Abstract
Although airway obstruction characterizes the functional defect in patients who have asthma as well as in patients who have chronic obstructive pulmonary disease (COPD), dif ferent mechanisms are thought to be respon sible for the obstruction. The airway obstruc tion can be quantitated by measuring airway or pulmonary resistance or by measuring max imal expiratory flow (MEF) from the lungs. The magnitude of the decrease in MEFis most commonly used to quantitate the severity of the obstruction; however, decreases in MEF may be due to a variety of pathogenetic mech anisms. MEF is related to the elastic recoil of the lung, which provides the driving pres sure for expiratory flow, the caliber of air waysupstream from the points where airways collapse and flow limitation occurs, and the mechanical properties of the airways at the sites of flow limitation. In patients who have asthma, the primary problem is one of air way narrowing alone and there is little evi dence for important changes in lung elastic recoil or large airway compliance, whereas in patients with COPD the decrease in MEF is more often caused by a combination of air way narrowing, loss of recoil, and altered air way collapsibility. Pulmonary and airway resistance are more specific measures of airway narrowing be cause they are less influenced by lung paren chymal recoil and are not influenced by air way collapsibility as flow-limiting segments do not develop during the tidal breathing. In addition, resistance or conductance may be a more pertinent variable to measure since
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