Lung Sounds Quiz

Airflow and associated turbulence within the airways is the major source of breath sounds. The branching network of the lung is such that inspiratory in-flow creates more turbulence and sound delivery to the lung because of flow separation at branch points whereas during expiration out-flow is converging. If inspiration has a shorter duration than expiration then inspiratory airflow must be somewhat greater than expiratory airflow. Higher flow when breathing in will create a louder signal than the lower flow when breathing out.

During a severe asthma attack when the patient is in extreme respiratory distress there may be little or no audible wheezing (the so-called silent lung). Following bronchodilator administration wheeze may appear indicating resumption of airflow.

It is the brief, intermittent, randomly repetitive character of these sounds that makes them discontinuous, contrary to sounds that persist (e.g. asthmatic wheeze), and therefore they are considered discontinuous.

During expiration while at rest airflow is passive, driven by elastic recoil. During inspiration active muscle effort produces a greater flow. In addition, during expiration the airways narrow with a corresponding increase in resistance to flow compared with the resistance to flow during inspiration. By extending the duration of expiration these effects are diminished so that the same volume of air that entered the lung can exit.

Crackles, also called rales, are brief, snapping-like sounds that can be heard in inflammatory or fibrotic pulmonary disease and in pulmonary congestion secondary to cardiac, kidney and other diseases. The sound of each crackle is generated by the sudden inspiratory re-opening of an airway that collapsed during the preceding exhalation. The sound is caused by the rupture of the fluid film that adheres to airway walls as they open. Experimental studies are consistent with the opening of previously collapsed small airways as the source of these sounds. Course, low pitch crackles may be created by the bubbling of air moving through fluid in large airways. If so, they are generally inspiratory and expiratory, and diminish or disappear with cough. Small pleural effusions do not compress lung parenchyma sufficiently to create crackles, but pleural friction rubs may resemble crackles.

As noted on the CD there are four separate “chunks” of acoustic information with each respiratory cycle — two silent intervals and two brief intervals of airflow.

See question 3 for an explanation of fine crackles. Small airway collapse and reopening occurs in both stiff, fibrotic lungs and in lungs that are congested and edematous from pneumonia or heart failure. In patients with pulmonary fibrosis or pneumonia the crackles are unchanged when the patient position is changed. On the other hand in patients with heart failure the distribution of crackles is often gravity dependent and changes according to the patient’s posture (sitting – reclining etc).