings and duration of snoring in habitual snming and obstructive apnea syndrome [in German]. Laryngorhinootologie 1989; 68:163-68 8 Wodicka GR, Stevens KN, Golub HL, et a!. A model of acoustic transmission in the respiratory system. IEEE Trans Biomed Eng 1989; 36:925-34 9 Flanagan JL. Speech analysis, synthesis and perception. New York: Springer Verlag, 1972 10 Ishizaka K, French JC, Flanagan JL. Direct determination of vocal tract wall impedance. IEEE Trans Acoust Speech Sign Proc 1975; 23:370-73 11 Weibel ER. Morphometry of the human lung. Berlin: Springer Verlag, 1963 12 Gupta V, Wilson TA, Beavers GS. A model for vocal cord excitation. J Acoust Soc Am 1973; 54:1607-17 13 Sanchez I, Pasterkamp H. Tracheal sound spectra depend on body height. Am Rev Respir Dis 1993; 148:1083-87 14 Pasterkamp H, Sanchez I. Tracheal sounds in upper airway obstruction. Chest 1992; 102:963-65 15 Rubinstein I, Bradley TD, Zamel N, eta!. Glottic and cervical tracheal narrowing in patients with obstructive sleep apnea. J Appl Physiol1989; 67:2427-31 16 Hellsing E. Changes in the pharyngeal airway in relation to extension of the head. Eur J Orthod 1989; 11:359-65 17 Pasterkamp H, Sanchez I. Effect of gas density on respiratory sounds. Am J Respir Crit Care Med 1996; 153:1087-92 18 Klatt DH, Klatt LC. Analysis, synthesis, and perception of voice quality variations among female and male talkers. J Acoust Soc Am 1990; 87:820-57
Clinical Investigations