1 Who invented lung auscultation?

Auscultation of the direct or immediate variety (that is, without the use of the stethoscope) has actually been around for a long time. References to breath sounds first appeared in the Ebers papyrus (c. 1500 BC), the Hindu Vedas (c. 1400–1200 BC), and the Hippocratic writings (4th century BC). In fact, Hippocrates himself taught and practiced auscultation, advising physicians to apply their ears to the patient’s thorax in order to detect various diagnostic sounds. Since then, chest auscultation was mentioned by Caelius Aeralianus, Leonardo Da Vinci, Ambroise Paré, William Harvey, Giovanni Battista Morgagni, Gerhard Van Swieten, William Hunter, and many others. The hypochondriacal Robert Hooke, an assistant to Robert Boyle and one of the first scientists to use the word cell (1664), even had a good insight in describing heart sounds. He wrote, “Who knows? It may be possible to discover the motions of internal parts. .. by the sound they make.” Yet, during the 18th and early 19th centuries, direct auscultation fell rapidly out of favor, being replaced by a newer diagnostic modality: chest percussion. It took a lot of serendipity (and plenty of shyness) to rekindle it as indirect auscultation, that is, one “mediated” by a newly invented cylindrical instrument, the stethoscope. The hero of this rediscovery was an introverted, diminutive, very asthmatic, very prudish, and very tuberculotic Breton physician, named René Théophile Hyacinthe Laënnec. In the fall of 1816 (a year after the battle of Waterloo), he was summoned to the bedside of a young woman with a chest illness. Because percussion was technically difficult (given the large size of the woman’s breasts) and since direct auscultation (i.e., placing the physician’s naked ear over the patient’s naked chest) was, in Laënnec’s own words, “inadmissible” (given the young lady’s age and gender), Laënnec came up with a totally different approach. He remembered that a few days before, while walking in the Tuileries garden in Paris, he had seen children scraping a stick of wood and listening to the other end. Imagining that something similar could be tried with patients’ chests, he fetched a cardboard, rolled it into a cylinder, applied it to the lady’s thorax, and to his amazement, was able to hear very distinct lung sounds. And all of this without even touching her! Being handy (he used to make flutes), Laënnec quickly manufactured a wooden contraption, shaped like a flute, which he started taking regularly on rounds. He dubbed it the cylinder (and this, in turn, gave his students a chance to dub him “the cylindromaniac”). Yet, in academic circles the tool came to be known as the stethoscope, from the Greek term for “inspector of the chest.” Whatever its name, the gadget allowed Laënnec to gather over 3 years an astounding wealth of clinical–pathological correlations, which he then published on August 15, 1819—in a two-volume book titled De l’Auscultation Mediate. There he reported masterly descriptions of several chest diseases, many previously unheard (no pun intended), like bronchitis, bronchiectasis, pleurisy, lobar pneumonia, hydrothorax, emphysema, pneumothorax, pulmonary edema, pulmonary gangrene and infarction, mitral stenosis, esophagitis, peritonitis, cirrhosis (hence the eponym Laënnec’s cirrhosis), and, of course, tuberculosis. And since autopsy was the ultimate benchmark for all these conditions, several ended up acquiring a pathological name. The book also presented an entirely new terminology, rooted in daily life examples and enriched by Laënnec’s fascination with Greek and Latin language. Among such neologisms were stethoscope, but also auscultation, rales, rhonchus, fremitus, crackled-pot sound, metallic tinkling, egophony, bronchophony, cavernous breathing, puerile breathing, veiled puff, and bruit. The first edition of De l’Auscultation sold for 13 francs (16 if purchased with a wooden stethoscope) and sold quite badly. But when the considerably rewritten second edition hit the press, stethoscopy had already become the standard of chest examination. By the time of Laënnec’s premature death from tuberculosis (in 1826, at age 45), many physicians were carrying stethoscopes, all personally made by Laënnec. In fact, the posthumous third and fourth editions of 1831 and 1837 sold very well, establishing the tool not only as a symbol of the art of medicine, but also as the centerpiece of bedside assessment. To reach a diagnosis, physicians could now rely on “objective” findings (instead of subjective symptoms reported by patients). They could finally tell their patients what they had wanted to say for a long time, “Shut up and let me listen to your lungs!” A new era had begun: one in which the patient was going to become first a sound, then a laboratory number, and, finally, a flickering computer image.

2 How do modern stethoscopes differ from Laënnec’s original cylinder?

Not a lot. The binaural stethoscope (invented in 1954 by Camman of New York) clearly helped. Yet, even today’s expensive stethoscopes remain primarily a simple conduit for transmitting sound between the patient’s chest and the examiner’s ears. Even as conduits, they have flaws. For one, most of them selectively amplify specific frequencies, such as those below 112   Hz (a welcome feature for cardiologists, who deal with the low-pitched S₃ and S₄, but a not-so-welcome feature for pulmonologists, who deal instead with higher-frequency sounds). That is also why pulmonary auscultation has benefited so much from sound analysis through computer technology.

3 In addition to issues of nomenclature, why is pulmonary auscultation difficult?

Because sounds are of too low frequency to hear well, plus they often overlap. This renders chest auscultation akin to listening to a group of people whispering at the same time. This is especially difficult in cardiac auscultation since heart sounds and murmurs have lower frequency, plus the cardiac cycle is shorter (0.8   second versus 2–3 for the respiratory cycle). To tackle these challenges, physicians develop pattern recognition, a crucial skill in clinical medicine, but one requiring practice.

4 How high is the interobserver variability of chest auscultation?

Quite high. In a study by Shilling et al., two physicians disagreed 24% of the time in identifying the abnormal lung sounds of 187 cotton workers. A similar figure was reported by (1) Fletcher et al. in specialists’ recognition of emphysema; (2) Smyllie et al. in the assessment by nine physicians of the crackles and rhonchi of 20 patients; and (3) Schneider and Anderson for the recognition of decreased breath sounds. Although this variability seems too high to be acceptable, it is actually not much higher than that found in data collection in general, including interpretation of radiographs.

5 What are lung sounds?

They are sounds generated by the lungs. Transmitted voice sounds are instead sounds generated by the larynx and subsequently transmitted through the lungs (Fig. 14-1).

Figure 14-1 The three categories of lung sounds: breath sounds, adventitious lung sounds, and transmitted voice sounds.

6 What are the major types of lung sounds (respiratory sounds)?

Each of these subgroups contains various other sounds (Table 14-1).

7 How are lung sounds produced?

By two major mechanisms: (1) air movement along the tracheobronchial tree (which is responsible for basic lung sounds, or breath sounds) and (2) vibration of solid tissue (which is responsible for adventitious [or extra] lung sounds).

8 What are breath sounds?

They are sounds heard over the chest of healthy (and diseased) subjects. They represent the background noise over which adventitious (or extra) sounds are occasionally superimposed.

9 What are the major types of breath sounds?

This traditional division is based on the sound’s site of production. Conversely, a more recent classification (based on physical characteristics) reports only two major lung sounds: (1) the normal ones (or vesicular breath sounds) and (2) the abnormal ones (or tubular breath sounds). The latter consist of three subvarieties: tracheal, bronchial, and amphoric. As for the bronchovesicular breath sound, it is in a league of its own and one that should probably be abandoned. (Fig. 14-2)

Figure 14-2 Diagrammatic representation of the three major types of breath sounds.

10 What is the air movement responsible for the production of breath sounds?

It depends on the size of the airway. Overall, three types of movement may take place along the tracheobronchial tree (Fig. 14-3). Some are silent and others noisy:

Figure 14-3 The three types of air movement that may take place along the tracheobronchial tree.

11 How are breath sounds produced?

Mostly by turbulent and vorticose flow in the trachea and central bronchi (see below, “tubular” breath sounds). Airflow in smaller and more peripheral airways is instead laminar and thus silent.

12 Can breath sounds be heard over both the chest and mouth?

Yes. Although produced in the central airways, they are transmitted both downward (to the chest) and upward (to the neck and mouth).

13 Are breath sounds at the chest different from those at the mouth?

Yes, because sounds’ characteristics depend on the tissues they traverse, especially their filtering properties. Alveolar air, for example, is a high-frequency filter that eliminates components >200   Hz. Since sounds transmitted to the mouth cross very little alveolar air, they will maintain all their original frequencies, including the highest. Sounds transmitted to the chest, however, traverse so much alveolar air to eventually lose most of their high frequencies. Since low frequencies are poorly perceived by the ear, sounds at the chest are typically softer than those at the mouth.

14 What are the acoustic characteristics of breath sounds at the mouth?

The dominant one is the high pitch (and loudness). Hence, sounds at the mouth have much wider frequencies, ranging between 200 and 2000   Hz—very much like white noise (Fig. 14-4).

Figure 14-4 Mouth versus chest sounds. Note that chest sounds are overall softer and lower-pitched than mouth sounds.

(Adapted from Forgacs P. Lung Sounds. London, Bailliere Tindal, 1978.)

15 What is the value of comparing breath sounds at the mouth with those at the chest?

The value of identifying airflow obstruction. Breath sounds heard at the mouth by the unaided ear have an intensity that is directly related to the spirometric degree of airway obstruction (i.e., the louder the sounds, the greater the obstruction). Conversely, breath sounds over the chest have an intensity that is inversely related to airflow obstruction, with distant sounds reflecting worse flow.

16 How do breath sounds at the mouth get produced?

By turbulent airflow in proximal bronchi and the trachea. In normal subjects, this flow is slow enough to barely make audible any noise at the mouth. Conversely, in patients with chronic obstructive pulmonary disease (COPD), the turbulence parallels airway narrowing, eventually causing very loud mouth breathing. This increased loudness is purely limited to breath sounds and thus can occur even in the absence of crackles or wheezes. In fact, loudness can become so high that the inspiratory breath sounds of patients with COPD are often heard across the room, even in patients breathing at rest. This concept is not new, since Laënnec himself had noticed an association between noisy mouth breathing and dyspnea, reporting a patient whose breath sounds could be heard at a distance of 20 feet. In fact, he devoted a full page of De l’Auscultation Mediate to this phenomenon, explaining in detail that what he meant by “loud breath sounds at the mouth” was just “loud breathing,” and not the noise of rattles, wheezes, or rhonchi.

17 Are there differences in intensity of breath sounds between the various types of airflow obstruction?

Yes (Table 14-2). In fact, the intensity of inspiratory breath sounds at the mouth can help differentiate emphysema from chronic bronchitis or asthma, since in only the last two conditions it directly correlates with (1) increased airway resistance; (2) reduced FEV₁ (forced expiratory volume in 1 sec); and (3) reduced peak expiratory flow rate (PEFR). Conversely, in emphysema, inspiratory breath sounds at the mouth are paradoxically quiet and almost silent because emphysema causes no direct narrowing of the bronchi, but only a dynamic expiratory airflow obstruction due to loss of elastic recoil.

Table 14-2 Changes in Lung Sounds with Pulmonary Disease

(From Wilkins R: Lung Sounds. St. Louis, Mosby, 1996.)

18 Are there any other unique breath sounds’ characteristics in patients with chronic bronchitis?

The most peculiar is indeed the paradoxical behavior of inspiratory sound intensity: increased at the mouth and softened at the chest. More often, however, chronic bronchitics tend to have noisy chests, not because their breath sounds are indeed louder (in fact, they are actually softer), but because there are so many superimposed adventitious sounds to make the overall intensity appear louder. These extra sounds include early inspiratory crackles and rhonchi (both of which may clear with coughing), but also end-expiratory wheezes.

19 How accurate is auscultation in identifying patients with chronic bronchitis?

Quite accurate, especially if computer aided. In a study of 493 subjects, computerized lung sound analysis—added to a screening program based on a symptom questionnaire plus spirometry—increased the sensitivity for detecting respiratory diseases from 71% to 87%. Half of all subjects with normal spirometry (but symptoms of chronic bronchitis) had abnormal lung sounds,primarily wheezing. Of the 24 subjects who only had abnormal lung sounds (but normal spirometry and no symptoms), three developed heart or lung disease at a 12- to 18-month follow-up.

20 Should patients with suspected chronic bronchitis be asked to cough during exam?

Yes, since crackles (and rhonchi) of airflow obstruction clear with coughing. This is because they originate from air-fluid interfaces of large to medium airways. Conversely, there are some crackles that may appear after coughing (posttussive crackles), especially over the apical lesions of tuberculosis. Hence, the relationship with cough is a good clue to the sound’s origin and should be routinely elicited. According to an old saying, you can tell a chest specialist from a generalist because the generalist never asks the patient to cough during auscultation, whereas the specialist always does.

(1) Tubular Versus Vesicular Breath Sounds

22 What are the main characteristics of tubular breath sounds?

Figure 14-5 Location and diagrammatic representation of tracheal (tubular) breath sounds.

23 Which of these characteristics is the most important?

The high frequency. Since they cross very little alveolar air, tracheal sounds (the quintessential tubular breath sounds) will contain higher frequencies than the vesicular ones, thus appearing louder and “hollow.” In fact, they have a range between less than 100 and more than 1500   Hz, with maximal intensity at 300–800. Exhalation also has a slightly higher intensity than inspiration.

24 What is the clinical significance of tracheal breath sounds?

It is indirect and linked to their resemblance of other (and more clinically relevant) tubular sounds: the bronchial.

25 What happens to tracheal sounds once they enter the chest?

Once the trachea enters the chest (and branches into bronchi and bronchioli), it gets surrounded by a mantle of alveolar air that acts as a muffler, dampening the intensity (and frequency) of the original tubular sounds and thus transforming them into vesicular sounds. Hence, alveolar air acts as the equalizer of your home stereo equipment, and also as a low-pass filter: it eliminates high-frequency (and thus also louder) components, while preserving low-frequency (and softer) tones.

26 What are the three characteristics of vesicular breath sounds?

27 Why are these sounds called vesicular?

Because Laënnec believed they were generated by “vesicles” (the alveoli), whereas in reality they are still generated by tubes (i.e., bronchi and bronchioli), albeit filtered (and modified) by alveoli.

28 What is the clinical significance of vesicular breath sounds?

They are the normal breathing-associated sounds of healthy people. In other words, vesicular breath sounds are the same as normal breath sounds.

29 Is the ability of the lung to act as a high-frequency filter a constant phenomenon?

No, it can be eliminated by replacing the alveolar air with a medium that transmits sound better—liquid, for example. This can come as pus (pneumonia), serum (pulmonary edema), or blood (alveolar hemorrhage). Alternatively, air can be simply “squeezed out” of the alveoli, as in patients with alveolar collapse. Both mechanisms produce an airless lung (i.e., consolidation), with liquid or solid replacing alveolar air. This allows better transmission of sound, including those high-frequency components that are normally filtered out. Hence, sound will be perceived as louder.

30 What are the acoustic differences between bronchial and vesicular breath sounds?

Bronchial breath sounds have a peculiar quality, similar to that of tracheal breath sounds: hollow, tubular, almost Darth Vader–like. They are also louder than vesicular breath sounds—mostly because they are richer in high frequencies. Hence, their respiratory cycle is graphically represented by thicker lines. Finally, they have a silent pause between inspiration and expiration, with a longer expiratory phase. Because of longer exhalation, bronchial breath sounds also have an inspiratory-to-expiratory (I:E) ratio that is usually 1:1 (instead of 3:1 or 4:1 for vesicular sounds).

31 What is the most striking physical characteristic of bronchial breath sounds?

Their high frequency. This is because consolidation is associated with an overall increase in lung density, which prevents it from functioning as a low-pass filter (i.e., as an equalizer that eliminates frequencies >200   Hz). Since airless lungs allow the unaltered transmission of high-frequency sounds, bronchial breath sounds will come across as loud. Also, both inspiration and expiration have similar component frequencies (between 100 to 1200   Hz) with maximal intensity of 300–900   Hz. These frequencies are much higher than those of vesicular breath sounds and are, in fact, similar to those of other tubular breath sounds, such as the tracheal sounds.

32 What is the clinical significance of tubular breath sounds?

It depends on location: they are entirely normal over the neck (i.e., originating in the trachea), but pathologic over the chest (originating in the bronchi). In this case, bronchial breath sounds (BBS) reflect absence of alveolar air and its replacement by media that better transmit high frequencies: liquid or solid (i.e., consolidation). Hence, they indicate patent airways in a setting of airless alveoli.

33 Where are vesicular breath sounds produced?

In large central airways, with the inspiratory component probably originating more peripherally than the expiratory one. Sounds so produced are then transmitted through the air-filled alveoli surrounding the bronchi. Since the mantle of alveolar air acts as a “low-pass” filter, vesicular sounds only retain low frequencies (100–500   Hz), with a steep cut-off greater than 200 and maximal intensity less than 100.

34 Are there acoustic differences in vesicular breath sounds between inspiration/expiration?

Expiration has lower pitch and intensity. In fact, its last two thirds are entirely silent. Hence, expiration is also shorter than inspiration, with an I:E ratio of 3:1 (in tubular sounds, it is 1:1).

35 Do vesicular breath sounds change with age?

Yes. Those of children (up to age 9) are higher pitched (and louder) than adults’. In turn, vesicular breath sounds of adults are higher pitched (and louder) than those of elderly. Laënnec was the first to notice this phenomenon and called it “puerile respiration.”

36 Why does this happen?

Probably because of the different resonance of small thoraces, leading to less power in low frequencies for children’s breath sounds (and also because of the progressive emphysema of the elderly, with an increase in “muffling” air). The smaller radius of children’s airways also may be responsible for the higher turbulence and loudness of their vesicular breath sounds.

37 Are vesicular breath sounds normally heard throughout the chest?

No. Although present over most lung fields of normal patients, vesicular sounds are classically absent in two narrow areas, corresponding anteriorly and posteriorly to the trachea and central bronchi (parascapular areas). Here, the vesicular sounds are replaced by bronchovesicular sounds (see also below, questions 60–62). Outside these narrow areas, presence of distinct vesicular sounds remains a sine qua non for a healthy lung (Fig. 14-6).

Figure 14-6 Vesicular sounds are classically absent in two narrow areas, corresponding anteriorly and posteriorly to the trachea and central bronchi (parascapular areas).

(Adapted from Lehrer S: Understanding Lung Sounds, Philadelphia, WB Saunders, 1984.)

38 What are the breath sounds characteristics of patients with pneumothorax?

The most striking is their softening. In fact, if the pneumothorax is large enough to collapse the entire lung, the corresponding hemithorax will be silent. The distant (or absent) breath sounds of pneumothorax are not only the result of reduced sound production (due to diminished airflow in the collapsed lung), but also of reduced sound transmission (due to the cushion of air in the pleural space). The same happens with pleural effusion (of course, in pneumothorax there is an increase in intensity of the percussion note, whereas in pleural effusion there is a softening). Still, air (or fluid) in the pleural cavity forms an acoustic barrier to sound transmission that usually muffles the breath sounds. The only exception is a layer of fluid so thin as to compress only alveoli but not bronchi.

39 Is the intensity of vesicular breath sounds important?

Yes, since decreased intensity usually indicates reduced airflow—assuming, of course, that (1) chest wall thickness is normal (i.e., no obesity); (2) pleural space is also normal (i.e., no collection of either air or fluid); and (3) respiratory muscles are functioning normally (i.e., no weakness). Hence, distant breath sounds are typical not only of patients whose right main bronchus has been selectively intubated by a misplaced endotracheal tube, but also of patients with obstructive lung disease. In turn, vesicular breath sounds of normal intensity virtually exclude a severe reduction in FEV₁. Finally, higher intensity can also be heard during post-exercise hyperventilation.

40 Is the intensity of breath sounds in airflow obstruction equally diminished at the mouth?

Not at all. In fact, it’s usually increased at the mouth.

41 What is the best bedside predictor for the presence of chronic obstructive lung disease?

A reduction in breath sound intensity (BSI). A total of 32 findings has been said to indicate COPD, with many arguing strongly for its presence (Table 14-3), yet BSI is the single best index of emphysema. Early inspiratory crackles also argue for obstruction (LR, 14.6), but mostly chronic bronchitis. If progressive over time, BSI reduction can help monitor methacholine challenge, even when wheezing is absent. Finally, any two of the following virtually rule in airflow limitation: >70-pack-years of smoking, decreased breath sounds, or history of COPD. Years of cigarette smoking, subjective wheezing, and either objective wheezing or peak expiratory flow rate also predict the likelihood of airflow limitation in males. Although other signs have been linked to obstruction (objective wheezing, barrel chest, positive match test, rhonchi, hyperresonance, and subxiphoid apical impulse), on multivariate analysis only three remain significantly associated with its diagnosis: self-reported history of COPD (LR, 4.4), wheezing (LR, 2.9), and FET >9 seconds (LR, 4.6). Patients with all three have an LR of 33 (ruling in COPD); those with none have an LR of 0.18 (ruling out COPD).

Table 14-3 Accuracy of Bedside Findings for the Evaluation of Obstructive Lung Disease: Likelihood Ratios, Point Estimates, and 95% Confidence Intervals

(Adapted from McGee S: Evidence-Based Physical Diagnosis. Philadelphia, WB Saunders, 2001.)

42 How can one objectively measure breath sounds’ intensity at the bedside?

By a scoring system originally devised by Pardee:

43 How good is interobsever reliability for BSI determination?

Very good. It had a correlation coefficient of 0.96 in two observers examining independently 20 patients. Hence, the BSI is an accurate indicator of airflow obstruction. In fact, even unscored lung sound intensity correlates closely with FEV₁ (although the BSI correlates even better, both with FEV₁ and FEV₁/FVC [forced vital capacity]). A BSI <9 argues strongly in favor of obstruction, whereas a BSI >15 argues against it.

44 In addition to airflow obstruction, is there any other process associated with distant breath sounds?

Pneumonia. A reduced BSI with fever and cough is very suggestive of it.

45 Can a change in lung sounds’ intensity help monitor patients’ response to airway challenge?

Yes. In patients with a positive methacholine test, a reduced BSI is typical of asthma. In fact, a gradual reduction in BSI may even precede wheezing, thus making it a great tool for monitoring bronchial provocation. Yet, with worsening airflow, the breath sounds’ pitch may paradoxically increase.

46 What is the mechanism of decreased BSI in COPD?

It is probably more a reduced sound transmission (due to parenchymal destruction, causing greater air-trapping and “muffling”) than a reduced sound production (due to diminished airflow). This is intuitive, considering that airflow limitation in COPD is more expiratory than inspiratory.

47 How does BSI compare to other bedside findings of airflow obstruction?

Quite well. In a study of COPD patients, the BSI was the best indicator of “obstructive emphysema,” as compared with 14 other physical findings and as judged against spirometry. The reason is its strong correlation with regional distribution of ventilation as measured by radioactive gas.

48 What is the best bedside predictor for severity of airflow obstruction?

The forced expiratory time (FET). To measure it, instruct patients to perform a forced-expiratory maneuver (i.e., to take a deep breath and blast it out as quickly and forcefully as possible) while you keep the bell of your stethoscope over the patient’s suprasternal notch. Then, clock the duration of audible expiration (FETo) to the nearest half-second. An FETo >6 seconds will correspond to an FEV₁/FVC <40%. Conversely, a FETo <5 seconds will indicate an FEV₁/FVC >60%. This simple bedside test is a good and reliable “poor man’s” spirometry. In a study by McAlister of 161 consecutive patients in six different countries, only three elements of the clinical exam were significantly associated with a diagnosis of COPD on multivariate analysis: self-reported history of COPD (adjusted LR, 4.4), wheezing (adjusted LR, 2.9), and FET >9 seconds.

49 Is there any finding that argues against the presence of COPD?

No single finding rules out airflow obstruction. Yet, a history of having never smoked argues strongly against it (especially if there is no wheezing on either examination or history).

(2) Bronchial Breath Sounds

51 How are bronchial breath sounds produced?

Like all other breath sounds: by air flowing rapidly through large and central airways. Their hollow quality and intensity, however, are due to better sound transmission, usually at the lung periphery.

52 What is the cause of this improved transmission?

1. Consolidation (i.e., replacement of alveolar air with a mantle of solidified lung that can better transmit higher frequencies). Consolidation reflects either alveolar collapse or alveolar fluid-filling:

Alveolar collapse (with patent airways) occurs in pleural effusions, whenever the amount of fluid is large enough to compress the alveoli but too small to compress the airways.

Alveolar fluid-filling occurs instead in situations of pneumonia (pus in the alveoli), alveolar hemorrhage (blood in the alveoli), or pulmonary edema (serum in the alveoli). In fact, in patients with cough and fever, the presence of bronchial breath sounds argues strongly in favor of pneumonia. Yet, its absence cannot rule it out, since the finding is specific but poorly sensitive.

2. Bronchial breath sounds also may be heard in situations of pulmonary fibrosis. This mechanism, however, requires severe fibrosis and tends to be less common than simple consolidation.

53 How deep should the consolidation be in order to generate bronchial breath sounds?

Quite deep. In fact, consolidation and/or fibrosis must extend all the way from the chest surface to 4–5   cm from the hilum (where large airways are located). Only in this way is the range of transmitted frequencies increased enough to make the breath sounds resemble a tracheal sound. This also is the basis for other signs of consolidation, such as egophony, bronchophony, and pectoriloquy.

54 Can one separate bronchial sounds of fluid-filled alveoli from those of collapsed alveoli?

Yes, by remembering that fluid in the alveoli is often associated with fluid in the interstitium and that this, in turn, is associated with adventitious lung sounds—such as crackles. Hence, BBS without crackles are usually the result of collapsed alveoli (with patent airways), whereas BBS with crackles are more often the result of fluid-filled alveoli (also with patent airways).

55 What is a common reason for bronchial breath sounds unaccompanied by crackles?

A pleural effusion. Fluid occupying half of the hemithorax presents with (1) vesicular breath sounds in the upper third of the chest (reflecting normal aeration); (2) tubular (or bronchial) breath sounds in the middle third (reflecting collapsed alveoli but patent airways); and (3) respiratory silence at the bottom (reflecting collapsed alveoli and airways, as a result of the gravity-dependent accumulation of fluid).

56 Other than consolidation, do bronchial breath sounds indicate anything else?

They may help rule out an endobronchial obstruction, thus avoiding unnecessary bronchoscopies. This is because a postobstructive pneumonia is unlikely to occur in patients with densities on chest x-ray but bronchial breath sounds on examination—which is intuitive considering that tubular sounds reflect patent bronchi. Patency can be easily confirmed by imaging, through the presence of air bronchograms (i.e., air-filled airways cast against a surrounding consolidated parenchyma). Bronchial breath sounds also may be clues, albeit indirectly, to the presence of tamponade and mitral stenosis.

57 Bronchial breath sounds can indicate tamponade and mitral stenosis?

Yes. Ewart’s sign (posterior dullness to percussion and bronchial breath sounds between the left scapular tip and the vertebral column) is a sign of compressive atelectasis caused by a distended pericardial sac. A similar finding occurs in the Ortner’s syndrome of mitral stenosis, which is due to the raising (and squeezing) of the left main bronchus by an enlarged left atrium. This, in turn, causes (1) compression of the recurrent laryngeal nerve between the aortic arch and the pulmonary artery (with resulting hoarseness and bitonal voice); (2) left-lower lobe atelectasis (with posterior dullness and bronchial breath sounds); and (3) dysphagia (from esophageal impingement).

58 Who was Ewart?

A British physician (1848–1929). Born in London of a French mother (and reared in England and Paris), Ewart graduated from Cambridge and then worked in a field hospital during the Franco-Prussian War of 1870. After the war, he lived in Berlin for a few years before returning to England, where he practiced at the Brompton and St. George’s hospitals until retiring in 1907. He reported his homonymous finding in 1896. A year later, the Dutch anatomist N. Ortner reported his syndrome.

(3) Amphoric Breath Sounds

(4) Bronchovesicular Breath Sounds

61 What are the three acoustic characteristics of bronchovesicular breath sounds?

62 What is the clinical significance of bronchovesicular breath sounds?

It depends on location. If heard over the parasternal and parascapular areas (both anteriorly and posteriorly), they are normal. Anywhere else, they indicate pathology—usually early consolidation (with enhanced transmission of high frequencies) or a thin pleural effusion, partially compressing the alveoli but not the bronchi. (Fig. 14-7)

Figure 14-7 Mormal location of bronchovesicular breath sounds.

63 What are adventitious lung sounds?

They are extra (i.e., adventitious) sounds that are normally absent in a respiratory cycle but become superimposed on the underlying breath sound (vesicular or bronchial) whenever disease occurs. Theirs is a confusing alphabet soup of rubs, squeaks, crackles, wheezes, stridor, and rhonchi. (Table 14-4)

64 How were these sounds first described?

By Laënnec, who through painstaking clinical–pathological correlation reported many of them in his 1819 treatise De l’Auscultation Mediate. He called them “bruits étrangers” (i.e., foreign sounds). He also referred to them as “râles” since many of his patients had tuberculosis, and thus rattling noises (râles in French) were indeed the sounds he most frequently heard. Yet, realizing that râles were easier to recognize than describe, he tried to teach them by using examples from “daily” life—all actually quite bizarre. For instance, he compared fine crackles to the “crackling of salt on a heated dish,” writing that these “humid râles” (or crepitations) were often present in patients with pneumonia, pulmonary edema, or hemoptysis. He then compared coarse crackles to the “gurgling of water from an upside down bottle,” adding that these “mucous râles” were often heard in patients with abundant secretions of the central airways. Finally, he likened wheezes to the “chirping of little birds” and rhonchi to the “cooing of a wood pigeon”—all bizarre and confusing examples.

65 When was the classification of adventitious lung sounds revised?

In 1977. The problem, of course, was Laënnec’s terminology and his original “daily life” examples. This was compounded by his inability to even use the term râle at the bedside, since it reminded his patients of the French expression “le râle de la mort” (the death rattle)—that is, the gurgling sound of dying people too ill to clear secretions. To avoid any bedside miscommunication, Laënnec often referred to these sounds as rhonchi, which was the Latin (and less scary) equivalent of rattles. Still, râles and rhonchi meant the same thing to him. This, however, escaped his first English translator, Dr. John Forbes, who decided that rhonchi should only describe long sounds, whereas râles should describe short sounds. Not all translators, however, complied with this rule, thus triggering the beginning of the end for Laënnec’s classification. By the 1970s, the confusion was so bad that Fraser and Pare reported that “every physician seems to have his own classification.” This eventually led to a reclassification by a team of international experts, with recommendations published in 1977, more than 150 years after Laënnec’s original terminology (Table 14-5).

66 What were the recommendations of the 1977 classification?

The most striking was the abandonment of Laënnec’s beloved term of “râle” in favor of a nomenclature based on acoustic and physical characteristics. Since priority was given to duration, adventitious lung sounds were divided into discontinuous (if lasting <250   msec) and continuous (if lasting >250   msec). The term crackle became the main descriptor of discontinuous sounds, replacing both the French râle and the British crepitation. Suffixes such as wet and dry were completely abandoned—as well as moist, sticky, atelectatic, close-to-the-ear, metallic, superficial, or consonating. Currently, the only acceptable modifiers for crackles are fine and coarse (in addition to indicators of the crackle’s respiratory timing—such as early, mid, or late).

67 So how should crackles be described?

68 How much has this terminology been implemented?

Not much. In common practice, outdated terms such as râles (or crepitations) are still encountered, as shown by several surveys of physicians and respiratory therapists. Even medical journals often rely on some of these old terms. A review of several case reports, for example, has shown the use of as many as 16 different terms to describe similar sounds.

69 How are adventitious lung sounds produced?

Mostly by vibration of respiratory structures, such as bronchi and pleura. This may occur in four ways:

Figure 14-8 Mechanism of production of coarse (early-inspiratory) crackles: air-fluid interface in large and central airways with rupture of fluid films or bubbles.

Figure 14-9 Mechanism of production of fine (late-inspiratory) crackles: reopening of partially collapsed distant airways with sudden equilibration of intra-airway pressure.

Figure 14-10 Postulated wheeze mechanism. The stability of the airway wall depends on a balance between internal air pressure and external forces and on the mechanical characteristics of the airway itself. When a narrowing of the lumen occurs, the air velocity must increase through the constricted region to maintain a constant mass flow rate. According to the Bernoulli principle, the increased air velocity leads to a decrease in air pressure, thus allowing external forces to further collapse the airway. When the lumen has been reduced so much that the flow decreases, the process begins to reverse itself as the pressure inside the airway begins to increase and reopen the lumen. When conditions are right, the airway wall flutters between nearly occluded and occluded positions and produces wheezing. Short open arrows indicate slower flow; long open arrows indicate faster flow. Large closed arrows indicate higher pressure; small closed arrows indicate lower pressure.

(1) Discontinuous Adventitious Lung Sounds

71 How useful are crackles?

Very useful. In fact, of all adventitious sounds, they are probably the most clinically valuable because of the strong correlation between inspiratory timing and site of sound production.

72 What do crackles sound like?

Forgacs vividly compared them to “miniature explosions,” which is definitely better than Laënnec’s “gurgling water” and “crackling salt.” Williams compared them in 1828 to the sound of “rubbing a lock of one’s hair between finger and thumb, close-to-the-ear.” In 1876, Latham spoke of “dry and moist râles.” Still, the term crackle is a recent addition, first introduced by Robertson and Cooper in 1957 as either coarse or fine, the latter being compared to the crushing of leaves. A more recent analogy, however—and one I particularly like—is the crepitation of Velcro, or the crinkling of cellophane, examples that would have surely defied Laënnec’s wildest dreams, or nightmares.

73 What is the underlying breath sound of crackles?

It depends on the type of crackles. For early and mid-inspiratory ones, it is vesicular, whereas for late-inspiratory crackles it is either vesicular or bronchial. This distinction may help differentiate the underlying disease. For example, a process that causes fluid-filling of the interstitium and alveoli (like pneumonia, pulmonary edema, or pulmonary hemorrhage) is much more likely to present with late-inspiratory crackles (due to interstitial fluid) and bronchial breath sounds (due to alveolar fluid). Conversely, scarring of the interstitium (i.e., pulmonary fibrosis) is much more likely to present with late-inspiratory crackles and vesicular breath sounds. This algorithm (Fig. 14-11) is simple but not simplistic and may be useful at the bedside.

Figure 14-11 Algorithmic approach to the differential diagnosis of late-inspiratory crackles.

74 How do crackles get produced?

It depends on their timing in the respiratory cycle (Fig. 14-12):

Figure 14-12 Graphic representations of crackles based on inspiratory timing.

75 What are the characteristics of early and mid-inspiratory crackles?

They are coarse, loud, low pitched, scanty, gravity independent, well transmitted to the mouth (because they originate in more proximal airways), and strongly associated with obstructive physiology. They vary in number, resolve with coughing, and cannot be extinguished with posture.

76 What are the characteristics of late-inspiratory crackles?

They are fine, soft, high pitched, profuse, gravity dependent, poorly transmitted to the mouth (because they originate in more peripheral airways), and strongly associated with restrictive physiology. They can be extinguished by a change in posture but not by coughing.

77 Are there any regional preferences for late-inspiratory crackles?

The dependent areas, like the posterior lung bases. These are regions of high interstitial pressure, where gravity can more easily cause the bronchiolar collapse that is key to these sounds.

78 Can crackles occur in normal people?

Yes. Although a sign of disease, crackles also may occur in healthy subjects. They are typically end inspiratory, high pitched, and fleeting—usually resolving after a few deep inspirations. Hence, they resemble the crackles of pulmonary fibrosis, including their predilection for lung bases, where gravity makes airway collapse more likely to occur. In fact, they indicate the reopening of atelectatic lung units, which occurs normally in most healthy subjects after a deep inspiration follows periods of quiet breathing—and especially in subjects that have been recumbent for prolonged time. Late-inspiratory crackles can be detected by careful auscultation in 63% of young nursing students, and in 92% if using an electronic stethoscope with high-pass filtration.

79 What should one do at the bedside when confronted with crackles?

First, separate early from mid-inspiratory and late-inspiratory crackles, since their etiology is different:

80 Summarize the characteristics of early, mid-inspiratory, and late-inspiratory crackles.

See Table 14-6.

Table 14-6 Characteristics of Inspiratory Crackles

81 How good is interobserver agreement for crackles?

Good for presence (or absence) of abnormal lung sounds and poor for grading and timing of crackles, especially the differentiation between coarse and fine. In this regard, Piirila et al. found agreement in only 60% of the cases. Differentiation between fibrosing alveolitis (i.e., late-inspiratory crackles) and bronchiectasis (i.e., mid-inspiratory crackles) was even worse. Interobserver agreement can, however, be improved by computer-assisted training.

82 Are the crackles of pulmonary fibrosis limited to late inspiration?

No. Although typically late in inspiration, these crackles may be mid-inspiratory or even early inspiratory. In fact, they may occur throughout inspiration. Their hallmark, however, is that they last until the end of inspiration. Similarly, bronchiectatic crackles predominate in mid-inspiration but may start earlier.

83 Are late-inspiratory crackles present in all interstitial lung disease?

No. Although reported in 65–91% of chronic interstitial pulmonary diseases (including asbestosis or idiopathic pulmonary fibrosis), they occur in only 5–20% of sarcoidosis cases. Fine crackles also are rare in other granulomatous disorders (like miliary tuberculosis, eosinophilic granuloma, or allergic alveolitis), and similarly rare in intra-alveolar processes (only 20% of pulmonary alveolar proteinosis cases). Still, whenever present, sarcoid crackles are basilar too, fine, and late-inspiratory (see Fig. 14-13).

Figure 14-13 Incidence and types of crackles according to clinical diagnosis in 657 patients.

(Adapted from Epler GR, Carrington CB, Gaensler EA: Crackles (rales) in the interstitial pulmonary diseases. Chest 73:33, 1978.)

84 Why are crackles so rare in sarcoidosis but so common in other fibrotic lung diseases?

Because of the different distribution in lung scarring, as clearly seen on high-resolution computed tomography (CT). Idiopathic pulmonary fibrosis tends to be associated with lower lobe location and subpleural scarring, which are strong radiologic predictors of the presence of crackles. Sarcoidosis is instead associated with upper lobe location and peribronchial fibrosis.

85 How common are crackles in asbestosis?

Very common. In large population studies, they are present in 15% of asbestos workers versus 3% of normal people. Crackles also are an early sign of disease, increasing in frequency and number with increased duration of exposure. By the time asbestosis is clinically evident, late-inspiratory, fine, and high-pitched crackles are heard in more than half of all patients. They are a good marker of disease severity, reflecting more on the duration of asbestos exposure than the vital capacity itself. Hence, crackles can be a valuable tool for the monitoring of exposed workers.

86 Where are asbestosis crackles localized?

Usually at the bases, first centrally (along the mid-axillary lines) and then posterolaterally.

87 Is there a correlation between the number of crackles and disease severity?

Yes. In asbestosis, for example, the number of crackles correlates directly with severity of the underlying disease. This rule applies also to other interstitial processes. Automatic crackle detection and counting have indeed been developed for both diagnosis and follow-up.

88 Are crackles common in patients with idiopathic pulmonary fibrosis (IPF)?

Yes. In fact, so common (up to 100%) that their absence argues strongly against the diagnosis.

89 Is there a correlation between late-inspiratory crackles and severity of IPF?

Yes. In addition to fewer crackles, milder forms of the disease have crackles that are only late inspiratory and gravity dependent (i.e., limited to the bases in upright patients). As the disease progresses, crackles become paninspiratory (even though still predominant in end-inspiration). They may also persist despite postural changes, eventually extending to higher lung regions. Finally, they may become associated with late-inspiratory squeaks (see below, questions 113 and 114).

90 Can crackles occur in exhalation?

Crackles are primarily inspiratory, and yet 10% do occur in exhalation—usually at mid- or late-expiration in patients with either obstructive or restrictive disease.

91 What is the mechanism of production of late-expiratory crackles?

There are two schools of thought: (1) they are produced by the closure (not the reopening) of stiff and fibrotic small airways, and (2) they are produced by the reopening of small airways, very much like late-inspiratory crackles. Using Forgacs’ model, this would occur as follows:

92 What is the clinical significance of expiratory crackles?

They are an important predictor of disease severity. In patients with interstitial lung disease, for example, the number of expiratory crackles has been shown to correlate directly with a reduction in diffusing capacity. In fact, because usually fewer than inspiratory crackles (and thus easier to count), expiratory crackles may be even more valuable for the assessment of disease severity.

(2) Special Problem—Pneumonia

94 What is the time course of these findings?

Variable, with crackles and diminished breath sounds usually appearing first, bronchial breath sounds and egophony developing 1–3 days after onset of symptoms (i.e., cough and fever), and dullness to percussion (plus increased tactile fremitus) occurring even later. This time lag usually allows for x-ray to preempt diagnosis, thus making exam irrelevant, since early detection by imaging translates into early institution of antimicrobial therapy, which in turn leads to aborted or never-developed physical findings. Hence, physical exam may be entirely normal in patients with pneumonia.

95 What about the presence of diminished breath sounds?

It also can occur in pneumonia, but usually in the setting of a concomitant pleural effusion.

96 What are the most valuable bedside predictors in pneumonia patients?

Hypothermia and hypotension, both strong predictors of poor outcome. Improvement of blood pressure and fever—together with lowering of cardiac and respiratory rates—is instead a favorable predictor. Finally, oxygen desaturation has little prognostic value in hospitalized patients.

97 Is there any diagnostic clue that may suggest pneumonia in ambulatory patients?

In patients with cough, fever, sputum production, and dyspnea, the findings of egophony, bronchial breath sounds, dullness to percussion, diminished breath sounds, tachypnea, and crackles all argue (in decreasing order of importance) in favor of a diagnosis of pneumonia.

98 What are the characteristics of crackles in pneumonia?

Although Laënnec considered them very similar to those of hemoptysis and pulmonary edema, their characteristics depend very much on the stage of pneumonia, as demonstrated by computerized sound analysis. In the acute setting, crackles are predominantly coarse and mid-inspiratory, resembling those of bronchiectasis. During recovery, however, they tend to become shorter, more end inspiratory, and thus similar to the crackles of pulmonary fibrosis.

99 What about crackles of congestive heart failure (CHF)?

They are very similar to those of pulmonary fibrosis: profuse, fine, high pitched, and late inspiratory. Both predominate in gravity (and posture) dependent regions. In fact, they are quite difficult to separate on auscultation, even though a differentiation can usually be made on clinical grounds (or by using computerized sound analysis). Still, the examiner should be aware of their similarity, especially when considering diuresis. As a rule of thumb, bibasilar fine crackles should suggest heart failure only in patients with no other indication of pulmonary disease.

(3) Special Problem—Posturally Induced Crackles (PICs)

101 What’s the best way to elicit PICs?

By following these steps (Fig. 14-14):

Figure 14-14 Standard procedure used to examine patients for PICs.

(From Deguchi F, Hirakawa S, Gotob K, et al: Prognostic significance of posturally induced crackles: Long-term follow-up of patients after recovery from acute myocardial infarction. Chest 103:1457–1462, 1993, with permission.)

102 How should this maneuver be interpreted?

See Table 14-7.

103 What is the clinical significance of PICs?

Ominous, both diagnostically and prognostically. PIC-positive patients have a higher pulmonary capillary wedge pressure, lower pulmonary venous compliance, and higher mortality. Deguchi et al. monitored for 6 years 262 patients after an acute myocardial infarction. PIC-positive patients had worse long-term prognosis: 28/143 (19.6%) died of cardiac causes as compared with 3/78 (3.8%) of PIC-negative patients. Cardiac deaths were even higher in patients with persistent crackles: 15/41 (36.6%). Hence, PICs provide a noninvasive, simple, and valuable bedside test. After the number of diseased coronary vessels and the patient’s pulmonary capillary wedge pressure (PCWP), PICs rank third as the most important predictor of recovery after acute myocardial infarction.

104 Do PICs represent an independent variable?

Yes. In fact, when the number of disease vessels is constant, PICs consistently predict a lower survival rate. They do the same when PCWP is high (≥13   mmHg). Hence, the lower survival of PIC-positive patients does not simply reflect an increased number of diseased vessels or a greater PCWP, but represents instead an independent variable.

(4) Continuous Adventitious Lung Sounds (CALS)

106 How long should these sounds be in order to qualify as “continuous”?

According to American Thoracic Society Guidelines, they should last >250   ms. In reality, CALs are rarely that long, lasting instead 80–100   ms.

107 What are the physical characteristics of CALs?

In addition to their long duration, they have a high-frequency range: from <100 to >1000   Hz. They have even higher frequency when recorded directly from within the airway.

108 What are monophonic and polyphonic CALs?

CALs that can be compared to either a solo singer (monophonic wheezes) or a polyphonic choir.

109 If a polyphonic CAL may have more than one frequency, how does one determine its pitch?

By its fundamental. A wheeze may contain several harmonically related frequencies, but its pitch is always determined by its lowest (or fundamental) frequency.

110 How are wheezes produced?

Not like the tone of an organ pipe (i.e., by vibration of air within the pipe, so that the pipe’s length and diameter correlate with the tone’s pitch [with larger and longer pipes producing the lower pitch]). If wheezes were generated this way:

Hence, wheezes are not generated like tones of organ pipe, but rather like notes of a toy trumpet’s reed—or, even better, like sounds of a harmonica’s reeds. In this model (first suggested by Forgacs in the 1960s), airflow sets each individual reed into oscillation between opening and closure, thus generating a note of constant frequency. Air flowing at high velocity through a narrow bronchus has a similar sucking effect on the airway wall, by pulling it inward and thus initiating a flutter (i.e., a wheeze) of closing and opening, resembling very much the vibration of a toy trumpet’s reed. This fluttering typically delivers a note of constant frequency that depends on the mass and elasticity of the bronchial walls, the tightness of the narrowing, and the rate of gas flow through it.

111 What is the physical principle behind this mechanism?

It is the Bernoulli principle, which centers on a local drop in intra-airway pressure whenever air flows at high velocity through narrowed pipes. The faster the flow at point of constriction, the lower the local pressure. Eventually, the drop in pressure becomes severe enough to collapse the airway. Since the collapse also reduces flow, the airway reopens and the fluttering cycle starts anew, repeating itself indefinitely (see Fig. 14-5). Thus, wheezes are not produced by vibration of air (as in organ pipes or woodwind instruments), but by vibration (fluttering) of airway walls. This is facilitated by fast jets of air, forced by high expiratory pressures through tightly compressed airways.

112 Is the pitch of a wheeze related to its site of production?

No. This widely held belief is based on the erroneous analogy with an organ pipe. Yet, wheezes are not the sounds of organ pipes. Hence, their pitch does not depend on the diameter and length of the airway, but on the degree of airway narrowing at the site where the sound is being generated. In other words, wheezes are generated whenever the bronchial diameter is narrowed to the point of dynamic compression. That’s why, in contrast to late-inspiratory crackles (and the high-frequency tones of an organ pipe), high-pitched wheezes do not originate in small peripheral airways. And low-pitched wheezes do not originate in large central bronchi.

113 How are CALs classified?

In addition to being classified according to dominant frequency (in either wheezes or rhonchi), CALs are also divided into:

Figure 14-15 Graphic representations of expiratory polyphonic CALs.

Figure 14-16 Graphic representations of random monophonic CALs.

114 What are the causes of a late-inspiratory squeak?

The three most common are pulmonary fibrosis, allergic alveolitis, and bronchiolitis obliterans. Still, any interstitial lung disease can produce them.

115 How are CALs graphically represented?

By bars, in a way very similar to the representation of musical notes:

116 What are the most common causes of airway narrowing responsible for wheezes?

Bronchospasm, peribronchial edema (from left ventricular failure), accumulation of secretions, and airway closure by a partially obstructing tumor.

117 Does the presence of wheezing rule in bronchial narrowing?

Not necessarily. Since wheezes reflect the degree of dynamic narrowing of the airway (and its flow rate, according to the Bernoulli principle), an expiratory flow that is forceful enough will produce a wheeze even in an entirely normal airway. This is why a forced expiratory maneuver has no value in unmasking “subclinical” asthma. In fact, wheezing on maximal forced exhalation has such a low sensitivity and specificity for asthma (57% and 37%, respectively) as to be completely unreliable for diagnosing subclinical airflow obstruction. Conversely, a weak expiratory flow might remain totally silent, even though the airway is quite narrowed (i.e., “beware of the asthmatic who stops wheezing while turning blue”). Thus, presence of wheezing does not rule-in bronchial narrowing. And its absence does not exclude it.

118 What are the underlying breath sounds of asthmatic patients?

They vary, depending on the degree of airway narrowing. In fact, one of the first signs of bronchospasm is an increase in frequency of the underlying vesicular breath sound—which takes place even before wheezes develop (especially in children). The opposite occurs during bronchodilator therapy. Thus, breath sounds of asthmatics tend to have higher frequency than regular vesicular breath sounds, but also lower intensity.

119 Asthmatics have breath sounds of lower intensity?

Yes. Even though wheezing during bronchial challenge is very suggestive of asthma, a softening of the breath sound may be the earliest (and only) manifestation of positive bronchoprovocation. In fact, this is as common as the appearance of a wheeze. An increase in frequency of breath sounds also is a useful clue to the unfolding of an asthmatic attack. Thus, the breath sounds of bronchospasm are indeed higher pitched (because of the effect of stiffer and narrowed airways on sound transmission) but also softer (because of diminished regional air flow).

120 Are there any wheeze characteristics that correlate with the degree of airflow obstruction?

One is the pitch. Shim and Williams have indeed shown that the worse the asthmatic attack, the higher the pitch of its wheezes. This is also why bronchodilator therapy lowers the frequency of wheezes. If pitch is a good indicator of asthma severity, length, however, is even better.

121 So how can wheezing help assess the severity of airflow obstruction?

This question was answered by Baughman and Loudon, who studied patients admitted to the emergency department for status asthmaticus. They recorded sounds at four standard chest sites and correlated findings with FEV₁ and FVC, both prior to and after treatment. In their analysis, neither the wheezing intensity nor the simultaneous presence of wheezes of different pitch (polyphonic wheezing) correlated with severity of obstruction. Instead, only two variables were consistently related to the degree of airway narrowing: (1) the proportion of the respiratory cycle occupied by the wheeze and (2) the frequency content of the highest-pitched wheeze. Hence, only pitch and length are useful predictors of airway narrowing: higher-pitched and longer wheezes reflect worse obstruction.

122 How does one express the length of a wheeze?

By the proportion of the respiratory cycle occupied by the wheeze (T_w/T_tot). In adults with moderate to severe obstruction, T_w/T_tot is inversely related to FEV₁. Hence, wheezing that occurs only in exhalation is not as severe as wheezing occurring both in exhalation and in inspiration; similarly, longer expiratory wheezes reflect worse obstruction than shorter ones.

123 What are then the acoustic characteristics of a resolving asthma attack?

A decrease in frequency of the highest-pitched wheeze component, and a decrease in T_w/T_tot.

124 Summarize the time course of status asthmaticus based on auscultation.

Findings depend primarily on the degree of obstruction. The most prominent is a high-pitched wheeze, first heard in exhalation, and then (as disease worsens) both in inspiration and exhalation. These wheezes are initially monophonic, but become polyphonic with progression:

125 How sensitive and specific are wheezes for the diagnosis of airflow obstruction?

Neither sensitive nor specific. Although wheezing on forced exhalation can occur even in healthy subjects (as long as they exhale with enough force), unforced wheezing argues strongly for chronic airflow obstruction. Still, it can be absent in 30% of patients with FEV₁ <1   L. It also may resolve in acute asthmatics whose FEV₁ remains at 63% of predicted value. In fact, in status asthmaticus, wheezing is the least discriminating factor in predicting hospital admission or relapse. Yet, its absence in acute asthma may be ominous. For instance, it may indicate flow rates too low to generate sound (a reminder of the lack of correlation between asthma severity and wheezing intensity, and of the time-honored dictum, “beware of the quiet asthmatic”). Thus, wheezes, although useful, are not that great diagnostically. They are much less valuable than crackles.

126 What about pulsus paradoxus?

Pulsus paradoxus has a significant and direct relation with hypercapnia in children with status asthmaticus and may thus serve as an indirect monitor when CO₂ cannot be measured.

127 And how about diaphoresis and orthopnea in asthma?

Diaphoresis and orthopnea on admission to an emergency center predict worse peak expiratory flow rates and greater need for admission.

128 What is the differential diagnosis of wheezes?

It is a rather broad one. Overall, wheezes are more frequent in asthma than COPD. Still, the old saying, “Not all that wheezes is asthma” is an important reminder that we should always exclude other etiologies before concluding that a wheezy patient is indeed asthmatic (Table 14-8). In a large epidemiologic study, for example, wheezes were present in 25% of the population, whereas the prevalence of asthma was only 7%. Among the extrathoracic causes of wheezing, vocal cord dysfunction is a particularly common one. And, of course, stridor is important, too.

Table 14-8 Clinical Conditions Associated with Wheezing

* Conditions that tend to be associated with a late-inspiratory squeak (or squawk).

129 What is cardiac asthma?

It’s wheezing in association with left ventricular failure. The traditional explanation is airway narrowing due to peribronchial and interstitial edema. In reality, cardiac asthma is indeed asthma. In fact, patients who wheeze when in pulmonary edema have positive methacholine challenge. The proposed mechanism is therefore a heightened airways reactivity, which leads to dynamic airflow obstruction whenever triggered by interstitial and peribronchial edema. That’s why only a minority of patients in left ventricular failure develop wheezing. The rest have crackles.

130 What about wheezes over the neck?

Wheezes louder over the neck may reflect upper airway obstruction. Note that even though stridor is primarily inspiratory, the wheezing of vocal cord dysfunction may be either inspiratory or expiratory. This might be misleading, unless coupled with careful auscultation of the neck. Exertional inspiratory stridor that spontaneously resolves with rest can occur in 5% of athletes (as compared to 2.5% in the general population), and is a manifestation of vocal cord dysfunction too, even though it is frequently misdiagnosed as exercise-induced bronchospasm.

(5) Stridor

132 Are there any acoustic differences between wheezes and stridor?

Definitely not pitch. The best discriminators are instead timing and location. Baughman and Loudon have analyzed the physical characteristics of these two sounds and found that stridor is exclusively inspiratory (and more prominent over the neck), whereas wheezes are more predominant over the chest (and never inspiratory only). Otherwise, there are no major acoustic differences.

133 What is the time course of stridor due to posttracheostomy tracheal stenosis?

A slow time course. First, the patient complains of dyspnea, cough, or problems with throat clearing. Only much later, stridor appears, usually indicating a critical tracheal narrowing <5   mm.

(6) Pleural Rub

135 What does a rub sound like?

It has been compared to a violin bow striking a string in a to-and-fro motion. According to this model, the chest wall, because of its large mass and springiness, behaves like the body of a string instrument, continuing to vibrate for a short time after each impulse transmitted by the pleural friction. Hence, the various components of the rub lengthen and even merge into a continuous and often musical sound, similar to a rhonchus or a wheeze.

136 Are rubs inspiratory or expiratory?

Usually both, because rubs are caused by the sliding on each other of both pleural layers. Since sliding is faster during inspiration, the inspiratory component of a rub is usually louder. At times, it may even be the only one audible. The expiratory component, on the other hand, is usually a bit longer, accounting for 65% of the entire rub duration. Overall, two thirds of rubs are present in inspiration and expiration. Some are inspiratory only. Very few are limited to exhalation.

137 How can one differentiate rubs from crackles?

With great difficulty. Rubs, in fact, are often misdiagnosed as crackles because they share similar characteristics. To help differentiate them, remember that in contrast to crackles, rubs: (1) occur both in inspiration and expiration; (2) do not change with coughing; (3) are usually longer, louder, lower pitched, and often palpable; and (4) are usually localized to a very small area.

138 How can one differentiate rubs from wheezes?

This is a bit easier. Although rubs can be confused with polyphonic wheezes (either medium- or low-pitched), they can be easily separated by remembering that they never occur in expiration only, whereas most wheezes do. Hence, an adventitious sound that is audible (or louder) only in inspiration is more likely to be a rub, whereas an adventitious sound that is audible only in exhalation is more likely to be a wheeze (or a rhonchus).

139 How can one separate pleural from pericardial rubs?

By asking patients to hold their breath. If the rub persists, it is more likely to be pericardial.

140 What is the natural history of a pleural rub?

Rubs are fleeting. They usually disappear as soon as the amount of pleural fluid gets large enough to separate the two layers, thus preventing them from rubbing against each other. Hence, if not carefully (and frequently) sought, transient rubs may be easily missed.

141 What is the histology underlying a pleural rub?

In normal subjects, the visceral and parietal pleura are lined by a single layer of flat mesothelial cells. These layers are smooth and lubricated by a thin film of fluid that allows them to slide easily and silently on each other during respiration. Yet, this smoothness is immediately lost as soon as fibrin and cells (neoplastic or inflammatory) cover the two pleural layers. As a result, the roughened pleural surfaces will rub against each other during respiration, thus creating a friction that is responsible for the pleural rub. The separation of the two pleural layers (because of fluid accumulation in the pleural cavity) will make the rub disappear. Pleural rubs, therefore, are pathognomonic of pleural inflammation. Noninflammatory effusions, such as those associated with congestive heart failure, nephrotic syndrome, or cirrhosis, are never associated with a rub.

142 What are the most common causes of a pleural rub?

Cancer, pneumonia, and pulmonary embolism. Serositis (as in collagen vascular diseases) may also produce one, despite an entirely normal chest radiograph. In this regard, rubs are common in lupus pleuritis but rare in rheumatoid effusion. They also are common in thromboembolic disease and parapneumonic pleuritis, but rare in tuberculous pleurisy. Similarly, rubs have variable frequency in neoplastic involvement. Cancers may produce a rub, either directly (through invasion of pleural layers) or indirectly (though inflammation of the pleura overlying a lung cancer). Finally, rubs often occur in lobar pneumonia (pneumococcal, staphylococcal, or gram-negative).

143 What are the physical characteristics of a rub?

The hallmark is a series of short, loud, creaky, and high-frequency sounds. These can be visualized as tall “spikes” superimposed on the underlying breath sound (Fig. 14-17). Hence, the soundwave of a rub is very similar to that of a crackle (although the rub tends to span throughout inspiration and expiration, whereas crackles predominate in inspiration). The frequencies of these spikes are medium to high pitched, but not as high as those of crackles. Still, rubs are well perceived by the human ear and appear loud. Their inspiratory components usually have higher intensity and sometimes may be the only audible sounds. Finally, the rub is characterized by what Forgacs defines as the “mirror image effect,” which refers to the apparent reverse sequence of the expiratory component of the rub as compared with the inspiratory component.

Figure 14-17 Soundwave characteristics of a pleural rub.

144 What are transmitted voice sounds? Why are they important?

They are sounds that are not produced by the patient’s lungs, but by the larynx. This is unlike other acoustic respiratory events, whether breath sounds or adventitious lung sounds. Voice-induced sounds may become abnormally transmitted in certain diseases, thus providing a valuable clue.

145 What are the most important transmitted voice sounds?

They are three, and all originally described (and named) by Laënnec. There also is a fourth and more recent type (the E-to-A change), but still a variation of Laënnec’s original description:

146 Is there any magic word that one should ask patients to say in order to elicit these sounds?

Not really. In the United States, we ask them to say “ninety-nine” (which is the same number used to elicit tactile fremitus). In Italy (smaller country), “thirty-three” is the number of choice. As Sapira points out, “ninety-nine” is nothing more than the translation of the German “neun und neunzig” (akin to the onomatopeic “oink-oink”), which actually changed the physical characteristics of the original sound, making it possibly less fit for the task. An alternative is to ask the patient to say, “one, two, three.” Still, for eliciting abnormally transmitted voice sounds, any sound will do (except, of course, for eliciting E-to-A changes; see below, questions 151–155).

147 What is the significance of these maneuvers?

They all mean the same thing: an abnormal transmission of spoken (or whispered) words across the lungs. More specifically, they indicate airless and consolidated lung parenchyma.

148 Are the bronchi of patients with abnormally transmitted voice sounds open or closed?

Open. If closed, there would be no sounds transmission across the chest.

149 When should one check for the presence of these sounds?

When suspecting abnormal sound transmission along the tracheal bronchial tree and across the lungs. In general, when suspecting consolidation.

150 How do voice sounds get produced and transmitted?

They are produced by vocal cords set in vibration by exhaled air. Normal voice sounds are then transmitted upward toward the mouth, and downward toward the chest. There, the air-filled lungs act as a low-pass filter, eliminating high-frequency components (>300   Hz) and allowing instead passage of only lower-pitched tones (100–300   Hz), which are eventually most of the sounds that reach the chest wall. This low-pass filtering also eliminates the higher-frequency components of the vowels, the so-called formants. Because recognizing vowels is essential to the comprehension of words (vowels have been called the spice of a language), the elimination of formants by the normal (and aerated) lung transforms voice sounds into a muffled, low-pitched, and unintelligible mumble. Since solids and fluids can transmit higher frequencies better than air, a consolidated (and airless) lung improves transmission of vowels, thus making voice sounds louder, clearer, and intelligible.

151 Who first described egophony?

Laënnec, who also introduced its complicated Greek term. “Egophony,” he wrote, “possesses one constant characteristic from which it has seemed to me suitable to name the phenomenon; it is quavering and jerky like the bleating of a goat.” The E-to-A changes were instead described later.

152 Who came up with the idea of asking patients to say “E”?

Good point. In fact, why not “U,” or “A,” or “O”? Whenever questions of this sort come up in history of medicine, there are usually three major requirements: a British missionary, a far-flung land, and lots of serendipity. In the case of E-to-A changes, the British missionary was a chap named Shibley, who in the 1920s was practicing missionary medicine in China. Part of his job consisted of auscultating chests while patients were saying “one, two, three”—which, since the patients were Chinese, was appropriately said in Mandarin, as “i, er, san.” Since the Mandarin for “one” (“i”) was pronounced “E” in the province where Shibley was working at the time, that “E” turned into an “A” whenever there was either pneumonia or pleural effusion. In fact, all five vowel sounds (A, E, I, O, U) became “A” in cases of effusion or consolidation. Shibley reported this “E-to-A change” in the Chinese Medical Journal in 1922. That same year, the Viennese Froschels and Stockert reported a similar observation (of course, their Austrian patients did not speak Mandarin, but still experienced a similar transformation of one vowel sound into another whenever “consolidated”). Of interest, “one” in Cantonese would have been “iat,” thus making Shibley’s “E-to-A change” a much less appealing “E-AT to A-AT change,” which would have never worked out.

153 What is the mechanism behind E-to-A changes?

It is, of course, consolidation—more precisely, consolidation that extends from the auscultated chest wall to the tracheobronchial tree. A less extensive process (as, for example, the consolidation of a pulmonary nodule) would not create a bridge long enough to cause egophony.

154 What are the most common causes of extensive consolidation?

The most common are either filling of the alveoli by a medium that transmits sound better than air (such as pus, blood, or serum) or collapse of the alveoli. In cases of pleural effusions, the layer of fluid must be thick enough to compress the alveoli (and thus make them airless) but also thin enough to leave the airways patent. Although generally valid (and intuitive), this rule has exceptions. There are, in fact, patients who have obstructed or collapsed bronchi and yet still manage to transmit the high frequencies of egophony and tubular respiration. In this case, the transmission does not occur along the airways but directly through the lung parenchyma.

155 How does consolidation transform an “E” into an “A”?

By changing the filtering properties of the lung, thus allowing it to transmit higher-frequency sounds. The fact that an “E” may turn into an “A” when heard over a consolidated focus remains, nonetheless, an acoustic paradox. In fact, when heard at the mouth, “E” is higher pitched than “A.” Thus, it seems counterintuitive that a consolidated lung (which is capable of transmitting higher frequencies better than a normal lung) should change a high-pitched sound like “E” into a low-pitched one like “A.” The explanation is that the sound “E” is a mixture of both high and low frequencies. The high frequencies are in the 2000–3500   Hz range, whereas the low are in the 100–400   Hz range. “A” also has low and high frequencies, but its low frequencies have a range that is a bit higher than that of the low-frequency components of “E” (in “A” they reach 600   Hz). When “E” or “A” is heard over the chest, none of its high-frequency components comes across, regardless of whether the underlying lung is consolidated. Thus, even though a consolidated lung can transmit higher frequencies better than a normal lung (close to 1000   Hz instead of 400), it still cannot transmit the highest frequencies (such as the 2000–3500 frequencies) that are so typical of “E.” In other words, a consolidated lung better transmits the low frequencies that are important features of “A” (the ones up to 600   Hz), but still cannot transmit the higher frequencies that are unique to “E.” As a result, “E” becomes “A,” as so do all other vowels when similarly analyzed.

156 What is the mechanism of production for whispered pectoriloquy?

It is still consolidation. Remember that whispered sounds consist almost entirely of high-frequency components. Thus, they are not transmitted by the aerated lung, but become audible only when the loss of alveolar air (due to consolidation) allows their transmission.

157 What breath sounds accompany these transmitted voice sounds?

Tubular (bronchial) breath sounds, because both transmitted voice sounds and tubular sounds reflect improved conduction of high-frequency components, typical of consolidation. Consolidation from alveolar fluid-filling is characterized by tubular sounds and late-inspiratory crackles, whereas consolidation from alveolar collapse is characterized by pure tubular sounds. In patients with cough and fever, the presence of egophony increases the likelihood of pneumonia.

158 What is the radiologic equivalent of abnormally transmitted voice sounds?

Air bronchograms. These are patent and air-filled bronchi silhouetted out against the white background of airless and consolidated alveoli. This radiographic finding is nonspecific and may be seen with atelectasis, lung hemorrhage, pneumonia, or pulmonary edema.

159 What is the most useful of all these transmitted voice sounds?

Probably egophony, closely followed by whispered pectoriloquy. In some patients, whispered pectoriloquy may be the first finding to appear in cases of consolidation.

160 Summarize disease processes associated with lung auscultation findings.

See Table 14-9.