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

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.

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

The data were analyzed by examining the relation­ship between sound amplitude and airflow at each airway size and between amplitude and airway size at each airflow rate. Since only the aggregate airflow was measured (at the trachea), the analyses were compar­ative; absolute airflow in individual branches was not measured. We used the Lowess curve fit procedure to objectively assess trends. This method produces a smoothed curve without first presuming the shape of the function. When deemed useful, least-square re­gression curve formulas were fitted to the data.

Although frequency analysis was not a primary goal of this investigation, sound spectrograms were made of all of the data, and the sounds were audibly monitored as well. The sound nearly always had the character, and the spectrograms the appearance of, band-limited white noise with frequency components extending from 5 to 1,000 to 1,500 Hz, rarely higher. Examples are shown in Figure 3.

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Airflow-Generated Sound in a Hollow Canine Airway Cast: MATERIALS AND METHODS

Because of availability and ease of handling, we decided to use a canine model. The goal of the experiment was to make a model of the lungs accurately representing all airway levels from trachea to 1-mm airways and to measure sound generated within the lumina at several airways generations within a range of airflows in the inspirator) and expiratory directions. The sound amplitudes could then be related to the airway sizes at each flow rate and to flow rate at each airway size.

Model Construction

The intact health) lungs and trachea of a 25-kg mongrel dog were excised after the dog had been killed after an unrelated experiment. The specimen was thoroughly washed, suspended by the trachea, and connected to an air hose in parallel with a water manometer. Air pressure of 20 cm was then applied at the trachea. This resulted in a constant flow through the lung, with the air apparently exiting through pores in the pleura, since we found it unnecessary to make additional holes in the pleura. After 48 hours the lungs had completely dried in inflation, assuming the appearance and consis­tency of Styrofoam. The dried lungs were removed from the air hose and immersed in an ice-water bath, taking precautions to avoid admission of water into the trachea. After two hours of cooling, the airways were filled with melted Ostalloy 117 (Arconium Corp.) at a temperature of 50°C. Ostalloy 117 is a metal alloy, similar to Wood s metal, but it melts at 47°C (117°F). The lung was chilled prior to filling to help avoid entry of the metal into the alveolar spaces. After waiting 24 hours, the preparation, now filled with solid metal, was immersed in a 20 percent solution of NaOIl for three days to remove the pulmonary tissue by corrosion. This resulted in a negative cast that was then pruned to remove all casts of acini and airways smaller than 1 mm in diameter.

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Airflow-Generated Sound in a Hollow Canine Airway Cast

The characteristic sound heard on the chest wall during breathing is known as the vesicular lung sound. Although the name implies that the source of the sound is the alveolar sacs (vesicles), the true source is not known. Several attempts at defining the site of origin has resulted in indirect evidence that the intrapulmonic airways generate the loudest compo­nent of the inspiratory sound in human lungs and that the expiratory component may arise from larger airways. To better define the source of these sounds, we decided to examine the spatial distribution of airflow-generated sound within a specially con­structed, hollow flexible model of canine airways. Read the rest of this entry »

The Heart Is Not Always in Good Hands: SQUARE WAVE BLOOD PRESSURE RESPONSE TO VALSALVA MANEUVER IN HEART FAILURE

This is also explicable by the analogy of the disten­sible segment in the siphon tubing. In failure, the intrathoracic and intra-abdominal vessels are dis­tended. Raising the pressure surrounding them in the chest squeezes them toward a normal caliber and the elevated extracardiac pressure lessens left ventricular load. The sustained output and the blood pressure increase from the high intrathoracic pressure is helped by the increased venous return from the compression of the engorged abdominal vessels by the equally raised intra-abdominal pressure. Since, when there is heart failure, there is little fall in systemic pressure during the Valsalva maneuver, the reflex overshoot of systemic pressure and consequent bradycardia does not occur.

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The Heart Is Not Always in Good Hands: Changes in Cardiac Output

Pulsus Paradoxus. It has long been a puzzle why intrathoracic pressure changes, as exemplified by the positive pressure Valsalva maneuver and the negative pressure Mueller maneuver, have such small effects on cardiac output in spite of the large pressures (-I-150 mm Hg to —75 mm Hg) which can be imposed. Yet, lung volume changes, which are associated with minor changes in pleural pressure (from about – 5 to about — 25 mm Hg), appear to cause rather profound effects.

A simple illustration (Fig 4) shows why the pressures in the chest, which are the same as those around the heart when the glottis is closed, have relatively little effect on cardiac output. Imagine you are holding a segment of a hose pipe about half-way along its length. It is attached to a faucet and is discharging through a sprinkler onto your lawn. The segment of the hose between your hands is the make-believe chest. The heart pump, in the hose between your hands, has been temporarily stopped. In this example, the inflow represents the venous return determined by the mean circulatory pressure. It makes no difference whether you lower the hose right down to the ground, dropping its vertical pressure, or hold it over your head—the outflow will not be changed. You could squeeze the hose upstream of one unidirectional valve with your right hand (right ventricle) and upstream of another with your left hand (left ventricle) to give a fixed impetus to the blood in each position of the hose without destroying the analogy. The pressure within the chest (the verticle pressure above ground level) does not affect flow because of the siphon effect as long as the tubing (blood vessels) are patent. The alveolar corner vessels have been shown to remain patent in spite of high alveolar pressures. They could maintain the column of blood through the chest necessary for the siphon under quite extreme collaps­ing pressures during the Valsalva maneuver.

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The Heart Is Not Always in Good Hands: Changes in Extracardiac Pressure

Lung Distension. In obstructed airflow disease, the end-tidal volume (FRC) is considerably enlarged and this volume characteristically rises further with the increase in ventilation demanded by infections or exercise. There are two important consequences of an increase in lung volume. One is the increase in right ventricular afterload, because the pulmonary vasculature is stretched and the resistance to flow through it is increased. The other is the distending force which stretches the heart and great vessels as it does the lungs (Fig 2). The pleural surfaces of the cardiac fossa and the surrounding lungs become more tense as the diaphragm descends and the rib cage expands.

Contrary to clinical lore, the average subcostal, intrapleural, or esophageal pressure does not increase much in obstructed airflow disease. The chest wall and diaphragm are still able to maintain the normal negative pressure average around the lungs. How¬ever, FRC expansion causes mediastinal pressures, particularly those around the heart in the cardiac fossa, to increase relative to subcostal intrapleural pressures. This could be because the lungs are bound together by the hilar structures and intrapulmonary ligaments so their expansion encroaches on the medi­astinal space, while they remain free to enlarge in the subcostal region (Fig 3).

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