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).

Table 14-1 Categories of Respiratory Sounds ^*

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

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

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.