Pleural pressure Ppi (kPa)

Expiration requires increased pressure

Bronchial compression

Labored expiration

Overdistension of lungs

Pulmonary hypertension \


Right heart failure o

Pulmonary Emphysema

Emphysema is characterized by an increase in the volume of the airways distal to the bronchioles. Centrilobular emphysema, with predominant distension of the alveolar ducts and respiratory bronchioles, is distinguished from panlobular emphysema, in which the terminal alveoli in particular are distended A). In ^ flaccid lung there is merely a loss of elastic ree coil. The disease can affect a circumscribed ala area (local emphysema), or the entire lung 00 (generalized emphysema). Emphysema is one in of the most frequent causes of death. 03 Centrilobular emphysema is caused mainly

3 by obstructive lung disease: in flaccid lung < there is a loss of connective tissue of unknown c cause; in panlobular emphysema there is additional loss of alveolar septa. In the elderly an ira increase in alveolar volume in relation to al-& veolar surface regularly occurs. In some pa-ai tients (ca. 2%) there is a deficiency in o^-pro-f teinase inhibitor (o^-antitrypsin), which normally inhibits the action of proteinases (e.g., leukocyte elastase). This enzyme is produced in the liver; its mutation can affect its secretion and/or function. In either case decreased inhibition of the proteinases leads to a breakdown and thus a loss of lung tissue elasticity. If secretion is disturbed, the accumulation of the defective protein in the liver cells can additionally lead to liver damage. Finally, a lack of proteinase inhibition can also affect other tissues, for example, renal glomeruli and the pancreas may be damaged. o^-antitrypsin is oxidized and thus inhibited by smoking, which thus promotes the development of emphysema even in someone without a genetic predisposition.

In addition to a lack of inhibitors, increased elastase production may be a cause of emphysema (e.g., of a serine elastase from granulocytes, a metalloelastase from alveolar macrophages, and various proteinases from pathogens). The excess of elastases in chronic inflammatory disease leads, for example, to a breakdown of elastic fibers in the lung.

When considering the effects of pulmonary emphysema, the consequences of reduced elastic recoil are important. In the end the lung's 78 elastic recoil generates the positive pressure in the alveoli in comparison to ambient air necessary for normal expiration. Although positive pressure in the alveoli can also be produced by external compression, i.e., by contraction of the expiratory muscles, this will also compress the bronchioles and thus bring about a massive increase in flow resistance. Maximal expiratory flow rate (Vmax) is thus a function of the ratio between elastic recoil (K) and resistance (Rl) (^ A, right). Reduced elastic recoil can thus have the same effect as obstructive lung disease (^ p. 76). Elastic recoil can be raised by increasing the inspiratory volume (^A, right), eventually leading to a shift in the resting position toward inspiration (barrel chest; ^ B). If tidal volume remains constant, both the functional residual capacity and the residual volume are increased, sometimes also the dead space. However, vital capacity is diminished because of the reduced expiratory volume. The loss of alveolar walls leads to a diminished diffusion area (^ p. 70); the loss of pulmonary capillaries to an increase in functional dead space as well as increased pulmonary artery pressure and vascular resistance with the development of cor pulmonale (^ p. 214). In centrilobular, but not panlobular, emphysema a distribution abnormality develops, too (^p. 72), because of differing resistances in different bronchioles. The abnormal distribution results in hypoxemia. Patients with centrilobular emphysema due to obstructive lung disease are called "blue bloaters" (^ A). In contrast, patients with panlobular emphysema at rest are called "pink puffers", because enlargement of the functional dead space forces them to breathe more deeply. It is only when diffusion capacity is greatly reduced or oxygen consumption is increased (e.g., during physical work) that diffusion abnormality will result in hypoxemia (^ p. 70).

Chronic obstructive lung disease

arproteinase inhibitor Elastase excess

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