COPD affects approximately 5 % of the population according to the Centers for Disease Control and Prevention [2] with a mortality of over 120,000 individuals per year [3]. Chronic bronchitis is defined as a chronic productive cough for 3 months over two successive years and emphysema occurs as a result of destruction to alveolar walls causing permanent airspace dilation distal to the terminal bronchioles. The inflammation leading to these two processes is characterized by the infiltration of neutrophils, macrophages, and CD 8+ T lymphocytes [4]. Cigarette use is the most common cause of this inflammation, although inhalational exposures and α-1 antitrypsin deficiency can contribute as well. The diagnosis of COPD is suggested by symptoms of dyspnea with or without exertion, by chronic cough and sputum production, and by spirometric evidence of irreversible airflow limitation during forced expiration, i.e., an FEV₁/FVC <70 % and FEV₁ <80 % of the predicted value not reversible with bronchodilators.

According to the National Institutes of Health National Asthma Education and Prevention Program, asthma affects approximately 22 million people of all ages in the United States [5]. The inflammation associated with asthma is distinct from that of COPD and involves eosinophils, mast cells, and CD4+ T lymphocytes [4]. This inflammation leads to the destruction of epithelium, the remodeling and thickening of airway walls, airway edema, mucous plugging, and bronchial hyperresponsiveness, all of which can lead to airflow obstruction characterized by wheezing, cough, dyspnea, and chest tightness. The diagnosis of asthma is suggested by episodic symptoms, by triggers such as exercise, cold air, and allergens, and by the presence of a family history of atopy. In contrast to COPD, patients with asthma demonstrate reversibility of their airflow obstruction. Spirometric data suggestive of asthma includes an FEV₁/FVC <70 % and an FEV₁ <80 % of the predicted value with a post-bronchodilator response demonstrating an increase in FEV₁ >12 % from baseline with at least a 200 mL increase in FEV₁ [6].

The pharmacologic management of COPD and asthma is very similar with some exceptions. An asthma attack may be acutely managed with short-acting bronchodilators (β2 agonists and anticholinergics) and systemic glucocorticoids. COPD exacerbations, in addition to bronchodilators and systemic glucocorticoids, may also be treated with antibiotics, as approximately 50 % of exacerbations are precipitated by bacterial infections [7]. Depending on the severity, chronic asthma can be controlled with a combination of multiple agents including short- or long-acting β agonists, inhaled corticosteroids, mast cell stabilizers, methylxanthines, leukotriene modifiers (receptor antagonists or lipoxygenase inhibitors), systemic corticosteroids, or immunomodulators. Table 18.1 delineates the recommended therapies according to severity of asthma [5, 8]. Epinephrine, as an intravenous bronchodilator, may be of benefit in severe attacks of asthma where massive bronchoconstriction and restrictive airflow limit the delivery of inhaled bronchodilators to the lungs [9, 10].

COPD may be managed with short- or long-acting β2 agonists, long-acting anticholinergics, and inhaled glucocorticoids (sometimes combined as triple-inhaler therapy), methylxanthines, and PDE-4 inhibitors [11].