In a patient with chronic obstructive pulmonary disease (COPD), what is the primary mechanism contributing to air trapping and hyperinflation?

The primary mechanism contributing to air trapping and hyperinflation in patients with chronic obstructive pulmonary disease (COPD) is the loss of elastic recoil in the lungs combined with airway obstruction. COPD is characterized by progressive airflow limitation that is not fully reversible. Emphysema, a common component of COPD, involves the destruction of alveolar walls. This destruction leads to a reduction in the elastic recoil of the lungs. Elastic recoil is the ability of the lungs to return to their original shape after being stretched during inspiration. When elastic recoil is reduced, the lungs become more compliant (easier to inflate) but less able to deflate passively and completely. Simultaneously, COPD involves airway obstruction, which can result from inflammation, mucus hypersecretion, and airway narrowing due to smooth muscle contraction and structural changes. The combination of reduced elastic recoil and airway obstruction causes air to be trapped in the alveoli during exhalation because the lungs cannot effectively push the air out. Over time, this trapped air leads to hyperinflation, which is an abnormal increase in the volume of air in the lungs at the end of exhalation (increased functional residual capacity). This hyperinflation flattens the diaphragm, making it less effective, increases the work of breathing, and impairs gas exchange.