Lidocaine topical anesthesia for flexible bronchoscopy.

965 percent decrease in resistance in an airway in which the wall area was 45 percent. Since an increase in airway wall thickness is one of the pathogenetic mechanisms that leads to the decrease in maximal expiratory flow in patients who have COPD,2 it would be expected that those patients with more severe baseline airflow obstruction would have thicker airway walls. Thus, another explanation for the relationship between starting FEy, and bronchodilator response is equal smooth muscle relaxation irrespective of starting FEy1, but a greater effect of the relaxation in those with the most inflamed and thickened airway walls. A similar mechanism may explain the exaggerated airway narrowing that develops in patients who have COPD in response to inhaled pharmacologic agents that stimulate smooth muscle contraction. A 30 percent muscle shortening in an airway in which the airway wall contributes 20 percent of the total area within the smooth muscle layer will result in a 600 percent increase in resistance, while the same amount of smooth muscle shortening will increase the resistance to 1,300 percent of baseline in an airway in which the wall area makes up 30 percent of the total area. These calculations show that changes in measures of resistance and maximal flow are not linearly related to changes in airway smooth muscle length. Similarly, changes in smooth muscle length, even if precisely known, would not allow an extrapolated conclusion about changes in smooth muscle activation. The degree to which smooth muscle will shorten when stimulated is influenced by the magnitude of the stimulus, the length of the muscle relative to optimal length, and the load that the muscle must overcome to shorten. There is evidence that smooth muscle in vivo does not contract isometrically or isotonically'3 but instead shortens under increasing tension provided by elastic afterloads. The elastic loads are related to the cartilage in the large airways and to the lung elastic recoil in the intraparenchymal bronchi and bronchioles. If there is a decrease in cartilage and/or lung elasticity, then the load on the contracting smooth muscle is less, and a given degree of muscle activation will produce more shortening and airway narrowing. Since a loss ofcartilage and lung elasticity are features of the development of COPD,4-5 this has direct relevance to the results reported by Gross and colleagues. As they in fact suggest, it is possible that the greater bronchodilatation in patients with more severe …