Chronic obstructive pulmonary disease (COPD) is a disorder characterized by reduced maximum expiratory flow and slow forced emptying of the lungs; features which do not change markedly over several months [1]. Most of the airflow limitation is slowly progressive and irreversible. The airflow limitation is due to varying combinations of airway disease and emphysema; the relative contribution of the two processes is difficult to define in vivo. The airway component consists mainly of decreased luminal diameters due to various combinations of increased wall thickening, increased intraluminal mucus, and changes in the lining fluid of the small airways.

Emphysema is defined anatomically by permanent, destructive enlargement of airspaces distal to the terminal bronchioles without obvious fibrosis [2]. Loss of alveolar attachments to the airway perimeter contributes to airway stenosis. Pathological changes occurring in COPD are discussed more extensively in Appendix A. Chronic bronchitis is defined by the presence of chronic or recurrent increases in bronchial secretions sufficient to cause expectoration. The secretions are present on most days for a minimum of 3 months a year, for at least two successive years, and cannot be attributed to other pulmonary or cardiac causes [3, 4]. This hypersecretion can occur in the absence of airflow limitation. Patients with COPD often exhibit minimal reversibility of airflow limitation with bronchodilators. Airway hyperresponsiveness to a variety of constrictor stimuli is common. These patients often have recurrent or persistent productive cough.