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Chronic Obstructive Pulmonary Disease II: Emphysema

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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.

Overview

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Emphysema, a major phenotype of chronic obstructive pulmonary disease (COPD), is characterized by irreversible destruction of alveolar walls and permanent enlargement of distal airspaces. Unlike chronic bronchitis, which primarily affects the airways, emphysema predominantly involves the lung parenchyma, where structural damage leads to airflow limitation.

Pathophysiology

It most commonly results from prolonged exposure to cigarette smoke and other toxic gases, particularly cigarette smoke. Inhaled oxidants and reactive oxygen species disrupt the balance between proteases and antiproteases. Normally, α₁-antitrypsin inhibits degrading enzymes, such as neutrophil elastase, protecting alveolar structures. In emphysema, oxidative stress and inflammation inactivate antiproteases, allowing proteases to degrade elastin and connective tissue. This, along with apoptosis and immune activation, causes progressive alveolar and capillary destruction. Histologically, inflammatory cells are present, but the main features are loss of alveolar walls and the formation of enlarged airspaces known as bullae (within the parenchyma) and blebs (adjacent to the pleura), which impair gas exchange and cause ventilation-perfusion mismatch.

Types of Emphysema

Centriacinar emphysema, linked to smoking, affects central acini.
Panacinar emphysema, associated with α₁-antitrypsin deficiency, involves uniform destruction of the entire acinus.
Bullous emphysema consists of localized over-distended airspaces compressing surrounding tissue.

Functional Consequences

Loss of elastic recoil, reduced surface area, and decreased capillary density cause airway collapse during expiration and airflow obstruction. Air trapping and hyperinflation increase lung compliance, flatten the diaphragm, and increase the work of breathing. Over time, hypoventilation leads to hypercapnia, while vascular loss raises pulmonary resistance, causing pulmonary hypertension and cor pulmonale.

Transcript

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Alveolar Destruction

Protease Antiprotease Imbalance

Centriacinar Emphysema

Panacinar Emphysema

Bullous Emphysema

Airway Collapse

Pulmonary Hypertension