Page 84 - Color Atlas Of Pathophysiology (S Silbernagl Et Al, Thieme 2000)

Restrictive Lung Disease
Restrictive lung disease is a term given to an prevented. The mediastinum is massively dis-
anatomical or functional loss of gaseous ex- placed by the increasing pressure toward the
change area. healthy side and breathing correspondingly
An anatomical loss occurs after removal (re- impaired. The increase in intrathoracic pres-
section) or displacement (e.g., by a tumor) of sure also reduces the venous return and thus
lung tissue. Atelectasis (→ p. 72) may also lead right ventricular filling, as a consequence of
to a decrease in diffusion area. which cardiac output falls.
A functional decrease in exchange area oc- the pleura is indistinguishable from that in
In whole-body plethysmography the air in
Acid–Base Balance example, in pulmonary edema (→ p. 80) or in the alveoli, because both are equally reduced
curs if plasma water is exuded into alveoli, for
on expiration. However, inspired test gas is
inflammation (increased vascular permeabil-
distributed only throughout the lung. In pneu-
ity, e.g., in pneumonia). In pulmonary fibrosis
mothorax, the intrathoracic volume measured
proliferating connective tissue displaces intact
by whole-body plethysmography is thus great-
pulmonary parenchyma (decrease in diffusion
area), infiltrates between capillaries and al-
er than the alveolar volume obtained with a
Respiration, veoli (increase in distance), and prevents the test gas.
Restrictive pulmonary disease causes a fall
normal expansion of the lung (impairment of
in compliance (C), vital capacity (VC), func-
alveolar air exchange). Pulmonary fibrosis can
tional residual capacity (FRC), and diffusion
be caused by inflammatory reaction against
abnormality (→ p. 70) and thus to hypoxemia
or by inhalation of dust which contains silicate
4 connective tissue (so-called collagen disease) capacity (→ p. 66). The latter leads to diffusion
or asbestos. Sometimes no cause is found (→ A; S O 2 = oxygen saturation of blood). Maxi-
(idiopathic pulmonary fibrosis [Hamman– mum breathing capacity (V ˙ max ) and forced ex-
Rich syndrome]). Local or generalized impair- piration volume in 1 second (FEV 1 ) are usually
ment of lung expansion can also occur in tho- reduced, but relative forced expiration volume
racic deformities, diaphragmatic paralysis, or (normally 80% of VC) is generally normal. To
adhesion of both pleural layers (as a result of in- inspire a certain volume, greater negative
flammation [pleural fibrosis]). pressure than normal is required in the pleural
Pneumothorax is also a restrictive lung dis- space (P p ˙ l ) and more energy thus has to be ex-
ease (→ B). If there is an open connection be- pended during breathing (increased work of
tween the pleural space and outside air (tho- breathing; → A; V ˙ = ventilation flow). Reduc-
racic injury; → B, top) or the alveoli (torn al- tion of the vascular bed by removing lung tis-
veolar wall due to overdistension), air enters sue or by compressing blood vessels increases
and the ipsilateral lung collapses. Breathing is vascular resistance. Greater pressure is re-
also impaired in the other lung, because the quired to pump the blood through the pul-
pleural pressure on the healthy side falls on in- monary vascular bed, pressure which must be
spiration and as a result the mediastinum is generated by the right heart. The consequence
displaced to the healthy side. On expiration is a raised load on the right ventricle (cor pul-
the pressure rises and the mediastinum moves monale; → p. 214).
toward the collapsed side. This mediastinal
flutter reduces the breathing excursion (VT) of
the healthy lung. If a valve-like mechanism de-
velops on the injured side, allowing air into the
pleural space but not out of it, tension pneumo-
thorax develops (→ B, bottom). It is especially
the burst alveoli that often act like valves: the
collapsed lung expands on inspiration, allow-
ing air to enter the pleural space through the
74 damaged alveolus, but when lung and alveolus
collapse during expiration the escape of air is
Silbernagl/Lang, Color Atlas of Pathophysiology © 2000 Thieme
All rights reserved. Usage subject to terms and conditions of license.