Air entry and breath sounds, are they the same?

No. And next time you hear a doctor reporting ‘good air entry’, you have a responsibility to slap them on the wrist and correct them. Let me explain why.

When you examine a patient, you report what you can hear and what you can see. You can then make inferences about what you have found. You cannot find sepsis on examination, but you can find signs of infection and tachycardia, tachypnoea or aberrant body temperature which together would make you think of sepsis.

The same is true here: you cannot hear air entry into the lungs because beyond the main bronchi, air flow is laminar and you cannot hear laminar air flow on auscultation. What you can hear is turbulent air movement in the trachea and bronchi and we tend to assume this air will enter the lungs. However, in certain pathologies such as in airway obstruction or collapsed lung, this may not be the case.

So let’s think about breath sounds. A breath sound is the sound of turbulent air in the large airways transmitting through the chest to the diaphragm of the stethoscope. Although you cannot hear laminar air flow, the lung parenchyma and air moving through the lower airways carry the sound of turbulent air from the upper airways. So with normal breath sounds it is likely that there is good air entry as nothing is interrupting the transmission of sound waves.

A normal breath sound is called a vesicular breath sound. As someone breathes in and turbulent airflow increases, the breath sound will get increasingly loud as sound is transmitted through the lung parenchyma. During expiration, air is expelled but beyond the first third of expiration, the sound of turbulent air flow is not transmitted to the lower airways and therefore we cannot hear it.

If part of a lung collapses, there is no lung parenchyma to carry the sound waves from the large airways to the diaphragm of your stethoscope. The breath sounds will therefore be reduced or absent.

Conversely, if there is fluid in the lungs (for example with consolidation in pneumonia), breath sounds will be increased. Why? Because sound waves are transmitted more effectively in liquids than gases. We now call this a bronchial breath sound – the same sound that you will hear if you place your stethoscope over the trachea. These are harsher sounds with a more discernible gap between inspiration and expiration than in vesicular breath sounds. This gap is emblematic of when turbulent air flow from inspiration ends, and before it begins during expiration. This gap is still there is vesicular breath sounds it is smoothly dissipated by the elastic recoil of the lower airways. The trachea does not have the same expansibility and recoil.

So why is this important? If there is reduced air entry into the lungs due to an airway obstruction, you will certainly hear reduced breath sounds (the sound of turbulent air flow cannot be transmitted). But the opposite is not necessarily true. You may have reduced breath sounds but air entry into the lungs may be normal. For example, breath sounds may be absent or reduced in pleural effusions or chest wall swelling. The air is reaching the lungs just fine but you effectively have a wall blocking sound from travelling from the distal lung fields to the diaphragm of the stethoscope. Likewise, in patients who are very thin, breath sounds might be louder for the opposite reason.

So next time you hear someone say air entry, ask what they really mean.


What is Stridor?

Stridor is a coarse, high pitched sound generated by anatomical abnormalities or obstruction of the upper airway. It is not a disease in itself. It can be inspiratory (most common), expiratory, or biphasic. Inspiratory stridor arises from obstruction of the extra-thoracic airway (larynx, pharynx, upper trachea). Expiratory stridor arises from obstruction of the intrathoracic airway (lower trachea and and bronchi). Biphasic stridor implies glottic involvement.

Inspiratory stridor is more common in children as they have relatively narrowed and flexible airways that are more predisposed to collapse. If we consider a gas at rest, it will exert pressure in all directions equally. However, during inspiration, air is drawn into the airways and the force the gas exerts in the direction it is moving parallel to the airways is greater than the pressure exerted on the walls of the airway. As this latter pressure falls, the airway can collapse and be obstructed, causing stridor. Because children’s airways are narrower, there are also more likely to develop stridor secondary to upper airway obstruction from inflammation, oedema, or foreign bodies.

Expiratory stridor is more complicated. Upon inspiration, the expansion of the chest and resultant negative intrathoracic pressure causes the intrathoracic portion of the trachea to be drawn open. Conversely, the extrathoracic, upper portion of the trachea experiences an external positive pressure and its diameter reduces. Conversely, during expiration, the extrathoracic trachea increases in diameter and the intrathoracic trachea narrows as the intrathoracic pressure increases. In a healthy individual, the trachea remains sufficiently patent during inspiration and expiration such that stridor does not occur. However, when the intrathoracic trachea narrows beyond normal limits, especially in the presence of secretions or oedema, the airway obstructs and stridor will be heard on expiration rather than inspiration.