ABSTRACT: Chest auscultation is a universally available diagnostic tool that may be underappreciated in these days of "high-tech" medicine. Abnormal breath sounds are marked by an unusual location, loudness, or pitch. Adventitious lung sounds are discontinuous (crackles) or continuous (wheezes and rhonchi). Fine crackles occur as many small bronchioles -- collapsed from fibrosis, pneumonia, or congestion--snap open at once. They are higher pitched and less intense than coarse crackles, which may be audible throughout inspiration. Often occurring in smaller bronchi, wheezes tend to be polyphonic, higher-pitched, and more intense than rhonchi, which have a monophonic snoring or moaning quality.
In his 1819 work, "De l'Auscultation Mediate," Rene Laennec described the normal and abnormal chest sounds he heard with his newly invented medical instrument, the stethoscope, and attached clinical significance to these sounds by comparing them with pathologic autopsy findings. Although the shape of Laennec's original wooden-tube stethoscope has changed radically, the general principles and clinical correlations of chest auscultation are the same now as they were in the early 19th century.
In Laennec's era, medical diagnoses were based largely on a patient's verbal account of his or her illness and some clinical observations. The stethoscope was one of the first objective tools available to physicians and added the discipline of auscultation to the physical examination. Tremendous strides have been made since that time in the development of more exact and expensive instruments for diagnosing lung disease.
Given the advent in recent decades of high-tech electronic diagnostic gadgetry, the stethoscope has fallen into a secondary role in the diagnosis of lung diseases. Some physicians have even described it (in a tongue-in-cheek manner) as "a decorative instrument in so far as its value in diagnosis of pulmonary diseases is concerned."
I contend, however, that chest auscultation is the single most useful technique in the diagnosis of lung disease, especially in light of the fact that it can be done by any physician, anytime, anywhere, without morbidity or mortality, and without any additional expense.
The diagnostic usefulness of the stethoscope is limited, however, by what goes between the earpieces. We who are in clinical practice can do both ourselves and our patients a great service by placing renewed emphasis on the art as well as the science of chest auscultation.
In this article, I will emphasize how to use this tool to the greatest advantage. I will review how breath sounds are produced and transmitted, their characteristics in normal and abnormal circumstances, and in which areas of the chest they are audible in both instances. Finally, I will review interpretation of breath sounds in the differential diagnosis of various pulmonary diseases.
Breath sounds may be classified as normal or adventitious. (The latter type is also referred to as added breath sounds.) Normal breath sounds, of course, are heard only in certain locations in the chest. When such sounds are heard outside of their "normal" area, this indicates a pathologic condition in the underlying lung or pleura and may thus be considered abnormal.
Adventitious sounds are superimposed on a patient's underlying breath sounds and usually indicate disease. The exact site of breath sound generation is not known. It appears that vesicular breath sounds are produced in the lung periphery - although a central source has not been totally excluded. Bronchial and tracheal breath sounds appear to be produced centrally, while the origin of bronchovesicular sounds may be somewhere between the two.
The majority of breath sounds, both normal and adventitious, are in the range of 16 to 200 Hz. This is at the lower end of the spectrum of normal hearing (16 to 16,000 Hz) The sensitivity of the human ear in detecting low-frequency sound is relatively poor; thus, breath sounds are difficult to appreciate with the stethoscope.
The character and quality of normal breath sounds depend on several factors, including low velocity, distance from the point of sound generation, airway patency, and the condition of the pleurae and chest wall.
Airflow velocity. Forceful exhalation and inhalation increase airflow velocity and cause greater air turbulence, greater amplitude of vibration in the bronchial wall, and a louder breath sound. Conversely, if the patient's rate or volume of respiration is so low that the air moves very slowly, less turbulence and, therefore, much less amplitude of normal breath sounds is produced. This is true for tracheal and bronchial breath sounds but may be less of a factor with vesicular breath sounds.
Distance from point of origin. Lung sounds are progressively filtered and attenuated as they travel toward the periphery through the chest wall. Filtering means that breath sounds generated at various frequencies are transmitted differently; this contributes to differences in acoustic quality of sounds heard at the mouth, upper chest, and lung base, as described below.
Sounds heard at the trachea and mouth, with a frequency between 200 and 2,000 Hz, are relatively unfiltered. At the level of the main-stem bronchi, the frequency is 200 to 1,000 Hz; at the lung base, it is 200 to 400 Hz.
Airway patency. Patency, of course, is necessary for transmission of breath sounds. Occlusion of a segmental or lobar bronchus by tumor or extrinsic compression creates a barrier to sound transmission. This obliterates or decreases the intensity of breath sounds that are perceived at the periphery.
Condition of pleurae and chest wall. Processes that separate the visceral and parietal pleurae, such as pleural effusion, pleural thickening, pleural tumor, and pneumothorax, decrease the loudness of lung sounds by interposing a sound barrier between the source of breath sound generation and the chest wall. Increased density of the chest wall caused by obesity, pleural tumor, or inflammation likewise can dampen normal breath sounds.
Heard over the entire lung field a healthy person, normal breath sounds consist of an inspiratory and expiratory phase. Four distinct types of sounds are audible during quiet respiration (Table I).
Tracheal. These breath sounds are high-pitched and loud, with a harsh and hollow (or "tubular) quality. The inspiratory and expiratory phases are of equal duration, and there is a definite pause between phases. Tracheal breath sounds usually have very little clinical usefulness.
Bronchial. Normally heard over the upper manubrium, these breath sounds directly reflect turbulent airflow in the main-stem bronchi. They are loud and high-pitched but not quite as harsh and hollow as tracheal breath sounds, The expiratory phase is generally longer than the inspiratory phase, and there is usually a pause between the phases.
Bronchovesicular. These breath sounds are normally heard in the anterior first and second intercostal spaces and posteriorly between the scapulas, where the main-stem bronchi lie. The inspiratory and expiratory phases are about equal in duration, with no pause between phases. Bronchovesicular sounds are soft and less harsh than bronchial breath sounds and have a higher pitch than vesicular sounds.
Vesicular. Audible over peripheral lung fields, these breath sounds are soft and low-pitched, without the harsh, tubular quality of bronchial and tracheal breath sounds. The inspiratory phase is about three times longer than the expiratory, with no pause between phases.
Breath sounds are considered abnormal if they are heard outside their usual location in the chest or if they are qualitatively different from normal breath sounds.
Unusual location. Bronchial breathing heard at any location other than the upper manubrium indicates the presence of pulmonary consolidation or atelectasis in that area. Such breathing may also be heard in areas of pulmonary fibrosis. It is believed that the consolidated, atelectatic, denser lung transmits sound generated the larger airways without significant loss of higher frequencies. Thus, the quality of the sound is much the same as if it were heard over the upper airway.
Qualitative differences. In contrast to the above situation, breath sounds are greatly reduced in intensity when there is hyperinflation (as occurs in severe emphysema) or when there is significant air trapping (as occurs in severe asthma). Theoretically, a hyperaerated, less dense lung transmits breath sounds poorly.
Although Laennec was very exacting in his original definitions of breath sounds, some confusion in terminology arose. This confusion stems from the original work of Laennec, who initially called adventitious sounds "rales," with appropriate modifiers. He used this term to describe fine and coarse crackles as wen as wheezes and rhonchi. However, since rale -- meaning "rattle" in French-was associated with the death rattle by the public, Laennec used the Latin equivalent, "rhonchus," in the presence of patients. By his own admission, the sounds he heard were easier to distinguish than they were to describe. Later, authors used the terms "rale" and "rhonchus" differently; this led to more than 150 year-s of confusing and misleading terminology.
Added lung sounds are divided into two general groups: discontinuous sounds, which are 250 milliseconds or less in duration, and continuous sounds, which last longer than 250 milliseconds (Table 2). Discontinuous sounds are further classified as either coarse or fine crackles; continuous sounds, as either wheezes or rhonchi.
Discontinuous. Crackles are explosive, sharp, discrete bursts of interrupted sound. They are classified as fine or coarse (Table 3). Fine crackles are heard over areas of abnormal partial deflation of the lung, in which many small airways are collapsed. The probable mechanism for the production of fine crackles is as follows. During inspiration, the air pressure on the "upstream" (mouth) side increases until it is able to overcome the forces that are closing the bronchiole. When this occurs, the airway snaps open as the pressure between the bronchiole and the alveolus is equalized (Figure). The resulting vibration in the airway causes a discrete, sharp sound of very short duration.
As hundreds of airways open sequentially, the characteristic crackling sound is produced. The sound of fine crackles can be simulated by rubbing a lock of hair between your fingers.
The bubbling sound of coarse crackles is produced when air passes over secretions in the larger airways (trachea and bronchi). Since air flows through the airways during inspiration and expiration, coarse crackles are more likely to be detected during both phases of the respiratory cycle. Fine crackles are usually appreciated only during inspiration.
Some clinicians maintain that the timing of onset of crackles aids in the differential diagnosis of parenchymal and airways-disease. Crackles auscultated during early inspiration are thought to be more indicative of airways disease, such as chronic bronchitis, emphysema, and asthma. Crackles auscultated during late inspiration are more suggestive of parenchymal disorders, such as pulmonary fibrosis, interstitial pneumonitis, and pneumonia.
Continuous. The rapid flow of air through narrowed bronchi produces wheezes and rhonchi. The walls and secretions of the bronchus vibrate between the closed and barely open positions, similar to the manner in which a reed vibrates in a musical instrument.
The pitch of the sound depends on the frequency of the vibrations; this is determined by the airflow rate and the mechanical properties of the affected segment of bronchus. Wheezes tend to be of higher pitch and greater intensity than rhonchi (Table 4). The rhonchus has a snoring or moaning quality.
Most wheezes and rhonchi are accentuated on inspiration and are less prominent or nonexistent during expiration. Wheezes are usually caused by many narrowed airways, each contributing its own pitch to the sound; because of this characteristic, they are called polyphonic.
Structural abnormalities and bronchial obstructions, such as smooth muscle hypertrophy, mucous plugging, and, less often, tumor or other external compression, usually generate wheezing in one airway. The resulting wheeze is monophonic and most frequently heard on inspiration.
Wheezes occur in the bronchi and bronchioles; rhonchi occur in large bronchi. Rhonchi are more frequently monophonic.
Polyphonic wheezes are the hallmark of asthma or acute bronchospasm, while rhonchi are more likely to be heard in patients with acute bronchitis or chronic obstructive pulmonary disease and in patients with poor clearance of secretions, such as those who are obtunded or in a post-operative state. Stridor is a continuous, high-pitched monophonic sound heard throughout respiration; this sound is accentuated during inspiration. It indicated upper airway obstruction at the laryngeal level. These characteristics distinguish stridor from a wheeze.
Other sounds. The visceral and parietal pleurae normally move silently against each other during respiration. However, when the pleurae are inflamed, the two thickened surfaces produce vibrations as they move irregularly over each other.
A pleural rub is the sound produced by the motion of inflamed pleurae. It tends to be a loud, grating sound confined to a relatively small area of the chest wall. A pleural rub is usually heard during inspiration and expiration. However, it is sometimes confined to inspiration; when this occurs, it is difficult to distinguish from pulmonary crackles. A pleural rub has also been described as a leathery sound. Usually, the inspiratory and expiratory components of the rub can be readily heard. When effusion separates the two pleural surfaces, the rub may disappear. However, the disappearance of a pleural rub does not necessarily mean that the pleural inflammation itself has resolved.
A pericardial rub usually has three components (atrial systole, ventricular systole, and ventricular diastole); it can usually be distinguished from a pleural rub by having the patient hold his breath. During breath-holding, a pleural rub disappears but a pericardial rub persists.
A mediastinal crunch is a grating, crunching sound heard in the center of the anterior chest. The sound coincides with the heartbeat and signifies the presence of free air in the mediastinum. The pathogenesis of mediastinal crunch is not clear, however, it may involve compression of the air by the beating heart and the mediastinal structures.
Egophony, bronchophony, and pectoriloquy all refer to auscultatory signs that can be heard over areas of pulmonary consolidation. The pathogenesis of these signs relates to the increased sound transmission through the consolidated lung. This results in transmission of sound-from the larger bronchi through the consolidated lung to the periphery without significant loss in sound quality.
Egophony is elicited by having the patient say the letter "E' while you listen with the stethoscope. When egophony is present the "E" sounds like "A."
Bronchophony is demonstrated by having the patient say a phrase as you auscultate; "ninety-nine" is the conventional phrase. The sound will be indistinct and muffled over the normal lung. However, the "ninety-nine" will be heard distinctly over the consolidated lung, without loss of clarity.
Pectoriloquy is similar to bronchophony, except it is usually elicited by having the patient say the phrase "one, two, three." The phrase will be muffled and indistinct when you auscultate over the normal lung and clearly audible when you auscultate over an area of consolidation.
The common obstructive diseases of the lung - chronic bronchitis, emphysema, and asthma - can frequently be distinguished solely on the basis of the physical examination. Patients with chronic bronchitis commonly have noisy chests because of crackles and wheezes. The breath sounds are vesicular in nature, however, there is a prolonged expiratory phase, which generally correlates with the degree of obstruction. Breath sounds at the mouth will be heard at normal intensity.
Patients with emphysema, on the other hand, present with a relatively quiet chest. Breath sounds are vesicular but significantly reduced in intensity Adventitious sounds are unusual unless bronchitis or asthma is present.
The expiratory phase of vesicular breath sounds is similarly prolonged, however, breath sounds heard at the mouth are usually reduced, in contrast to what is normally heard with chronic bronchitis or asthma.
Wheezing is the hallmark of clinical asthma. In patients with mild or early asthma, wheezing is usually heard over the central airways only during expiration. As bronchospasm worsens, the wheezes are heard over the entire chest and in both phases of respiration. The breath sounds are vesicular, and there is a prolonged expiratory phase that tends to correlate with the degree of bronchial obstruction. Breath sounds heard at the mouth are of normal intensity. Interstitial pneumonitis and fibrosis are characterized by the presence of fine inspiratory crackles. With early or mild disease, the crackles are heard at end-inspiration; however, as the disease progresses, they may occupy more of the inspiratory cycle - it is often difficult to hear the underlying breath sounds because of the intensity of the crackles in interstitial fibrosis, but the sounds are vesicular with no prolongation of expiration.
Pulmonary consolidation, as in lobar pneumonia, yields bronchial breath sounds over the affected area. Also, coarse or fine crackles may be heard. Expiration is not prolonged unless obstructive disease exists.
Left-sided heart failure. Pulmonary congestion associated with left sided heart failure is characterized by transudative fluid in the interstitium and alveoli. The bronchial mucosa may also be swollen.
Breath sounds in left-sided heart failure are vesicular, although they sometimes have a prolonged expiratory phase secondary to bronchial mucosal edema. Fine crackles are heard in mild to moderate pulmonary edema, while coarse crackles and polyphonic wheezes occur in severe pulmonary edema.
Pleural effusion. Pleural fluid or pleural thickening muffles the transmission of all lung sounds to the periphery. Vesicular sounds are decreased or absent Because the adjacent lung is compressed, bronchial breath sounds are sometimes heard at the area just above the pleural effusion. The reason for this is unclear. I believe the compressed edematous lung, which is immediately above the effusion, acts as a consolidation and causes increased sound transmission.
Pneumothorax. With a small or mild pneumothorax, decreased vesicular breath sounds may be heard on the side that is affected. Breath sounds are absent if a more extensive pneumothorax is present.
Consultant, February 1997, pp 415-427.