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* From the Pneumology Department (Drs. Fiz, Izquierdo, Lores, and Morera), Germans Trias i Pujol University Hospital, Badalona, Spain; and from the Department ESAII (Drs. Jané, Salvatella, and Caminal), Centre de Recerca en Enginyeria Biomèdica. Universitat Politècnica de Catalunya, Barcelona, Spain.
Correspondence to: Jose Antonio Fiz, MD, C/Canyet s/n, planta 11 Neumología, Badalona, Spain; e-mail: jafiz{at}ns.hugtip.scs.es
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Abstract |
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Material and methods: Seventeen
nonsmoking asthma patients (9 were male, 8 were female) who had been
suffering from the disease for 
15 years were included in the study,
as were 15 normal subjects (7 were male, 8 were female). The average
age (± SD) was 56.5 ± 15.2 years (FVC, 2.7 ± 0.9 L
[63.4%]; FEV1, 1.5 ± 0.6 L [53.0%]). The tracheal
sounds were collected during three forced expiratory maneuvers with a
sampling frequency of 5,000 Hz and were analyzed by applying a
16-parameter autoregressive model.
Results: The centroid frequency decreased after the bronchodilator was given at different flow segments between 1.2 and 0.4 L/s, with significant changes between 0.6 and 0.4 L/s.
Conclusions: Patients with asthma showed changes in the spectral acoustic analysis frequencies after the administration of a bronchodilator drug (terbutaline) during forced expiratory maneuvers.
Key Words: acoustic analysis • asthma • respiratory sounds
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Introduction |
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Materials and Methods |
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Patients were treated with inhaled corticosteroids and sustained action bronchodilator drugs. Patients abstained from inhaled ß-stimulants for at least 12 h before the test, while inhaled corticosteroids were continued unchanged.
Spirometry was performed using a spirometer (PFT; Horizon; Manchester, OH) on all patients and normal subjects at baseline and at 20 min after the inhalation of 1 mg terbutaline (2 puffs of 500 µg each administered via an inhaler [Pulmicort Turbuhaler; Astra Draco AB; Lund, Sweden]), according to criteria of the American Thoracic Society.1 Wheezing was present by auscultation in all patients during the FVC maneuvers before and after terbutaline inhalation.
The respiratory sound was collected using a piezoelectric contact microphone (PPG sensor; Technion University; Haifa, Israel) with a flat response between 50 and 1,800 Hz with a resonance frequency at 2,600 Hz. The microphone was applied directly to the patient's skin and placed laterally to the trachea at the level of the cricoid cartilage, using an elastic band. At the same time, the airflow in the mouth was recorded from a pneumotachograph (Screenmate; Jaeger; Germany). The sound signal was amplified and filtered using a pass-band filter of between 80 and 2,000 Hz by means of a filtering system (KH 39168; Butterworth; England). The sound and flow signals were digitized with a sampling frequency of 5,000 Hz. The sound was analyzed after automatic segmentation of flow by means of an algorithm between 1.6 and 0.4 L/s of airflow, with ranges of 0.2 L/s for all the patients and control subjects. To compute the tracheal sound spectrum of each forced expiration, we used a 16-parameter autoregressive model. Parameter number was determined by means of Akaike's final prediction error criterion.6 Analysis was done using the average of three forced expirations made after an earlier deep inspiration.
The following parameters were calculated: (1) maximum frequency (Fl), defined as the frequency that contains 90% of the total power of the spectrum, measured in hertz; (2) peak frequency (Fp), defined as the frequency that contains the maximum power of the spectrum, measured in hertz; (3) centroid frequency (Fc), defined as the frequency that includes half of the total power of the spectrum, measured in hertz.
A Mann-Whitney test for unpaired samples was applied to compare anthropometric and spirometric parameters between asthma patients and normal subjects.
For the comparisons of frequency parameters, one-factor and two-factor analyses of variance (ANOVAs) were applied, with the results registering a p < 0.05 being considered as statistically significant. ANOVA was followed by Newman-Keuls post hoc testing.
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Results |
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FEV1 15%; group 2,
FEV1 < 15%). Group 1 had more severe
bronchial obstruction than group 2.
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), p < 0.048;
Newman-Keuls test, 0.6 to 0.4 L/s; F = 6.42; p < 0.017).
Control groups have not shown differences after bronchodilator tests.
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For Fl and Fp, the ANOVA two-factor analysis did not show significant changes with bronchodilator.
Fl was higher in group 2 for the majority of flow segments (Table 3 ; ANOVA one-way t test, 2.36; p < 0.034). There were no differences for Fp and Fc frequencies between groups 1 and 2. Also, there were no differences in changes of Fc, Fp, or Fl between groups 1 and 2. Mean intrasubject variation coefficients for basal Fc, Fp, and Fl are expressed in Table 4 .
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Discussion |
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Several studies have shown that the inhalation of a methacholine or histamine bronchoconstrictor leads to changes in the breathing sound spectrum frequencies, during both ordinary breathing and forced expiratory maneuvers,8 9 10 while in healthy subjects there are no significant changes at the same bronchodilator concentrations. The mean frequency increases after inhaling the bronchoconstrictor agent, usually accompanied by changes in the spectral power intensity.10 11 The effect of the bronchodilator has also been seen after airway challenge tests. The mean spectral frequency decreases, compared with the state of maximum bronchoconstriction when a ß-stimulant is given.9 Baughman and Loudon4 used spectral analysis of lung sounds to study the responses of 20 asthmatic patients to ß-adrenergic stimulants. They noted that, during ordinary breathing, the maximum spectral power frequency dropped after inhalation of the bronchodilator from 440 ± 128 Hz to 298 ± 76 Hz. This change was accompanied by a reduction in the wheeze duration time during the respiratory cycle (time with wheezes/total breathing cycle time [TOTT]) from 58 ± 20 to 30 ± 15. Changes in mean spectral frequency usually paralleled the changes observed in the FEV1. An increase in FEV1 was associated with a reduction in mean frequency, and vice versa. In our study, the mean Fc of the sample, consisting of 17 asthmatic patients whose baseline spirometric parameters were below normal, decreased after inhalation of the bronchodilator. This result was consistent with the above-mentioned studies and reflected the changes that occur in the airway when the bronchodilator is given. There were no bronchodilator effects in the control group.
Wheezing during forced exhalation was heard in all the studied subjects. Although wheezing was not processed in this study, changes in frequency parameters were probably associated with changes in wheeze characteristics. Charbonneau et al12 detected wheezing during forced exhalation, before and after peak flow. Frequency of wheeze ranged from 375 to 1,080 Hz (mean [± SD], 636 ± 200 Hz). This frequency was similar to the values for trachea Fc for all subjects (range, 210 to 1,286 Hz; mean, 620.5 ± 202.9 Hz), measured between 1.6 and 0.4 L/s of air flow. Marini et al13 and King et al14 found that wheezing during forced exhalation was not correlated with either degree of obstruction or bronchodilator response and was neither sensitive to nor specific for airway hyperreactivity in asthma and chronic airflow obstruction patients. These studies were made by direct auscultation without sound analysis techniques.
According to the flutter theory,15 16 wheezing is linked to airflow limitation in the involved bronchial area. In this area, an increase in speed of the air particles passing through it above a given level (flutter speed), together with changes in transpulmonary pressure, cause the bronchus/fluid to oscillate and generate sound, the frequency of which depends on the air speed and morphologic characteristics of the airway. A drop in the air speed in the affected airway is linked to a decrease in the frequency of the sound generated, as would be the case in the bronchodilator effect. On the other hand, a reduction in the intrabronchial lumen as a result of bronchoconstrictor substances would lead to an increase in the frequencies of the sound generated. Also, changes in equal pressure points after bronchodilator can explain the effect on Fc.17 The dilatation effect on segmental airways moves the equal pressure points downstream and, in consequence, the flow limitation locus of the affected airway. Eddy-induced wall oscillation is a possible alternative mechanism even if the flow is not limited.16
In this study, the frequencies of the tracheal sound spectrum of patients with a significant response to the bronchodilator and of those who showed no changes in the spirometry tests decreased after the bronchodilator was used. This is consistent with the recent study carried out by Gavriely et al3 on 493 active workers, applying frequency-power log-log ratios. The authors identified 14 subjects whose medical histories were compatible with chronic bronchitis and the results of whose spirometry tests were normal, although the results of lung sound analyses proved to be abnormal. This means that spirometry is not always capable of identifying changes in the airway.
Another interesting point of this work was that asthma patients with low responses to the bronchodilator had higher Fl frequencies than asthma patients with positive higher responses. One hypothesis to explain this difference is that the asthma group with higher responses to the bronchodilator could have a higher proportion of small airways affected than the asthma group with low responses, generating more wheezes during the expiratory maneuvers with lower frequencies. In fact, Fl frequencies of low-response asthma patients were similar to those of the control group.
To conclude, our study showed that in asthma patients the inhalation of a ß-stimulant bronchodilator (terbutaline) caused changes in the tracheal sound spectral power during forced expiratory maneuvers. Such changes consisted of a decrease in tracheal sound frequencies after administration of the bronchodilator. This fact was seen both in patients whose FEV1 increased by 15% or more after inhalation of the bronchodilator and in those whose increase in FEV1, compared to baseline values, were under 15%.
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Footnotes |
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Received for publication May 22, 1996. Accepted for publication April 7, 1999.
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This article has been cited by other articles:
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  J. A. Fiz, R. Jane, A. Homs, J. Izquierdo, M. A. Garcia, and J. Morera Detection of Wheezing During Maximal Forced Exhalation in Patients With Obstructed Airways* Chest, July 1, 2002; 122(1): 186 - 191. [Abstract] [Full Text] [PDF]
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