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Twenty patients, with a mean age of 43 years, were studied. Eighteen of the 20 were female. All 20 had audible wheezing before treatment; 12 of them still had some wheeze after treatment. All patients showed improvement in their FEV1 the mean value for the group rose from 1.15±0.39 L (mean±SD) before treatment to 1.49 ±0.43 L after treatment. Peak expiratory flow rates improved from 150 ±67 L/sec to 192 ±66 L/sec. The probability that either improvement resulted from chance was less than 1:1,000 (p<0.001).
In Figure 3, the relationship between FEVX and Tw/Txt is shown for all cases in whom a wheeze was identified, 20 patients before therapy and 12 patients with persistent wheeze after therapy. There is a significant correlation, with a correlation coefficient of 0.46 (p<0.01). It will be noted that the two patients with FEV1 less than 600 ml had less wheeze; the correlation coefficient is 0.59 if these two patients are excluded. There is no significant correlation between Tw/Txt prior to treatment and the percent increase in FEV1 after treatment.
Changes in FEV1 and in Tw/Txt are shown in Table 1 for the 12 patients with wheeze after treatment. They had a statistically significant increase in FEWl (p<0.001), a significant decline in Tw/Txt (p<0.001), and a significant reduction in the highest measured sound frequency, from a mean for the group of440 Hz to 298 Hz (p<0.01). An example of the change for one patient is shown in Figures 4 and 5. Before treatment (Fig 4), a wheeze was present both during expiration (0.1 to 1.5 seconds) and inspiration (1.8 to 2.1 seconds), giving a Tw/Txt ratio of 0.86. After treatment, Figure 5 shows the peak corresponding to wheeze heard only during expiration, from 0.3 to 1.0 second; the ratio has fallen to 0.31.
The intensity of wheezing and the simultaneous presence of wheezes of different pitch (polyphonic wheezing) can be readily examined by this technique. There was no correlation between these characteristics and the FEV1 or the response to therapy in the patients studied.
Wheezing sounds are a well recognized and frequently obvious physical finding in patients with asthma. Dodge and Burrows found that 20 percent of a general population sample was aware of wheezing at one time or another, but only 6.6 percent were diagnosed as having asthma. Patients with chronic airflow obstruction who were referred for pulmonary function tests were shown by Marini and colleagues to have a greater probability of responding favorably to bronchodilators if wheezing was heard during the expiratory phase of unforced deep breathing. They defined a wheeze as a continuous musical sound that commenced at any time during expiration, and wheezing was scored on an arbitrary scale. Forgacs observations on wheezing sounds heard clinically and heard experimentally using excised bronchi led him to propose the toy trumpet as a musical instrument analogue of the wheezing airway. Rapid linear airflow through severely narrowed airways appears necessary for the production of these sounds, and Forgacs suggests that apposition of the bronchial walls may be necessary for their initiation. Grotberg and Davis have developed mathematical models which are based upon an interaction between vibrating airway walls and the flowing air column in sound production.
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Objective measurement of the pulmonary sound signals makes it easier to decode them and to relate their characteristics to changes in structure and function. Analysis of these sound signals has been made easier by technical advances such as sound spectrum analysis. This has been applied to vesicular and bronchial breath sounds by Gavriely et al, who noted a peak in the frequency spectrum which was associated with wheezing. Charbonneau et al showed a higher mean frequency in spectra recorded at the larynx from patients with asthma than in spectra from normal subjects.
Our method of analysis allows more exact measurement of changes (for example, those resulting from treatment) in terms both of frequency content and of timing in the respiratory cycle. By making observations at the same site, differences due to sound conduction from site of origin to the surface of the chest wall are minimized. While the changes in wheezes with relief of obstruction cannot as yet be explained in terms of specific changes in airway characteristics, a modest beginning has been made in the description of relationships. Potential advantages for our method of analysis are suggested by the correspondence. These measured changes in the objective, recorded sound signal can in turn be related to the subjective perceived changes in sound. The attributes of wheezing most likely to be altered by effective bronchodilatation (Tw/Txt and pitch) are indicated for the consideration of the interested auscultator.
Figure 3. Linear relationship between FEV, and duration of wheeze over total breath cycle is shown. Relationship is significant (r = 0.459; p <0.01). Two values with FEV, of less than 600 ml have shorter wheeze than expected. This may represent quiet chest of severely ill asthmatic subject. If we consider only those patients with FEV, of more than 600 ml, r = 0.593 (p <0.001).
Figure 4. Complex set of wheezes in asthmatic subject in acute bronchospasm. Line 1 represents beginning of expiration. Wheezing was heard on inspiration and expiration, and several peaks are identified, even at same moment in breath cycle (polyphonia). Ibis patient has wheezing in 19 of the 22 segments making up her breath cycle. Her T/T = 1.9 second/2.2 second = 0.86. Highest pitch of any wheeze is 500 Hz.
Figure 5. Same patient as in Figure 4 after bronchodilators. Line 1 marks beginning of expiration. Time of wheezing is now 0.8 second of a total of 2.6 seconds (T/T = 0.31). Highest frequency is now 300 Hz.
Table 1 — Data from 12 Patients with Wheeze after Treatment
|Case||IFEV L||before Bronchoc||Lilators Highest Frequency,Hz||A FEV, L||Her Bronchodi||lators Highest Wheeze,Hz||Change|