Internationally, the Global Obstructive Lung Disease (GOLD) study recommends that COPD classification be based on post-bronchodilator spirometry.4 This global consensus advocates spirometry testing for all smokers over the age of 45 in the primary care setting. Experts uniformly agree that early detection and treatment can significantly impact the human toll of these diseases.

COPD, such as bronchitis and emphysema, is defined as a disease state characterized by the presence of airflow limitation that is generally progressive and may be partially reversible.The airflow limitation is caused by a combination of abnormal inflammatory response, mucous hypersecretion, cilliary dysfunction, structural bronchospasm remodeling, and hyperinflation. The causative factor is, in most cases, cigarette smoking.The pathology of emphysema, one form of COPD, includes dynamic airflow limitation and over-inflation, and is frequently associated with chronic processes such as bronchitis. Although COPD has irreversible components, quality of life can be significantly improved by targeting the underlying processes that can relieve the hyperinflation or inflammation. Asthma is defined as a disease syndrome that can be chronic and progressive or be very acute and transient. Asthma is also characterized by bronchospasm, an abnormal inflammatory response, and hyperinflation that may be partially or completely reversible but, unlike COPD, asthma has highly variable presentation of symptoms and dysfunction.

Bronchospasm, abnormal inflammatory response, and mucous hypersecretion increase airway resistance by reducing the airway cross-sectional area. Since airway size is mechanically linked to lung volume, significant airway obstruction can cause a compensatory hyperinflation in an attempt to maintain acceptable levels of airway resistance by distending the airways.

Indeed, this mechanical -coupling- of lung volume and airway caliber is the most important mechanism controlling airway size. During normal breathing, increased driving pressure can sustain airflow within normal limits as long as dynamic airway collapse during expiration does not occur.

As an example, a patient with emphysema due to alpha- 1 antitrypsin deficiency compensatory hyperinflation maintains a relatively normal airway resistance during quiet breathing.However,airflow is significantly limited during forced expiratory efforts by airway collapse and forced inspiratory efforts especially during states of high airflow, e.g. exercise. Regardless of the mechanism, the increase in airway resistance ultimately progresses to a degree that cannot be compensated for or overcome.

Evaluating Airflow Limitation and Reversibility Using Spirometry Charles G Irvin, PhD, is the Director of the Vermont Lung Center at the College of Medicine, University of Vermont. In 1998, he was recruited to the University of Vermont to re- establish the well known Vermont Lung Center. Dr Irvin has studied lung physiology and the mechanisms of asthma for 30 years and enjoys an outstanding international reputation. His research is translational in nature and he has published extensively on animal models as well as patient- oriented research into the mechanisms of asthma and other lung diseases.

Asthma Treatment As recommended by GOLD, classifications of disease diagnosis and severity can be made using pre- and post-bronchodilator tests to assure proper classification and identify appropriate treatments.4 Appropriate treatment depends on the underlying obstructive mechanisms. Beta agonists, anticholinergics, and methylxanthines primarily induce smooth muscle relaxation and improve lung emptying. Inhaled corticosteroids can be effective in treating inflammatory responses, which may also improve airflow and lung emptying. Evaluating the response to bronchodilator can improve classification and guide the course of treatment. The increased airway resistance and hyperinflation lead to dyspnea as a result of increased work of breathing; hence, treatment with bronchodilators and anti- inflammatory medications can directly affect airway caliber and reduce crippling dyspnea.

One of the challenges of early detection of airflow limitation is that many of the early symptoms can be dismissed as a natural result of aging, obesity, or poor fitness. Significant airway obstruction commonly causes a compensatory mechanism of over-inflation. By increasing lung volume,the airways are distended by the expansion of the thoracic cage, which in turn acts to lower airway resistance.While this compensation may reduce work of breathing at rest, it will significantly compromise the ventilatory reserve needed for exertion. The compensation may also obscure the evidence of airway reversibility.5 Reducing the work of breathing sufficiently to eliminate the compensatory over-inflation may leave the airway resistance at an elevated or unchanged level.