Physiologic similarities and differences between asthma and chronic obstructive pulmonary disease

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Abstract
This review examines the physiologic mechanisms responsible for persistent maximum expiratory airflow limitation in nonsmoking patients with acute and chronic moderate to severe persistent asthma in comparison to chronic obstructive pulmonary disease. The phenomenon of acute but reversible loss of lung elastic recoil during acute asthma is reviewed, although no plausible pathophysiologic explanation has been offered. Nonsmoking adults with stable asthma and persistent maximum expiratory airflow limitation, despite optimal polytherapy, were shown to have unsuspected and unexplained marked loss of lung elastic recoil in the absence of lung computed tomography scored emphysema. This condition resulted in up to 50% reduction in maximum expiratory airflow. Furthermore, these patients remain at high risk for adverse clinical events, including near-fatal asthma. In chronic obstructive pulmonary disease, reduction in maximum expiratory airflow is related to variable extent of loss of lung elastic recoil secondary to emphysema and concurrent intrinsic airway obstruction or obliteration of small airways. There is also an unexplained loss of lung elastic recoil in primary intrinsic small airways disease in the absence of emphysema. Nonsmoking patients with moderate-severe persistent asthma and patients with smoking-related chronic obstructive pulmonary disease share similar physiologic mechanisms of expiratory airflow limitation, but probably caused by different anatomic abnormalities.

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