Airflow-Generated Sound in a Hollow Canine Airway Cast: DISCUSSION

Posted by James

The so-called vesicular lung sound is heard over the lungs of humans and many animals. Through empiric observation and pathologic correlation, this sound has been found useful for clinical diagnostic purposes since early in the 19th century. Nevertheless, little scientific investigation into the site and mechanism of generation of the vesicular lung sound has been attempted. The available experimental evi­dence supports an intrapulmonic source for the inspiratory component of the vesicular lung sound but does not distinguish more precisely among the many possible intrapulmonic locations. Bullar et al found that in freshly excised lungs of sheep, inspiratory lung sounds were produced within the lung during airflow and were not dependent on the presence of the larynx. Kraman found that the inspiratory lung sounds of healthy subjects appeared to come entirely from within the lungs, whereas the expiratory sounds had an origin, at least partially, in the trachea although not from the larynx. Hardin and Patterson, working with simple, rigid airway models, postulated a sound- generating mechanism driven by vortices that would produce sound in small airways. These investigators predicted the production of musical tones of specific frequencies depending on the airway generation in­volved, which, in aggregate, would be perceived as a “vesicular” sound. To our knowledge, no one has confirmed this last study, and in the present study, we perceived no tones at any level under any of the examined airflow rates.

Our findings suggest that the expiratory component of the vesicular lung sound is produced in large airways as a relatively simple function of airway cross-sectional area but that the inspiratory component is a more complex function distinguished by prominent sound generation within airways of 8 and 5 mm in diameter, corresponding to locations (in the human adult lung) within the range of lobar to subsegmental airways. We make the comparison with man because we are aware of no previous experimental data on lung sound lo­cations in dogs. In inspiration and expiration, changes in sound amplitude at any airway level seemed to be linearly related to the square of changes in the airflow. By design, these conclusions are descriptive in nature, and we will not try to imply mechanisms of sound production that could explain these findings. Although changes in airflow are directly related to changes in the Reynolds number (Re), we cannot attribute any of the noted changes to development of turbulence because we were unable to measure the absolute airflow in the branch airways and so could not calculate Re.
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In interpreting the present findings, we will make the assumptions that the mechanisms of sound pro­duction in human airways are the same as those in canine airways and, furthermore, that our model was an acceptable representation of these airways. We believe that the first assumption is reasonable because of the universal presence of vesicular-sounding lung sounds in humans of all ages and sizes and in many, if not all, air-breathing animals. The physics of the sound could not, therefore, be terribly sensitive to the precise size and morphology of the system. We will use the same argument to excuse any deviations (if any) of our model from the anatomy of the in vivo canine lung from which it was made. We do not know how the compliance of the models walls differed from the live animal and acknowledge that this may be an important issue, although it is one that we cannot resolve at present. We do know from observation and manipu­lation of the model that the Silastic walls maintained their shape during the experiments, never noticeably ballooning nor collapsing.

Strictly speaking, the probe-tipped microphone was detecting transient pressure fluctuations within the flowing gas. We cannot state with certainty that these fluctuations were directly translatable to the sound made by ventilated lungs. As pointed out by Olson and Hammersley, energy within flowing fluids may be dissipated by mechanisms other than sound pro­duction, so-called pseudonoise. Nevertheless, we know that sound is produced by airflow within airways and are thus making the assumption that the observed pressure fluctuations were mechanistically related to the sound generation itself.

We are encouraged in the previous assumptions by comparisons of our data with current knowledge about lung sounds in humans. This includes findings by Bullar et al, Ploysongsang et al, and Kraman that inspiratory lung sounds are generated within the lung and of Kraman that expiratory lung sounds have a measurable tracheal component. Our finding of a direct relationship between airway sound amplitude and the square of the airflow is the same as was found by Shykoff et al in human studies. Although Kraman had previously reported a linear relationship between lung sound amplitude and airflow, we acknowledge that the scatter of the data and the elimination of data points below 1.4 L/s could have easily masked a low- level exponential function.
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We conclude that the aggregate evidence of this and of previous research supports intrapulmonic sources of the inspiratory vesicular lung sound, with predom­inant sound production within lobar to subsegmental airways, and that the expiratory lung sound is gener­ated predominantly within the trachea and large bronchi.