EMPHYSEMA



Emphysema is characterized by two features. Anatomically, it is defined as an abnormal en­largement of the airspaces distal to the terminal bronchioles, accompanied by destructive changes in the alveolar walls. Physiologically, it is char­acterized by a loss of elastic recoil and thus an increased lung compliance. The correlation be­tween the anatomic and physiological criteria is good but not invariable.

The pathogenesis of emphysema has yet to be determined with certainty, although most workers favor an imbalance of proteases and antiproteases in the lung, with resultant lung destruction. This theory is based on the discovery of a small number of patients with an inherited deficiency of alphai-antitrypsin, the major antiprotease, who develop emphysema at a young age even without other risk factors. Cigarette smoke, the major etiologic factor in the development of emphysema, has been shown to increase the numbers of alveolar mac­rophages and neutrophils in the lung, enhance protease release, and impair the activity of anti­proteases. However, other factors must determine susceptibility to emphysema, as less than 10 to 15 per cent of smokers develop clinical evidence of airway obstruction. Patients with emphysema usually present with dyspnea, exercise intoler­ance, and in its purest form minimal cough and sputum production. On physical examination they have hyperinflation, decreased breath sounds, and prominent use of accessory muscles. They are usually thin, even cachectic looking, and rarely have evidence of congestive heart failure. Despite severe obstructive lung disease, they usu­ally preserve their arterial oxygen saturation and are generally normocapnic.
In the absence of pathological material, the di­agnosis of emphysema is inferred from the clinical and laboratory findings. Chest roentgenograms demonstrate hyperinflation with depressed diaphragms, increased anteroposterior diameter, and widened retrosternal airspace. These findings, however, are seen whenever hyperinflation is present, and more specific features in emphysema include attenuation of the pulmonary vasculature and the presence of bullous lines. The routine pul­monary function studies are also nonspecific, showing a decrease in the VC and increased RV, FRC, and TLC, along with decreased forced ex­pired volume in 1 sec [FEVt) and flow rates. While flow rates may increase with bronchodilator ad­ministration, the improvement is less than that observed in asthma. The one finding that corre­lates well with the anatomical presence of em­physema is a reduction in diffusing capacity be­cause of the loss of alveolar capillary surface area.