Page 86 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Obstructive Lung Disease
In order to reach the alveoli air must pass retract (flaccid lung, → p. 78) can also lead to
through the respiratory tract or airways obstructive lung disease, because reduced
(→ p. 68), which present a resistance to the elastic recoil (increased compliance) of the
flow. This resistance is determined by the lu- lung requires an increase in pressure during
men in the tract. In particular the narrow lu- expiration, resulting in compression of the in-
men of the bronchioles can be further nar- trathoracic airways (see below).
rowed by mucus and the contraction of the Extrathoracic increase in resistance occurs,
bronchial musculature. Mucus is secreted in for example, in paralysis of the vocal chords,
Acid–Base Balance transported toward the mouth by the cilia of compression (e.g., by tumor or goitre; →
order to trap pathogens and dirt particles. It is
edema of the glottis, and external tracheal
the lining epithelium and then swallowed. As
p. 282ff.). In tracheomalacia the tracheal wall
is softened and collapses on inspiration.
the cilia cannot propel very sticky mucus, an
The effect of obstructive lung disease is re-
electrolyte solution is usually secreted that
lifts the mucus from the cilia, so that mucus
duced ventilation. If extrathoracic obstruction
moves toward the mouth on a thin fluid layer.
occurs, it is mainly inspiration that is affected
Respiration, The lumen can be narrowed by the action of (inspiratory stridor), because during expira-
tion the pressure rise in the prestenotic lumen
the bronchial muscles, which increases the
widens the narrowed portion. Intrathoracic ob-
likelihood of pathogens being caught in the
mucus. The disadvantage, however, is that nar-
struction mainly impairs expiration, because
spiration widens the airways. The ratio of the
diseases are characterized by an increased flow
4 rowing raises flow resistance. Obstructive lung the falling intrathoracic pressure during in-
resistance. duration of expiration to that of inspiration is
Intrathoracic increase in resistance is usual- increased. Obstructed expiration distends the
ly due to a narrowing or obstruction of the alveolar ductules (centrilobular emphysema;
bronchi, by either external compression, con- → p. 78), lung recoil decreases (compliance in-
traction of bronchial muscles, thickening of creases), and the midposition of breathing is
the lining mucus layer, or obstruction of the lu- shifted toward inspiration (barrel chest; →
men by mucus. Most of these changes are the p. 78). This raises the functional residual ca-
result of asthma or chronic bronchitis. In asth- pacity. Greater intrathoracic pressure is neces-
ma there is an allergy to inhaled antigens sary for expiration because compliance and
(e.g., pollen). These antigens cause an inflam- resistance are increased. This causes compres-
mation of the bronchial mucosa leading to the sion of the bronchioles so that the airway pres-
release of histamine and leukotrienes (called sure increases further. While the effort re-
slow reacting substances in anaphylaxis quired to overcome the elastic lung resistance
[SRSA]). The bronchial muscles contract and is normal or actually decreased, the effort re-
mucus secretion as well as vessel permeability quired to overcome the viscous lung resistance
(mucosal edema) are increased (→ A, top) un- and thus the total effort of breathing is greatly
der the influence of these mediators. In addi- increased (→ A, middle). The obstruction re-
tion to the inhaled antigens, microorganisms duces maximum breathing capacity (V ˙ max )
in the mucosa may also act as antigens (infec- and FEV 1 (→ table 2 on p. 66), and the differing
tious–allergic asthma). Here there is no clear- ventilation of various alveoli results in abnor-
cut distinction between asthma and bronchi- mal distribution (→ p. 72). The hypoxia of un-
tis. Obstructive lung disease can also be the re- derventilated alveoli leads to vasoconstriction,
sult of cystic fibrosis (CF). As the result of an au- increased pulmonary vascular resistance, pul-
tosomal recessive genetic defect of the CF monary hypertension, and an increased right
transmembrane regulator (CFTR; → p.162) ventricular load (cor pulmonale; → p. 214).
there is decreased secretion and hyperreab-
sorption of fluid, and mucus can no longer be
76 cleared from the airways. The result is obstruc-
tive lung disease. The lung’s reduced ability to
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
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