Biomedical Engineering Reference
In-Depth Information
fluid and induced sputum demonstrate a marked increase in macrophages
and neutrophils (16,17). In contrast to asthma, eosinophils are not promi-
nent except during exacerbations or when patients have concomitant
asthma (13,18).
Fixed narrowing of small airways, emphysema, and luminal obstruc-
tion with mucus secretions may all contribute to airflow limitation in
COPD, but there is debate about which mechanism is most important.
There are differences between patients and at different stages of disease
progression in the contribution of each of these processes, but problems
in making accurate measurements in patients have made it difficult to eval-
uate the importance of each mechanism in an individual patient.
B.
Small Airways
It has long been recognized that there is narrowing of small airways in
patients with COPD (19-22) (Fig. 1). There is an increase in the thickness
of small airways with increased formation of lymphoid follicles and depo-
sition of collagen in the outer airway wall that may restrict airway opening
(23). The lumen of small airways is reduced by mucosal thickening
containing an inflammatory exudate, which increases with the severity of
disease. The mechanism for lymphoid follicle formation in more severe dis-
Figure 1
Mechanisms of airflow limitation in COPD. The airway in normal sub-
jects is distended by alveolar attachments during expiration, allowing alveolar emp-
tying and lung deflation. In COPD, these attachments are disrupted because of
emphysema thus contributing to airway closure during expiration, trapping gas in
the alveoli and resulting in hyperinflation (17). Peripheral airways are also obstructed
and distorted by airways inflammation and fibrosis (chronic obstructive bronchioli-
tis) and by occlusion of the airway lumen by mucous secretions which may be
trapped in the airways because of poor mucociliary clearance.
