ABSTRACT
Acute exacerbations are the most frequent cause of medical visits, hospitalization, and death among patients with chronic obstructive pulmonary disease (COPD) (1). Although it is generally regarded that worsening airway inflammation is the primary inciting event of an exacerbation, the recent evidence suggesting that long-acting bronchodilators and mucolytics reduce the frequency and severity of exacerbations (2,3) indicates that factors other than airway inflammation may be important as well. Our knowledge of the pathophysiologic changes that occur at the time of exacerbation continues to grow. Although detailed studies of patients who have been hospitalized with acute respiratory failure requiring mechanical ventilation have provided clearer insights into the mechanisms that underlie severe exacerbations, considerably less is known about the physiologic derangements that accompany the mild-to-moderate exacerbations, which are more commonly encountered in clinical practice. It is reasonable to assume, however, that exacerbations share common pathophysiologic mechanisms and that these changes may occur along a spectrum of severity that is determined by both host factors (including severity of underlying disease) and environmental influences (such as severity of the inciting illness or insult). This review will summarize our current understanding of the effects of exacerbation on pulmonary function, mechanics [including the central concept of worsening expiratory flow limitation (EFL) and dynamic hyperinflation (DH)], gas exchange, and cardiopulmonary interactions in patients with COPD.
