Adventitious Sounds: Crackles
SOUND PRODUCTION
Crackles, formerly known as rales, are discontinuous, intermittent, nonmusical sounds that are described according to their timing and duration within the respiratory phase, intensity, pitch, and location. These short, explosive or popping sounds are heard primarily through the chest wall with a stethoscope, but they may also be heard at the mouth with or without a stethoscope. Crackles are characterized as fine or coarse. Fine crackles have a soft, high-pitched, very brief nature and coarse crackles are louder, lower in pitch, and are brief but slightly longer than the fine ones. The characteristics of crackles change, depending on the underlying cause. Two different mechanisms are thought to generate crackles: air bubbling through secretions and the sudden, explosive opening of airways.
Air bubbling through secretions
Air bubbling through secretions in the airways is widely accepted as one way crackles are produced. According to Dr. Paul Forgacs, this explanation is probably true when the trachea and mainstem bronchi are full of sputum, as commonly occurs with severe pulmonary edema and chronic bronchitis. However, Forgacs argues that the air bubbling theory doesn’t explain why crackles are heard mainly during inspiration and why they’re heard over diseased lungs when sputum is usually absent. Further, in the smaller airways, airflow resistance—produced by the surface tension and viscosity of secretions—is too high to be overcome by the air pressure gradients that are present in healthy lungs during inspiration and expiration. Thus, another mechanism must explain how crackles are produced in the smaller airways.
Sudden, explosive opening of airways
At the end of expiration, peripheral airways in the lung bases close. At the beginning of inspiration, these peripheral airways remain closed, and inspired air flows to each lung apex first. The airways that are distal to the closed peripheral airways remain
underexpanded until airway pressures and external forces, such as diaphragmatic movement and rib cage expansion, snap the airways open. The sudden opening of multiple collapsed peripheral airways and the associated explosive changes in air pressures are thought to produce the crackles heard over the lung bases in a healthy person who inhales deeply after a maximum exhalation. This mechanism is also thought to be responsible for the crackles heard in patients with atelectasis and interstitial lung disease.
underexpanded until airway pressures and external forces, such as diaphragmatic movement and rib cage expansion, snap the airways open. The sudden opening of multiple collapsed peripheral airways and the associated explosive changes in air pressures are thought to produce the crackles heard over the lung bases in a healthy person who inhales deeply after a maximum exhalation. This mechanism is also thought to be responsible for the crackles heard in patients with atelectasis and interstitial lung disease.
Crackles are acoustic alterations that follow abrupt equalization of pressures or a change in elasticity resulting from the sudden opening of abnormally closed airways. Crackles are characterized by a repetitive rhythm and loudness. These characteristics suggest that the airways open in the same sequence, at the same point in the respiratory cycle, and at the same approximate lung volumes. Crackles may be present in the lung bases of older individuals and occasionally in other healthy individuals. These crackles clear with coughing and have no pathological significance.
AGE ISSUE
Crackles aren’t usually heard in infants; however, if present, they could indicate respiratory tract infection.
DOCUMENTATION
The timing of crackles is described as early inspiration, midinspiration, or late inspiration or early expiration, midexpiration, or late expiration. The duration, indicating the length of time that the crackles can be heard during inspiration or expiration, varies. Sound intensity is described as soft, intermediate, loud, or very loud. Pitch is considered high or low. The density of crackles in the thoracic region is described as diffuse or scanty.
LATE INSPIRATORY CRACKLES
Late inspiratory crackles are high-pitched, explosive sounds of variable intensity and density. These are heard mostly over dependent or poorly ventilated lung regions.
Related conditions
Conditions associated with late inspiratory crackles include atelectasis, resolving lobar pneumonia, interstitial fibrosis, and left-sided heart failure.
Atelectasis
Atelectasis, the incomplete expansion of a lung area, is seen in postoperative and immobile patients and in patients with impaired diaphragmatic function. Resorption of alveolar air occurs secondary to prolonged hypoventilation, gravitational forces that close airways and deflate the lung bases, obstruction from secretions, and mucus plugging the airways. The result is poor ventilation
in the affected areas and possible collapse of segmental or lobar bronchi. If small peripheral airways are involved, clinical findings may not be detectable. However, if a larger airway is involved, the clinical findings of decreased chest wall movement, a dull percussion note, and bronchial breath sounds are easily noted. The transmission of vocal sounds, such as egophony, bronchophony, and whispered pectoriloquy, suggests atelectasis.
in the affected areas and possible collapse of segmental or lobar bronchi. If small peripheral airways are involved, clinical findings may not be detectable. However, if a larger airway is involved, the clinical findings of decreased chest wall movement, a dull percussion note, and bronchial breath sounds are easily noted. The transmission of vocal sounds, such as egophony, bronchophony, and whispered pectoriloquy, suggests atelectasis.
Crackles associated with atelectasis are produced by the sudden opening of collapsed small airways and adjoining alveoli. These crackles are high-pitched, explosive sounds heard late in inspiration. (♦Sound 85)
AGE ISSUE
Premature infants may develop atelectasis secondary to a surfactant deficiency. Older adults on prolonged bed rest are especially susceptible to atelectasis due to changes in their musculoskeletal systems (such as kyphosis, which decreases lung expansion) and decreased respiratory and expiratory forces.
Sound characteristics
In a postoperative patient who hasn’t been coughing and deep breathing adequately, late inspiratory crackles are heard over the posterior bases of both lungs. This area is located between the eighth and tenth intercostal spaces from the left posterior axillary line to the right posterior axillary line. The crackles begin late in inspiration and become more profuse toward the end of inspiration. They vary in intensity but are high-pitched. (♦Sound 85)
Because crackles associated with atelectasis are poorly transmitted to the chest wall surface, their intensity and density change when the stethoscope is moved only a short distance. Crackles are not audible at the mouth. The patient’s position affects the detection of crackles. For example, in an immobile patient, profuse
crackles are heard in the dependent lung regions, but crackles are absent or scanty in the nondependent lung regions. Also, crackles associated with atelectasis may clear somewhat with coughing.
crackles are heard in the dependent lung regions, but crackles are absent or scanty in the nondependent lung regions. Also, crackles associated with atelectasis may clear somewhat with coughing.
Lobar pneumonia
In patients with resolving lobar pneumonia, crackles can be auscultated over lung areas where many alveoli are still filled with exudate, but the surrounding alveoli are aerated and have higherthan-normal ventilation. A large increase in air pressure gradients in the airways reaching these unaerated alveoli generates crackles as the airways are snapped open during late inspiration. These crackles have a sound similar to that of late inspiratory crackles heard over atelectatic areas, but are not affected by coughing or position changes. (♦ Sound 86)