Chronic Obstructive Pulmonary Disease II: Emphysema

Emphysema, a major phenotype of COPD, involves permanent enlargement of the distal airspaces due to destruction of alveolar walls.

It often results from prolonged exposure to toxic gases such as cigarette smoke, which generate harmful oxidants.

These oxidants disrupt the protease–antiprotease balance by inactivating protective enzymes, such as α₁-antitrypsin, allowing unchecked proteases, like neutrophil elastase, to degrade elastin and connective tissue in the alveolar septa.

As damage progresses, alveolar walls deteriorate, and airspaces merge into large, nonfunctional cavities called bullae within the lung parenchyma and blebs near the pleura. These impair gas exchange and lead to ventilation–perfusion mismatch and hypoxemia.

Functionally, the loss of elastic recoil and alveolar surface area impairs expiratory airflow, causing air trapping and lung hyperinflation. As the diaphragm flattens, the lungs expand less efficiently, increasing the effort needed to breathe.