Lung Auscultation

Generalities

Lung auscultation has long suffered from a complex and onomatopoeic terminology that goes back to the original stethoscope and its inventor. Recent application of computer technology has rekindled this art by facilitating acoustic analysis. Still, its major difficulty lies not in the identification of sounds (which is much easier than for cardiac sounds and murmurs), but in their interpretation. And despite recent attempts at standardization, terminology remains a vexing issue.

Lung and thoracic ultrasound, as well as related applications, are discussed at the conclusion of this chapter. Like auscultation, lung ultrasound was once viewed as having a “foreign” character destined for limited dissemination. However, this opinion has been dramatically reversed in recent years, and is now regarded as perhaps the most clinically useful applications of POCUS for the generalist.

• 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 S ₃ and S ₄ , 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 a 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.

  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. 12.1 ).

  

• 5.

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

  • Basic lung sounds (also called breath sounds )

  • Adventitious (i.e., extra ) lung sounds

  Each of these subgroups contains various other sounds ( Table 12.1 ).

  Table 12.1

  Categories of Respiratory Sounds ^a

  (Adapted from Pasterkamp H, et al. Respiratory sounds. Am J Respir Crit Care Med . 1997;156: 974–987.)

  RESPIRATORY SOUND	MECHANISMS	ORIGIN	ACOUSTICS	RELEVANCE
  Basic Sounds
  Normal lung sound ( vesicular )	Turbulent flow vortices, unknown mechanisms	Central airways (expiration), lobar to segmental airway (inspiration)	Low-pass filtered noise (range <100 to 1000 Hz)	Regional ventilation, airway caliber
  Normal tracheal sound ( tubular )	Turbulent flow, flow impinging on airway walls	Pharynx, larynx, trachea, large airways	Noise with resonances (range <100 to >3000 Hz)	Upper airway configuration
  Adventitious Sounds
  Wheeze	Airway wall flutter, vortex shedding	Central and lower airways	Sinusoid (range ~100 to >1000 Hz; duration, typically >80 ms)	Airway obstruction, flow limitation
  Rhonchus	Rupture of fluid films, airway wall vibrations	Large airways	Series of rapidly dampened sinusoids (typically <300 Hz and duration >100 ms)	Secretions, abnormal airway collapsibility
  Crackle	Airway wall stress – relaxation	Central and lower airways	Rapidly dampened wave deflection (typical duration <20 ms)	Airway closure, secretions

  a This table lists only the major categories of respiratory sounds and does not include other sounds, such as squawks, friction rubs, grunting, snoring, or cough. Current concepts about sound mechanisms and origin are listed, but these concepts may be incomplete and unconfirmed.

• 6.

  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).

A

Breath Sounds (Basic Lung Sounds)

• 7.

  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.

• 8.

  What are the major types of breath sounds?

  • Vesicular breath sounds

  • Bronchial breath sounds (BBS)

  • Bronchovesicular breath sounds

  • Tracheal breath sounds

  • Amphoric (cavernous) 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. 12.2 )

  

• 9.

  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. 12.3 ). Some are silent and others noisy:

  • Laminar airflow is characteristic of small peripheral airways. It is so slow that airflow in the alveoli almost comes to an end. Hence, this is a silent movement.

  • Vorticose airflow is a bit faster and typical of medium-sized branching airways. “Branching” separates airflow in different layers with different velocities, whose interaction generates eddies and vortices – all noisy . This air movement is often called mixed (or transitional) because it resembles both laminar and turbulent airflow.

  • Turbulent airflow is very rapid, complex, and typical of large central airways (trachea and major bronchi). Air molecules randomly collide against each other and onto the airway walls. This air movement is characteristically noisy .

  

• 10.

  How are breath sounds produced?

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

• 11.

  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).

• 12.

  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.

• 13.

  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. 12.4 ).

  

• 14.

  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.

• 15.

  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.

• 16.

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

  Yes ( Table 12.2 ). 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 FEV ₁ (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.

  Pearl

  Noisy mouth inspiration argues in favor of asthma or chronic bronchitis, where it can predict the degree of airflow obstruction even more reliably than wheezing.

  Table 12.2

  Changes in Lung Sounds with Pulmonary Disease

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

  LUNG DISEASE	BREATH SOUNDS	ADVENTITIOUS LUNG SOUND
  Pneumonia	Bronchial or absent	Inspiratory crackles
  Atelectasis	Harsh/bronchial	Late inspiratory crackles
  Pneumothorax	Absent	None
  Emphysema	Diminished	Early inspiratory crackles
  Chronic bronchitis	Normal	Wheezes and crackles
  Pulmonary fibrosis	Harsh	Inspiratory crackles
  Congestive heart failure	Diminished	Inspiratory crackles
  Pleural effusion	Diminished	None
  Asthma	Diminished	Wheezes

• 17.

  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, patients with chronic bronchitis 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.

• 18.

  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.

B

Adventitious Lung Sounds

• 61.

  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 12.3 )

  Table 12.3

  Classification of Adventitious Lung Sounds

  ACOUSTIC CHARACTERISTICS	AMERICAN THORACIC SOCIETY NOMENCLATURE	COMMONLY USED SYNONYMS(OLD TERMINOLOGY)	LAËNNEC EXAMPLE
  1. Discontinuous (<250 msec)	Coarse crackle	Coarse râle	Water gurgling from a bottle
  Fine crackle	Fine râle crepitation	Crackling of salt on a heated dish
  2. Continuous (>250 msec)	Wheeze (high-pitched)	Sibilant rhonchus	The chirping of little birds
  Rhonchus (low-pitched)	Sonorous rhonchus	The cooing of a wood pigeon

• 62.

  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.

• 63.

  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 12.4 ).

  Table 12.4

  Outline of Classification of Lung Sounds

  ACOUSTIC CHARACTERISTICS	WAVEFORM	RECOMMENDED ATS a NOMENCLATURE	TERMS IN SOME TEXTBOOKS	A BRITISH USAGE	LAËNNEC’S ORIGINAL TERM	LAËNNEC’S MODEL
  Discontinuous, interrupted explosive sounds		Coarse crackle	Coarse rale	Crackle	Rale muquex ou gargouillement	Escape of water from a bottle held with mouth directly downward
  Loud, low in pitch
  Discontinuous, interrupted explosive sounds		Fine crackle	Fine rale crepitation	Crackle	Rale humide ou crepitation	Crepitation of salts in a heated dish
  Less loud than above and of shorter duration; higher in pitch than coarse rales or crackles						Noise emitted by healthy lung when compressed in the hand
  Continuous sounds Longer than 250 ms, high-pitched; dominant frequency of 400 Hz or more, a hissing sound		Wheeze	Sibilant rhonchus	High-pitched wheeze	Rale sibilant sec ou sifflement	Prolonged whisper of various intonations; chirping of birds; sound emitted by suddenly separating two portions of smooth oiled stone.
  						The motion of a small valve
  Continuous sounds		Rhonchus	Sonorous rhonchus	Low-pitched wheeze	Rale sec senore ou ronflement	Snoring; bass note of a musical instrument; cooing of a wood pigeon
  Longer than 250 ms low-pitched; dominant frequency about 200 Hz or less; a snoring sound

  Although the terms used to name the categories of lung sounds vary widely, the categorization scheme itself has changed little since Laennec. The most recent names recommended for adoption by the American Thoracic Society and terms used by others are shown here, accompanied by acoustic descriptions and examples of typical sound wave-forms for each category.

  a American Thoracic Society

• 64.

  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).

• 65.

  So how should crackles be described?

  • Depending on their number , as either scanty or profuse

  • Depending on their predominant frequency , as high-pitched (fine) or low-pitched (coarse)

  • Depending on their amplitude of oscillations, as either faint or loud

  • Finally, depending on their timing during inspiration, as either early, mid, or late inspiratory

• 66.

  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.

• 67.

  How are adventitious lung sounds produced?

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

  • Rupture of fluid films or bubbles: this is responsible for coarse crackles (discontinuous adventitious lung sounds [DALs]) and occurs whenever air flows through large central airways coated with thin secretions. The air–fluid interface causes the rupture of fluid films and bubbles, resulting in crackling noises. These are typical of acute and chronic bronchitis and were called by Laënnec “râles gargouillement,” an expression which included the death rattle . ( Fig. 12.8 )

    

  • Sudden equalization of intraairway pressure: this is responsible for fine crackles, which are also DALs, but more typical of pneumonia, pulmonary hemorrhage, pulmonary edema, and pulmonary fibrosis. Sudden equalization of intraairway pressure occurs whenever small airways that are partially collapsed suddenly “pop” open in inspiration. The partial collapse of distal airways is due to high interstitial pressure, the result of either scarring (pulmonary fibrosis) or fluid (pus, blood, serum). ( Fig. 12.9 )

    

  • Fluttering of the airway wall: this is responsible for wheezes , which are instead continuous adventitious lung sounds (CALs). Fluttering occurs whenever air flows rapidly through airways that have been narrowed by either bronchospasm or thick secretions/edema. The underlying mechanism is the Bernoulli principle, which also governs the water vacuum pump of many labs. In the case of the pump, it is the water rapidly flowing through a narrow tube that produces a sucking effect (which, in turn, draws in air through a hole in the tube). In the case of wheezes, however, there is no hole in the airway wall. As a result, air flowing rapidly through a narrow bronchus will simply draw-in the airway wall, thus creating a fluttering and a wheeze ( Fig. 12.10 ).

    

  • Rubbing of inflamed pleural surfaces: this is responsible for the pleural friction rub. The two pleural layers are roughened by inflammation and covered with fibrin, and they grate against each other during respiration. This produces a leather-like sound that is typically inspiratory and expiratory.