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5.2 HUMAN RESPIRATORY TRACT PHYSIOLOGY 207
the lungs and causing the lungs to expand. Air enters the respiratory tract
from the surrounding atmosphere when the inspiratory pressure exceeds air-
way resistance. Expiration occurs when the diaphragm and intercostal mus-
cles relax, causing elastic recoil from the pleura, which reduces the forces
expanding the lungs. When lung viscoelastic forces overcome pleural pres-
sure, the lungs constrict and air is expelled.
Movement of the chest wall in relationship to lung volume can be rep-
resented on a pressure-volume diagram (Fig. 5.19). The pressure term re-
fers to pleural pressure, a measure of pressure within the space between the
pleural membranes surrounding the lungs. The volume term represents
changes in percent vital capacity (%VC), changes in lung volume, or other
convenient measures of lung volume. Hysteresis, i.e., the failure of the
chest wall and lungs to follow identical pressure-volume paths during in-
spiratory and expiratory loads, is caused by viscoelastic and plastic prop-
erties of the lung and chest wall. Specifically, mechanical differences
between lung surfactant properties and alveolar recruitment, on the one
hand, and chest wall skeletal muscle and elastic fiber properties, on the
other, are believed to account for most of the observed hysteresis. It is
worth noting that posture also affects pressure-volume relationships by
shifting gravitational forces within the abdomen.
Gases entering the airways first fill the volume of the anatomical dead
space (conducting airways) before filling the pulmonary airway. Alveolar
ventilation (V^) defines the volumetric rate of gas passing through
pulmonary airways that participate in O 2 and CO 2 exchange, with O 2 up-
take (VoJ and CO 2 production (VcoJ determined by metabolic demands.
FIGURE 5.19 Relationship of transpleural pressure to volume in normal and asthmatic individuals.