Page 88 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Pulmonary Emphysema
Emphysema is characterized by an increase in necessary for normal expiration. Although
the volume of the airways distal to the bron- positive pressure in the alveoli can also be pro-
chioles. Centrilobular emphysema, with pre- duced by external compression, i.e., by con-
dominant distension of the alveolar ducts and traction of the expiratory muscles, this will
respiratory bronchioles, is distinguished from also compress the bronchioles and thus bring
panlobular emphysema, in which the terminal about a massive increase in flow resistance.
alveoli in particular are distended (→ A). In Maximal expiratory flow rate (V ˙ max ) is thus a
flaccid lung there is merely a loss of elastic re- function of the ratio between elastic recoil (K)
Acid–Base Balance area (local emphysema), or the entire lung tic recoil can thus have the same effect as ob-
coil. The disease can affect a circumscribed
and resistance (RL) (→ A, right). Reduced elas-
(generalized emphysema). Emphysema is one
structive lung disease (→ p. 76). Elastic recoil
can be raised by increasing the inspiratory
of the most frequent causes of death.
Centrilobular emphysema is caused mainly
volume (→ A, right), eventually leading to a
shift in the resting position toward inspiration
by obstructive lung disease: in flaccid lung
there is a loss of connective tissue of unknown
(barrel chest; → B). If tidal volume remains
Respiration, cause; in panlobular emphysema there is addi- constant, both the functional residual capacity
and the residual volume are increased, some-
tional loss of alveolar septa. In the elderly an
times also the dead space. However, vital ca-
increase in alveolar volume in relation to al-
pacity is diminished because of the reduced
veolar surface regularly occurs. In some pa-
teinase inhibitor (α 1 -antitrypsin), which nor-
leads to a diminished diffusion area (→ p. 70);
4 tients (ca. 2%) there is a deficiency in α 1 -pro- expiratory volume. The loss of alveolar walls
mally inhibits the action of proteinases (e.g., the loss of pulmonary capillaries to an increase
leukocyte elastase). This enzyme is produced in functional dead space as well as increased
in the liver; its mutation can affect its secre- pulmonary artery pressure and vascular resis-
tion and/or function. In either case decreased tance with the development of cor pulmonale
inhibition of the proteinases leads to a break- (→ p. 214). In centrilobular, but not panlobular,
down and thus a loss of lung tissue elasticity. emphysema a distribution abnormality devel-
If secretion is disturbed, the accumulation of ops, too (→ p. 72), because of differing resis-
the defective protein in the liver cells can addi- tances in different bronchioles. The abnormal
tionally lead to liver damage. Finally, a lack of distribution results in hypoxemia. Patients
proteinase inhibition can also affect other tis- with centrilobular emphysema due to obstruc-
sues, for example, renal glomeruli and the tive lung disease are called “blue bloaters”
pancreas may be damaged. α 1 -antitrypsin is (→ A). In contrast, patients with panlobular
oxidized and thus inhibited by smoking, which emphysema at rest are called “pink puffers”,
thus promotes the development of emphyse- because enlargement of the functional dead
ma even in someone without a genetic predis- space forces them to breathe more deeply. It
position. is only when diffusion capacity is greatly re-
In addition to a lack of inhibitors, increased duced or oxygen consumption is increased
elastase production may be a cause of emphy- (e.g., during physical work) that diffusion ab-
sema (e.g., of a serine elastase from granulo- normality will result in hypoxemia (→ p. 70).
cytes, a metalloelastase from alveolar macro-
phages, and various proteinases from patho-
gens). The excess of elastases in chronic in-
flammatory disease leads, for example, to a
breakdown of elastic fibers in the lung.
When considering the effects of pulmonary
emphysema, the consequences of reduced elas-
tic recoil are important. In the end the lung’s
78 elastic recoil generates the positive pressure
in the alveoli in comparison to ambient air
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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