Normally, the intrapleural pressure (Pip), or the pressure in the space between the lung’s visceral and parietal pleural layers, is slightly negative relative to the atmosphere (Patm). This is due to the chest wall and lungs recoiling away from each other. During a forced expiration, expiratory muscles can increase the Pip (as noted in the diagram). This pressure is transmitted to the alveolus, increasing pressure within the airway. I’ve termed this bronchial pressure (Pbr). Flow occurs from regions of high pressure to those of lower pressure, so since Pbr > Patm, air is expired.
As air exits the lung (alveoli → bronchioles → bronchi → trachea), it encounters airway resistance causing Pbr to decrease. If the patient has obstructive physiology as in chronic obstructive pulmonary disease (COPD), expired air encounters more resistance leading to a precipitous drop in pressure (+20 down to +10 cm H2O, in this example).
In either case, Pbr stents open the airway, and Pip tries to collapse it. The point along the airway where Pbr = Pip is called the equal pressure point (EPP). Normally during forced expiration, the EPP occurs proximal in the tracheobronchial tree where cartilage reinforces the airway and prevents collapse; however, in patients with COPD, the EPP is much more distal, causing airway collapse near the alveolus (parts of the airway NOT reinforced with cartilage) leading to hypoventilation, hypoxemia, air trapping, etc.
This explains why patients with COPD habitually exhale through tightly pursed lips. By limiting the rate at which air is exhaled, the patient can maintain a higher airway pressure (Pbr) to help stent the airway where it wants to collapse.
Be sure to check out my other post on the basic physiology of breathing, and drop me a comment below with questions! 🙂
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