The term pulmonary emphysema literally means excess air in the lungs. However, this term is usually used to describe a complex obstructive and destructive process of the lungs caused by many years of smoking. It results from the following major pathophysiological changes in the lungs:
1. Chronic infection, caused by inhaling smoke or other substances that irritate the bronchi and bronchioles. The chronic infection seriously deranges the normal protective mechanisms of the airways, including partial paralysis of the cilia of the respiratory epithelium, an effect caused by nicotine. As a result, mucus cannot be moved easily out of the passageways. Also, stimulation of excess mucus secretion occurs, which further exacerbates the condition. Inhibition of the alveolar macrophages also occurs, so they become less effective in com bating infection.
2. The infection, excess mucus, and inflammatory edema of the bronchiolar epithelium together cause chronic obstruction of many of the smaller airways.
3. The obstruction of the airways makes it especially difficult to expire, thus causing entrapment of air in the alveoli and overstretching them. This effect, combined with the lung infection, causes marked destruction of as much as 50 to 80 percent of the alveolar walls. Therefore, the final picture of the emphysematous lung is that shown in Figures 1 (top) and 2.
Fig1. Contrast of the emphysematous lung (top) with the normal lung (bottom), showing extensive alveolar destruction in emphysema. (Courtesy Patricia Delaney and the Department of Anatomy, The Medical College of Wisconsin.)
Fig2. Lung alveolar changes in pneumonia and emphysema.
The physiological effects of chronic emphysema are variable, depending on the severity of the disease and the relative degrees of bronchiolar obstruction versus lung parenchymal destruction. Among the different abnormalities are the following:
1. The bronchiolar obstruction increases airway resistance and results in greatly increased work of breathing. It is especially difficult for the person to move air through the bronchioles during expiration because the compressive force on the outside of the lung not only compresses the alveoli but also com presses the bronchioles, which further increases their resistance during expiration.
2. The marked loss of alveolar walls greatly decreases the diffusing capacity of the lung, which reduces the ability of the lungs to oxygenate the blood and remove CO2 from the blood.
3. The obstructive process is frequently much worse in some parts of the lungs than in other parts, so some portions of the lungs are well ventilated, whereas other portions are poorly ventilated. This situation often causes extremely abnormal ventilation-perfusion ratios, with a very low V̇A / Q̇ in some parts (physiological shunt), resulting in poor aeration of the blood, and very high V̇A / Q̇ in other parts (physiological dead space), resulting in wasted ventilation, with both effects occurring in the same lungs.
4. Loss of large portions of the alveolar walls also decreases the number of pulmonary capillaries through which blood can pass. As a result, the pulmonary vascular resistance often increases markedly, causing pulmonary hypertension, which in turn overloads the right side of the heart and frequently causes right-sided heart failure.
Chronic emphysema usually progresses slowly over many years. Both hypoxia and hypercapnia develop because of hypoventilation of many alveoli plus loss of alveolar walls. The net result of all these effects is severe, prolonged, devastating air hunger that can last for years until the hypoxia and hypercapnia cause death—a high penalty to pay for smoking.
