Before reading this post, it’s important to understand the basic physiology behind breathing. Normally, intrapleural pressure (Pip) isnegative, but during a forced expiration, the usage of expiratory muscles can drive the Pip upward. This, in turn, compresses the alveolus increasing pressure within the airway which, due to pressure gradients, exceeds the atmospheric pressure (Patm) causing airflow to move outward
In the diagram below, the normal lung on the left shows how the airway pressure (I’ve called it bronchial pressure, Pbr) drops from +20 to +18 to +16 and so on as air exits the alveolus in transit to the atmosphere. This pressure dropoff is due to resistance within the airway. If the patient has obstructive physiology (ie, chronic obstructive pulmonary disease), significant obstruction can cause a more precipitous drop in pressures along the distal airways.
In either case, one can imagine the Pbr stents open the airway and Pip is trying to collapse it. The point at which these two are equal is called the equal pressure point. In forced exhalation of normal lungs, this point occurs fairly proximal in the tracheobronchial tree where cartilage reinforces the airway and prevents collapse. In patients with COPD, this point occurs much more distal causing airway collapse near the alveolus (parts of the airway that are NOT reinforced with cartilage) leading to hypoventilation, hypoxemia, etc.
This explains why patients with COPD habitually exhale through tightly pursed lips. By limiting the rate at which air is exhaled, the patient is able to maintain a higher airway pressure (Pbr) to help stent the airway where it wants to collapse.
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