COPD: Overview of Definitions, Epidemiology, and Factors Influencing Its Development: Mechanisms of Airflow Obstruction
The mechanisms by which these various diseases lead to expiratory airflow limitation differ. In asthma, the “classic” mechanism for expiratoiy airflow limitation is smooth muscle contraction with narrowing of the airway lumen. In emphysema, destruction of alveolar walls is associated with loss of lung elastic recoil. As a result, following inspiration, there is less tension in the alveolar walls. It is this stored mechanical energy that generates expiratoiy pressure in the alveoli, and the reduction in this pressure contributes in two ways to expiratoiy limitation in emphysema. First, there is less pressure driving air from the alveoli into the proximal airways. Second, the peripheral airways lack supporting cartilage and their patency depends to a large extent on pressure within their lumen which, in turn, is generated by the elastic recoil of the alveolar structures. In emphysema, intraluminal pressure in the terminal airways is reduced. As a result, small airways cannot maintain patency, particularly during forced expiratory maneuvers. The collapse of these airways with forced expiration results in effort independent limitation of airflow. That is, no matter how hard a person tries, airflow is limited because increasing expiratoiy pressures simply collapse airways more. diabetes amaryl
In chronic bronchitis, two processes exist and these may be present independently. Hypertrophy of glandular structures and goblet cell metaplasia in the proximal airways likely contribute to the increased mucus production, the expectoration of which is the defining characteristic of chronic bronchitis’ (Table 1). These changes are not strongly associated with airflow limitation, although it is possible that secretions in large airways may contribute to airflow limitation, particularly during acute exacerbations. The best histologic correlate of airflow limitation in patients with moderately severe COPD is inflammation, fibrosis, and narrowing of the small airways. In this regard, peribronchiolar fibrosis of the terminal airways resembles scarring in other tissues. That is, deposition of collagenous connective tissue is associated with contraction of that tissue which results in circumferential narrowing of the airways and, as a result, limitation of airflow. These two independent features of chronic bronchitis likely both result from the same initiating stimulus. Cigarette smoke, for example, can result in airway inflammation, which in turn can lead to mucus hypersecretion and cough. Similar inflammatory processes initiated by cigarette smoke can independently result in fibrosis and scarring of the small airways. Thus, airflow limitation is epidemiologically linked with mucus hypersecretion. However, in a given patient, hypersecretion may be present without airflow limitation, while in other patients the opposite may develop.
Table 1—Definitions in COPD
|Condition||Key Features in Definition||“Universe” of Definition|