These sounds are commonly, and INACCURATELY referred to by many as rales . End-inspiratory crackles are generally sharp and high-pitched, as they are occurring in the very small airways (bronchioles or terminal bronchioles) and/or in the air sacs (alveoli). They are the sound of the explosive "popping-open" of those collapsed lung parts when the patient is at the end of their inspiratory cycle. They often result from:
ATELECTATIC crackles, as the name would suggest, are heard when a portion of the lung is collapsed and airless. They are relatively quiet, end-inspiratory crackles. They are often heard posteriorly:
After the patient takes many deep breaths, the loudness and the area over which the crackles were heard will generally decrease, and/or the breath sound will occur later in the inspiratory cycle. Incentive Spirometry (IS) or Intermittent Positive Pressure Breathing (IPPB) may be indicated for patients with atelectatic crackles.
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Atelectatic crackles often change characteristics after the patient takes many deep breaths.
Another end-inspiratory crackle is called a CREPITANT crackle. With these sounds, the alveoli collapse from excessive fluid pressure within the capillaries around the alveoli. This can occur from fluid overload from excessive IV fluid administration, or from congestive heart failure. These sounds do not change with deep breaths, but will often clear with diuresis. Look for:
Hydrostatic pressure is gravity-specific, therefore this sound is usually auscultated in the bases. When a patient is lying on his/her side, the crackles may be heard predominantly on that side. As the problem becomes more severe, one can expect to find crepitant crackles in more lung fields. As a patient's condition worsens further, the fluid may leak into the lungs. The patient now has "pulmonary edema", and those lung sounds may even be heard on expiration. At that point, they are classified as SUB-CREPITANT crackles.
Sometimes an isolated area of crepitant crackles can be found in an upper lung field. This finding may be indicative of a pulmonary tubercle, as found in tuberculosis. Please note, crepitant crackles are not "crepitus" (sub-cutaneous emphysema), though a similar, but louder, crackling sound is heard when a stethoscope is first placed on skin containing sub-cutaneous air.
FIBROTIC crackles, though not listed as such in Laennec's work, are heard in pulmonary fibrosis. Again, it is the sound generated by the "popping-open" of collapsed bronchioles and alveoli. In this scenario, the presence of scar tissue is causing a loss of lung compliance. These are slightly louder and sharper than the previous crackles. They can be heard in patients with lung injuries from environmental exposures, as in those who are/were employed in factories where a large amount of dusts, fibers, caustic fumes, and other pollutants are airborne. Fibrotic crackles are not gravity or body-weight specific, therefore can occur in any lung field. They are usually present over large areas of the lung. Deep breaths and/or diuretics have little effect on these lung sounds. Glucocorticoids, such as prednisone, are usually indicated here.
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Fibrotic crackles are louder and duller than atelectatic crackles