Auscultation: a New Appraisal

Why is physical examination of the chest being neglected? Why do so many clinicians want to see an X-ray film before they make a physical examination of the chest? Is it because they lack confidence in physical examination? Will the roentgenogram give more information than they can obtain from a personal study of the patient? Will it give all the information desired? Or, does the fault lie in the uncertainty of the facts obtained by examining the chest by the eye, the ear and touch? 

It is common knowledge that neither physical nor X-ray examination always reveals fully the pathological condition in the lungs. The one contains the elements of strength and weakness involved in a human study of a human being; the other, the accuracy and inaccuracy of a mechanical approach to the same. Neither procedure, in itself, is fully satisfactory, but they supplement each other. Tuberculosis is the most interesting chest disease to study by means of the physical senses because it exhibits every form of pathological process that involves the lungs and pleura–pneumonitis, bronchitis, emphysema, cavity, pleural inflammation and effusion (both simple and purulent), and pneumothorax. 

Let us now inquire why physical examination is not more satisfactory. 

Normal respiratory sounds: Most physicians depend more on auscultation than on other methods of physical examination but have difficulty in interpreting their findings. The reason for this difficulty is not hard to find if one compares auscultatory sounds as heard in chests with their description found in textbooks and taught to medical students. 

The first basic error is the inaccurate description of the respiratory murmur itself. It is stated in textbooks that inspiration is to expiration as five to three, three to two, two to one, and so on, according to the authority consulted. Yet if one will listen carefully throughout the normal respiratory cycle, he will find there is very little difference in the length of inspiration and expiration. Inspiration is heard throughout the inspiratory phase, and expiration throughout the expiratory phase. 

Spirometric tracings made by Dr. Max Pinner (personal communication) and Dr. George C. Leiner on 6 normal persons show that the expiratory phase of respiration is even longer than inspiration. The last aspect of restoring the lung to its resting phase may be scarcely audible or inaudible. 

Pinner states: “In them [i.e. 6 normal persons] the average relative lengths of expiration to inspiration are as follows: 5.6:5.0; 6.0:5.0; 7.8:5.6; 6.4:4.6; 6.0:4.6; 8.0:5.0. The first figure refers to expiration and the second to inspiration in each case. As you see, the relation is consistent and the total average is 6.6:5.1.”

The probable reason expiration is apparently shorter on stethoscopic records is that inspiration is a much more forceful act than expiration. While both inspiration and expiration take place as a result of muscular activity, the expiratory effort is normally weaker than the inspiratory. Part of expiration and the final settling of the lung to its resting condition are due to the restoration of pressure equilibrium between the intraabdominal and intrathoracic cavities. This latter is probably attended by very little force; in fact, is almost passive. 

It is also taught that expiration follows immediately on inspiration in normal vesicular respiration but that there is a break between inspiration and expiration in bronchial breathing, whether found in normal or pathological chests. The facts are that this break may or may not be present in pathological chests. It is not a constant factor in pulmonary infiltrations. 

Cause of respiratory sounds: An important error arises from considering the effect of the column of air on the respiratory passages as the main factor in producing the respiratory murmur. I questioned this in my early writings.¹ 

Laennec² stated: “The sound of respiration presents different characters according as it takes place in the pulmonary tissue, the larynx, the trachea, or the large bronchial trunks.” He believed the sounds are produced by the air stream pressing against the trachea, bronchi and alveoli. He described the vesicular murmur as “a gentle but distinct murmur which indicates the penetration of air into the pulmonary tissue and its expulsion.” He recognized bronchial breathing as being heard normally in the first interspace and over the superior portion of the interscapular space, near and over the bifurcation of the bronchi and also over consolidations in the lung. 

In 1834, Beau³ suggested that respiratory sounds are caused by the air passing through the glottis, the trachea, bronchi and alveoli, each producing its characteristic quality, the whole being transmitted as one sound to the surface of the lung. In normal chests the alveoli are supposed to dominate the picture, hence the name “vesicular murmur.” In infiltrations bronchial elements are supposed to modify, causing “bronchovesicular” sounds; or dominate, causing bronchial sounds. Beau’s suggestion of the cause of the sounds has determined our teaching for more than a century. 

If the sounds are caused by the air rushing through the glottis and on into the finer air chambers, what causes the sound of expiration? Here the air is passing the other way. What causes the weakness of the murmur in abdominal as compared with costal breathing? The air rushes in–in the same volume and with similar speed. It enters the bronchi and the alveoli the same as in costal breathing. Why is it so weak in emphysema and rigid thorax? It still enters through the glottis. 

An experiment is reported by Bondet and Chauveau⁴ quoted by Powell and Hartley.⁵ A horse had pneumonia of the lower half of the left lung. “Exaggerated breathing was heard over the upper half of the left and the entire right lung, while ‘tubular’ breathing was heard over the infected portion of the left lung.” The trachea was then opened by an incision 20 centimeters long. The respiratory bruit was almost completely absent below the incision when held wide open. On auscultation over the consolidated portion of the lung no “tubular” sound could be heard on inspiration and only a faint sound on expiration. Over the remainder of the left lung and the entire uninfected right lung normal respiratory sounds were heard. They apparently accepted the idea of the sounds originating in the larynx, but concluded that the “pulmonary element takes an important share in the production of the normal respiratory sounds.” While some of their findings seem contradictory, we must recognize that they suggested to the authors that there is a pulmonary element in the production of respiratory sounds. 

It is necessary to bear in mind that these descriptions and suggestions were made by early observers who were working in a virgin field. Their experience in tuberculosis was probably confined to the far advanced. Their examinations were made at great disadvantage compared with to-day. The human chest was usually examined through clothing. Laennec said a bare chest was unnecessary. Structural pathology was undeveloped. The living pathology as we follow it now with the X-ray was decades in the future. The physiology of respiration was not understood. It was believed that air rushes from the glottis to the alveoli. 

We have no evidence that anyone prior to Laennec had tried to describe or explain minutely what was heard on auscultation, although Greek physicians are reported to have listened to the lungs by placing their ears on the chest wall. 

It is remarkable that Laennec could have given a description of the respiratory murmur and a classification of râles that should have endured for a century and a quarter. It is all the more remarkable when we recall that he died at the age of forty-five. Some of us have examined chests for fifty years and still are unable to clarify respiratory sounds to our full satisfaction. 

Without belittling the opinions of these early workers it is time to add what we can, in the light of recent discovery, to make physical examination more inviting and more dependable. 

Ornstein⁶ has given careful study to the cause of the sounds and has come to the conclusion that they may be explained on the basis of physical laws and suggests that “the mechanism is similar to the production of a sound in a labial pipe,” and that “the sounds are produced throughout the length of the bronchial tree wherever the inrushing column of air strikes the sharp edge of the bifurcating bronchus.” 

Sahli⁷ observed a patient with congenital fissure of the sternum and reported that increased intraabdominal tension caused the lung to protrude and that the filling of the alveoli produced a murmur with vesicular qualities. The same has been found in inflating and deflating lungs removed from a cadaver. 

I have taught for years that muscle sounds may simulate the respiratory murmur.^8,9,10,11,12 If one listens over a contracting and relaxing muscle, for example the biceps, he may hear sounds similar to those over the chest, which vary in pitch and intensity according to the tension in the muscles. A sound like a weak “respiratory” murmur may also be heard over the abdominal muscles below the costal margin, stronger in abdominal breathers. 

Having found that sounds similar to the respiratory sounds can be heard over muscles in various phases of contraction; that a weak respiratory murmur often may be heard over the side of the chest in which a lung is partially collapsed and separated from the chest wall by air or fluid; that it is weak in high-grade emphysema where the intercostals are markedly distended and unable to function normally; and in rigid thorax where the muscles are functioning very little; I cannot but believe that we must change our opinion of the cause of respiratory sounds and assign them to a more complicated mechanism. 

The air current, the bronchi, the alveoli, the lung mass, the respiratory muscles and the bony cage are all intimately involved in the respiratory act. That the larynx is limited as a factor is shown by the fact that the sounds are heard during bronchoscopy when the air enters through the tube, the same as in the experiment of Bondet and Chauveau, in which the air entered a wide incision in the trachea of a horse, as quoted above. The musculature of the bronchi which lengthens and dilates on inspiration and contracts and shortens on expiration undoubtedly influences the flow of the air and may cause some sound on its own part. The muscles of respiration, particularly the intercostals, are unquestionably important factors. The contraction of the crus and central tendon of the diaphragm and the abdominal muscles influences the murmur and enters into the sound directly. Size and form of the chest cavity, its elasticity, and the superficial muscles as well as those more intimately concerned with respiration, are all to be considered as factors. 

Not only will careful auscultation show that the inspiratory murmur occupies the entire inspiratory phase whatever its length may be, but also that the expiratory murmur, while often weaker, occupies the expiratory phase. It will also show that the basic murmur qualitatively and quantitatively differs in different individuals and in different portions of the chest in the same individual. Pulmonary sounds, both normal and pathological, fail to conform to standardization. 

Our premises are that respiratory sounds are expressed in vibrations set up by the entire respiratory mechanism: The vibrations are not limited to the column of air, nor the air plus the tubes through which it passes, nor these and the alveoli. They are wide-spread and involve the air column, the air passages, the pulmonary tissue, the muscles of respiration and bony thorax. 

That muscles cause sound vibrations may be shown by placing the stethoscope over contracting muscles such as the biceps, or abdominal muscles below the costal border as mentioned above. Vibrations not unlike those heard over the lung are conducted to the ear during contraction and relaxation. 

As the inspiratory muscles contract, the inrushing air itself vibrates. Moreover, vibrations are set up in the bronchi, alveoli and the superficial structures covering the chest. There is no doubt that the pressure of the air against the bronchial walls and in the alveoli, as suggested by Laennec, causes sound vibrations. Moreover, there is no doubt that the air column, passing through the narrow glottis as suggested by Beau, is thrown into vibrations. It may be that the onrushing air striking the sharp edge of bifurcating bronchi causes sound similar to a “labial pipe” as suggested by Ornstein. But it seems to me that all these explanations are too limited. There is more to be considered than the air column. 

When once we get a conception that the respiratory sounds are caused by all of the factors which form a part of the respiratory mechanism we will have a more rational approach to our problem. We will then understand that vibrations will continue throughout both the inspiratory and expiratory phases of respiration, and that the character of the sounds will be altered as the various factors in their production vary. We will then see that our findings on auscultation will be modified directly by our findings on inspection, palpation and percussion. 

The normal respiratory murmur is not a definite sound. Nor is the mechanism responsible for respiration a definite fixed quantity. 

That the muscles are an important part of the respiratory murmur may be inferred, as above mentioned, by analyzing those conditions in which intercostal action is limited, such as emphysema; calcification and ankylosis of the costal cartilages which immobilize the bony cage; and breathing which is predominantly abdominal in character. In all these conditions the respiratory murmur is weak no matter if the same inrush of air enters the lung as in costal breathing. 

A complete respiratory cycle consists of the inspiratory phase in which the diaphragm and external intercostals contract, the abdominal muscles relax, and the intrathoracic space is increased. The air rushes in and the elongated and dilated bronchi and the alveoli are filled. In the expiratory phase the diaphragm returns to its resting position as a result of the contraction of the abdominal muscles which increases the intraabdominal tension, and, with the aid of the internal intercostal muscles, restores the thoracic portion of the respiratory mechanism to its resting condition. During this last phase the air is expelled from the lungs, completing the cycle. 

Active muscular effort takes part in both the inspiratory and expiratory phases of respiration. Respiratory vibrations continue throughout both phases, unless interfered with by some anomaly in the mechanism or by some pathological interference. 

Pathological respiratory murmurs: An infiltrated area adds a hindrance or obstruction according to the degree to which the bronchi and alveoli are blocked and the elasticity of the pulmonary tissue is decreased. Infiltration interferes with both the ingress and egress of air. Air may not enter at all, or, if it does, it enters less easily. The respiratory movement is retarded. The lung expands more slowly and less completely than normal and takes longer to deflate. Part of this reduced movement of the chest wall is a muscular reflex and part of it is due to reduced expansion caused by the infiltration. The intercostal muscles prolong their inspiratory and expiratory action, and this influences the length and quality of the respiratory note. 

In case of infiltration, it is evident that the sound vibrations in the air current, the bronchial musculature, the alveoli, the bony thorax and the muscles of respiration may all be altered; but altered differently in different individuals and according to the nature of the infiltration. 

So the effect of infiltration on the respiratory murmur is an impeding or lengthening of inspiration and slowing (prolongation) of expiration, probably raising the pitch somewhat and prolonging the phases because the air does not have the normal contractility of the alveolar tissues and bronchi to receive and expel it. Possibly an increased effort on the part of the respiratory muscles might be required, too. It is evident that the sounds would vary greatly with different types of infiltration and the different degrees of interference with the various factors which take part in the respiratory mechanism. 

In limited infiltrations the variation may be so slight as to be imperceptible, while in extensive infiltrations it may be very marked. Different portions of the respiratory mechanism predominate at different times. The more complex the mechanism for causing respiratory sounds, the more will the sounds differ in different individuals even with the same morbid change. So, if the entire respiratory mechanism enters into the production of the respiratory murmur, we have a more reasonable explanation for the variation in sounds than we have if we consider only the changes in the current of air. 

The blocking of a stem bronchus by a tuberculous lesion may allow very little air to enter the lung. This may diminish but I have not seen it obliterate the respiratory sound. The intercostal muscles still contract both on inspiration and expiration. If anything diminishes or increases the movement of a hemithorax, both inspiration and expiration may be weakened or exaggerated, prolonged or shortened according to the nature of the pathological change and the extent to which the movement is interfered with. 

In emphysema the intercostal muscles, both external and internal, are stretched, and the intercostal spaces are widened and the action of the muscles is interfered with. The same is true in chronic asthma with addition of bronchial constriction. Under these conditions the muscular element is lessened and, while the patient may be able to breathe with fair ease when at rest (showing that the column of air enters the lungs), the respiratory sounds show degrees of weakness which now and then amount almost to inaudibility. The expiration is prolonged because of the inefficiency of the expiratory muscles and the overstretching of the pulmonary tissues and their lessened ability to contract. On extra effort the patient attempts to breathe fast but the muscles cannot respond. Every factor in the respiratory mechanism goes awry. 

In certain patients with poliomyelitis in whom the intercostal muscles were involved, years after the attack I found the ribs horizontal, the intercostal spaces widened, the muscles distended and inefficient and the respiratory note prolonged and markedly diminished in intensity. 

The rigid and emphysematous chests of the aged show a weak respiratory murmur, although there may be no recognized dyspnea. 

Thus the column of air in emphysema, chronic asthma, the poliomyelitis chests above mentioned, rigid chests and abdominal breathers, enters the air passages and penetrates the alveoli, but the vibrations set up are weak and the respiratory murmur is of low intensity. The muscular element is reduced in all these conditions. 

An increased cellular and fluid content of the tissues, air cells and small bronchi, such as we see in pneumonia or the exudative type of tuberculosis (tuberculous pneumonia), may be accompanied by the usually described bronchial breathing. However, the transmission of the voice does not dominate the picture. On the other hand, in a preponderantly proliferative tuberculosis in which the fibrous elements predominate (scar tissue) the vibrations of the air column and tissues are high-pitched and prolonged and their transmission predominates over all other factors which cause respiratory vibrations. 

A similar condition is met in case of cavitation. A cavity with soft walls in the midst of tissues which are infiltrated with inflammatory elements (the so-called silent cavity of Dunham) may not be detected by any characteristic respiratory sound. All the usual elements of the respiratory mechanism may contribute their vibrations but that of the voice and pulmonary tissues is not prominent. 

On the other hand, a cavity with fibrous walls and open bronchus in the midst of dense fibrous tissue will transmit exaggerated air and tissue vibrations which produce a characteristic respiratory sound. If the mouth is held open and the syllables “ha ha” are repeated in a whisper and prolonged, a low-pitched blowing may be heard differing mainly in pitch from the sound heard over a dense scar without excavation. 

The vibrations in the presence of extensive scar tissue, either with or without cavity, are predominantly of air column and tissue origin, the muscle element being overshadowed. 

Adventitious sounds: Sounds which accompany respiration (râles or adventitious sounds) are of great diagnostic significance. They have borne the name “râles” since first described by Laennec. His division of dry, moist and crepitant râles is still followed and still supposed to designate the same conditions to which he assigned them one hundred and twenty-five years ago. We have not reexamined the respiratory sounds or the “râles” which often accompany them either in the light of more recent pathology or the findings of the X-ray. 

One would get the idea from reading the literature of tuberculosis that râles are nearly always heard over tuberculous infiltrations. But such is not the case. Nor are all râles heard in a tuberculous chest of pulmonary origin. Many of them are extrapulmonary; and it is necessary to appreciate these as well as those of pulmonary origin. 

All who are interested in râles should read the paper by Coplin¹³ on the inflammatory and degenerative changes which take place in the pleura and intercostal tissues in diseases of the lungs and pleura. He gives a pathological basis for these adventitious sounds which are persistent after pleural involvement. I quoted from his paper extensively in Clinical Tuberculosis11 and also in my forthcoming book on tuberculosis. 

I have found clinically that râles may persist when the pleura has previously been involved. They originate in both the pleura and the intercostal structures and usually are accompanied by an easily recognized degeneration of the overlying skin and subcutaneous tissue. These areas too are frequently the seat of recurrent and not infrequently of persistent pain. 

That these râles are not of pulmonary origin may be inferred from the fact that they are frequently present when the X-ray film shows no abnormal pulmonary shadow. However, when they are present and the underlying pulmonary structure is also diseased, one cannot be so sure of the origin of the râles; they may arise either in the pulmonary or pleural tissues. Nevertheless, I have made it a rule to suspect, at least, a partial nonpulmonary origin if the overlying soft tissues are degenerated; for the trophic reflex in case of the pleura lies in the zones immediately overlying the inflamed area. 

No doubt the cause of this degeneration is twofold: one reflex through injury of the intercostal nerves by long stimulation the same as in case of the trophic reflex in the cervical (particularly third, fourth and fifth) zones when the lung is chronically inflamed; the other is the direct effect of the chronic infection by continuity as suggested by Coplin. 

I cannot emphasize too strongly the importance of recognizing the presence of these nonpulmonary râles. They cannot be differentiated by their sound or their size from the subcrepitant and the crackling râles which arise in the lung and which are usually described as being caused by mucus in the air passages. 

It is usually taught that râles may be determined as being of pulmonary origin if they are detected following expiration, mild cough and prompt light inspiration. These nonpulmonary râles are heard following the same procedure. Nonpulmonary, usually designated as pleural râles, are supposed to be nearer the ear, but differentiating the location of râles within a distance of a centimeter or two, to say the least, is uncertain. 

Of course, the whistling and gurgling, the rhonchi and wheezes, are a different story. They are definitely of pulmonary and bronchial origin.

 

Discussion

With the inaccuracy in description of the normal respiratory murmur, the probably wrong explanation of the mechanism of its production and the inaccuracy of our knowledge of râles, is it any wonder that there should be confusion on the part of clinicians in interpreting the data obtained on auscultation? That physicians examine better than their teaching would warrant, goes without saying; for each learns certain sounds and certain modifications of them which he interprets in a certain manner. 

Another important fact must be understood. No type of murmur or modification of that type always means the same pathological change. We would like to think that whenever pneumonia is present a given sound will be found; and that, whenever we find that sound, pneumonia will be present. We would like the same for the various pathological changes found in tuberculosis, lung abscess, bronchitis, bronchiectasis and so on. But it is not true. 

If all lungs were of the same volume and had the same degree of elasticity; all bony thoraces were equally elastic or rigid; all musculature of equal volume and tension; all larynges were of equal capacity; all pleurae and mediastina were free; and the respiratory demands were the same on each individual, then the normal respiratory murmurs could be described as fixed and definite, and a given departure might mean a definite pathological alteration. But since these things are not true, each clinician must learn that variability is the rule in both normal and pathological chests. 

Moreover, it must always be remembered that pressure on the stethoscope decreases the intensity of respiratory sounds and that the fundamental characteristic of tones heard varies with different stethoscopes according to the size and nature of the bell and the character of the rubber tubes used. In teaching respiratory sounds, teacher and student should use the same kind of stethoscope if they would speak the same language, or one bell with multiple ear pieces. 

Any good diagnostician has doubtless been confused on auscultating chests by finding sounds which he was not able to interpret according to the descriptions found in the books. He may find the so-called vesicular murmur over a cavity and bronchial respiration over apparently normal pulmonary tissue and absent over infiltrations where he has learned it should be. He frequently will find râles that he has been taught to consider as belonging to a tuberculous infiltration where other signs fail to show such lesions. Yet if he will carefully inspect, palpate, percuss and auscultate, and as carefully analyze the phenomena discovered, he will find that even without an X-ray examination he is able to determine pulmonary and pleural lesions with great accuracy. 

If the respiratory sounds are the product of vibrations originating in all parts of the respiratory mechanism, it is all the more necessary to interpret the knowledge gained on auscultation in accordance with that obtained by other methods of physical examination. So it is important to recall the data which may be derived by inspection, palpation and percussion and discuss briefly how this may affect the respiratory mechanism. 

Inspection: Aside from giving the examiner a general idea of the patient and acquainting him with any deformities or gross departures from the normal, careful inspection will provide valuable information of what is going on within the chest at the time of the examination and what has transpired previously that may modify the respiratory murmur. In combination with palpation, inspection will reveal reflex spasm and atrophies which indicate both present and past disease and cause the examiner to suspect changes in the respiratory murmur. 

Palpation: Textbooks teach that by palpation one can note such things as the texture of the skin, the presence or absence of enlarged lymph nodes, and the vibrations caused by the spoken voice. But these are least important from a diagnostic standpoint of all the things that may be detected by palpation. 

Increased tension of the apical muscles is important confirmatory evidence when an active tuberculosis is present in the underlying lung. Degeneration of the same muscles and the skin and subcutaneous tissue above the second rib anteriorly and the spine of the scapula posteriorly is evidence that the lung is the seat of a chronic or healed lesion, usually tuberculosis. These are important diagnostic data, and a knowledge of their presence is necessary to the proper interpretation of auscultatory findings. Likewise, the boardiness of the intercostal muscles immediately over an acute pleurisy, and the degeneration of the skin, subcutaneous tissue and intercostal muscles when the pleurisy persists for any length of time are of great diagnostic value and indicate probable changes in the respiratory sounds. This degeneration may be found anywhere between the second rib anteriorly and the spine of the scapula posteriorly above, and the margin of the ribs below. 

In chronic or healed pleurisy adventitious sounds are heard frequently and sometimes persistently over these same areas that show degeneration of the intercostal muscles and overlying subcutaneous tissues. These râles are sometimes heard without coughing but oftener when the patient gives two or three easy coughs and follows with a short quick inspiration. The roentgenogram may show nothing at all, but the effects of the former changes in the pleura and intercostal tissues may be clearly seen in the atrophied superficial tissues. In this connection it must be stated that râles are not always present even though the degeneration of tissues shows that pleurisy was formerly present. However, some degree of lessened motion is usually present. Many times pain is felt in these areas under conditions of stress such as tiring, emotional upsets, menstruation and change in weather. This pain is due to injury of the intercostal nerves as a result of the chronic inflammation. Understanding the origin of this trophic reflex and pain is essential to the interpretation of the respiratory sounds heard under these circumstances. 

Lagging and lessened motion of the chest wall in some particular area or on one side, or as a whole, is of great diagnostic significance. Of importance, too, is the detection of different degrees of density in the tissues according to the underlying pathological changes noted on palpation. 

It is important to know that infiltrations and emphysema, and fluid and air in the pleura, can be determined by palpation as well as percussion, and that these alter the percussion note. 

The data obtained on palpation have bearing on the auscultatory sounds in proportion to the degree that they cause changes in the respiratory mechanism. 

Percussion: Physicians learn to recognize differences in quality, intensity and pitch of the percussion note. Their fingers are trained to perceive different degrees of resistance over percussed areas. Many depend far more on the sensation conveyed to the fingers than on the sound elicited; and many of our best diagnosticians pay little or no attention to sound but learn to percuss almost without producing sound. This is only one step removed from detecting different degrees of density by palpation. The data derived by percussion, the same as by palpation, suggest an alteration in the respiratory note to the extent that they interfere with the respiratory mechanism. 

This discussion may at first seem to take away the whole basis on which auscultation stands. Instead, more careful study will show that it only broadens the base and furnishes an explanation for the difficulties and inaccuracies which have heretofore confused the clinician. By suggesting auscultation as being a method of studying the whole respiratory mechanism instead of the air current, it gives a better conception of what is going on within the respiratory system.

 

Summary

1. The long taught description of the relative length of inspiratory and expiratory breath sounds is erroneous. They are about equal in length–inspiration occupying the entire inspiratory phase and expiration occupying the entire expiratory phase. 
2. The suggestions that the respiratory murmur is caused by air pressing against the walls of the bronchi, dilating and closing the alveoli as suggested by Laennec, by passing through the glottis as suggested by Beau, or by striking the sharp edges of the bifurcating bronchi as suggested by Ornstein, simplify the respiratory murmur too much. While all may be factors they are not the whole cause. The cause is very complex and includes vibrations in all parts of the respiratory mechanism. Inspiration is caused by contraction of the external intercostal muscles and diaphragm, enlarging the chest cavity and causing the lung to expand, the bronchi to dilate and lengthen, and the alveoli to open. Expiration is caused by the contraction of the abdominal and internal intercostal muscles, and relaxing and restoring the diaphragm to its resting position, diminishing the size of the thoracic cavity and allowing the lung to return to its normal resting size, shortening and lessening the lumen of the bronchi and relaxing the alveoli. 
3. Râles are both pulmonary and extrapulmonary. The latter may be caused by a chronic pleuritis extending to the intercostal structures, or to reflex trophic effects in the same structures. 
4. There is no definite sound that denotes a definite disease. The respiratory mechanism would always have to be the same to make the respiratory note always the same.

 

Sumario

 La Auscultación–Una Re-Avaluacion 

 

1. La vieja descripción de la relativa duración de las fases inspiratoria y expiratoria de los ruidos respiratorios peca de errónea. Su duración es aproximadamente igual, ocupando la inspiración toda la fase inspiratoria y la expiración toda la expiratoria.
2. Las sugerencias de que el soplo respiratorio es producido por el aire, que al comprimir las paredes de los bronquios, dilata y cierra los alvéolos, según insinuara Laennec, o al atravesar in glotis, según Beau, o al herir los agudos bordes de las bifurcaciones bronquiales, según Ornstein, simplifican demasiado el soplo respiratorio. Aunque todos esos fenómenos pueden ser factores, no constituyen toda la causa. Esta es muy compleja y comprende las vibraciones de todas las partes del mecanismo respiratorio. La inspiración tiene por causa la contracción de los músculos intercostales externos y del diafragma que dilata la cavidad torácica y hace que el pulmón se expanda, que los bronquios se dilaten y alarguen y que los alvéolos se abran. La expiración se debe a la contracción de los músculos intercostales abdominales e internos y a la dilatación y restablecimiento del diafragma en su posición de reposo, y la disminución del tamaño de la cavidad torácica, que al dejar que el pulmón recupere su tamaño normal en descanso, acorta y achica la luz de los bronquios y dilata los alvéolos. 
3. Los estertores son tanto pulmonares como extrapulmonares, pudiendo deberse los últimos a una pleuritis crónica que se extiende a los tejidos intercostales, o a efectos tróficos reflejos sobre los mismos. 
4. No existe ningún ruido bien definido que denote una enfermedad bien definida. El mecanismo respiratorio tendría que ser siempre el mismo para producir una nota respiratoria siempre idéntica. 

 

References Cited:

1. Pottenger, F. M.: The Diagnosis and Treatment of Pulmonary Tuberculosis, Wm. Wood & Co., New York, 1908, p. 21.
2. Laennec, R. T. H.: A Treatise on Mediate Auscultation, and on Diseases of the Lungs and Heart, English Edition, edited by Theophilus Herbert, London, H. Bailliere, 1846, p. 23.
3. Beau, M.: “Recherches sur la Cause des Bruits Respiratoires percus au Moyen de l’Auscultation,” Archives Generales de Medecine, Paris, 1834, II série, tome V, p. 557. 
4. Bondet, A., and Chauveau, A.: “Contribution à l’étude du mécanisme des Bruits respiratories normaux et anormaux,” Rev. Mens. de Méd. et de Chir., Paris, 1877, 1, 161.
5. Powell, Sir Douglas, and Hartley, P. Horton Smith: Diseases of the Lungs and Pleurae, London, H. K. Lewis & Co., 1921, Sixth Ed. 
6. Ornstein, G. C., and Ulman, D.: Physical Diagnosis in Pulmonary Tuberculosis, chap. VII, in Clinical Tuberculosis by Benjamin Goldberg, 1935, Philadelphia, F. A. Davis Co. 
7. Sahli, H.: Correspondenblatt für Schweitzer Aertzte, 1892, quoted from 1.
8. Pottenger, F. M.: “Muskelspasmus und Degeneration. Ihre Bedeutung für die Diagnose Intrathorazischer Entzündung und als Kausalfaktor bei der Produktion von Veränderungen des knöchernen Thorax, und leichte Tastpalpation,” Beitr. z. Kiin. d. Tuberk., 1912, 22, 1. Published in English: Muscle Spasm and Degeneration in Intrathoracic Inflammation and Light Touch Palpation, 1912, St. Louis, C. V. Mosby Company. 
9. Pottenger, F. M.: “Spasm of chest muscles, particularly the intercostals as a physical sign of disease of the lungs,” Am. J. M. Sc., 1909, 137, 669. 
10. Pottenger, F. M.: “Inspektion, Palpation, Perkussion und Auskultation bei der Frühdiagnose der Lungentuberkulose,” Beitr. z. Klin. d. Tuberk., 1915, 53, No. 1. 
11. Pottenger, F. M.: Clinical Tuberculosis, Vol. I, C. V. Mosby Co., St. Louis, 1917, p. 429. 
12. Pottenger, F. M.: Tuberculosis in the Child and the Adult, C. V. Mosby Co., St. Louis, 1934, p. 264. 
13. Coplin, W. M. L.: “Changes in the intercostal muscles and the diaphragm in infective processes involving the lungs and pleura,” Am. J. M. Sc., May, 1904.
14. Pottenger, F. M.: Clinical Tuberculosis, Vol. II, C. V. Mosby Co., St. Louis, 1917, p. 61.