Adrenergic Beta Agonists and Anticholinergics in Obstructive Lung Diseases

ABSTRACT

Airflow obstruction in chronic obstructive pulmonary disease (COPD) is due to the combination of airway disease and emphysema, may be accompanied by airway reactivity, and may be partially reversible. Aerosol deposition is affected by airway geometry. Deposition patterns in COPD are increasingly abnormal as the forced expiratory volume in 1 second (FEV₁) percentage deteriorates. More advanced COPD is characterized by the formation of multiple impactions in the central airways and a marked reduction in peripheral deposition. Vagal innervation is most prominent in the central airways, although beta-adrenergic receptors are more widely distributed in small airways. Anticholinergics and beta agonists are effective bronchodilators in COPD. With large doses of either ipratropium or beta agonists, most studies have demonstrated equivalent bronchodilation in stable COPD. Small, conventional doses of the two agents are additive, and large doses are not. In COPD patients with acute exacerbation, nebulized anticholinergics or beta agonists improve pulmonary function similarly. Two different clinical circumstances, i.e., acute exacerbation and stable disease, can result in the same response to the bronchodilators. Recent data suggest that extended ipratropium therapy is associated with improvement in baseline lung function, whereas long-term therapy with beta agonists results in no significant change in lung function. The inhaled route for beta agonist and anticholinergic delivery results in the newest adverse effects. Many devices are available, including metered-dose inhalers and dry-powder inhalers. Nebulizers are easier to use to achieve a good response during acute exacerbations.