In the lung there are millions of tiny, thin-walled, elastic air sacs called alveoli (see Anatomy of the Respiratory System). These tiny sacs perform the crucial task of replenishing the blood with oxygen (via inhalation) and ridding the body of carbon dioxide (CO2) in exhalation.
Emphysema is the enlargement of the alveoli accompanied by destruction of their walls. In "smokers emphysema" an agent in cigarette smoke sets off a self-perpetuating, low-grade inflammation that causes the release of enzymes (elastase) from inflammatory cells that break down collagen and elastin - substances that maintain the structure and elasticity of alveoli - in the alveolar walls. The NHLBI (National Heart, Lung and Blood Institute) reports that this creates an imbalance between the elastin-degrading enzymes and their inhibitors. They also found that oxidants in cigarette smoke inactivate a significant number of elastase inhibitors, thereby decreasing the amount of active antielastase available to protect the lung and further upsetting the elastase-antielastase balance.
This disruption of the alveolar walls and elastin leads to a decrease in the elastic recoil of the lungs, limiting the ability of the alveoli to passively shrink and to exhale. This accounts for the main limitation to exhalation seen in severe COPD. The disruption of the alveolar walls also leads to their increase in size, making the lungs larger and placing the chest at a mechanical disadvantage. Disruption of the alveolar walls also makes exchange of oxygen from the alveoli to the capillaries and carbon dioxide from the capillaries to the alveoli more difficult. Collapse of the bronchial walls occurs when the cartilage in the bronchial walls has been weakened.