C h a p t e r 2 1
Control of Respiratory Function
525
another, and change their velocities. Whether turbulence
develops depends on the radius of the airways, the inter-
action of the gas molecules, and the velocity of airflow.
It is most likely to occur when the radius of the airways
is large and the velocity of flow is high. Turbulent flow
occurs regularly in the trachea. Turbulence of airflow
accounts for the respiratory sounds that are heard dur-
ing chest auscultation (i.e., listening to chest sounds
using a stethoscope).
Airway Compression During Forced Expiration.
Airway resistance does not change considerably during
normal quiet breathing, but is significantly increased
during forced expiration, such as occurs during vigor-
ous exercise. The marked changes that occur during
forced expiration are the result of airway compres-
sion. Airflow through the collapsible airways in the
lungs depends on the distending airway (intrapulmo-
nary) pressures that hold the airways open and the
external (intrathoracic) pressures that surround and
compress the airways. The difference between these
two pressures (airway minus intrathoracic pressure)
is called the
transpulmonary pressure.
For airflow to
occur, the distending pressure inside the airways must
be greater than the compressing pressure outside the
airways.
During forced expiration, the transpulmonary pres-
sure is decreased because of a disproportionate increase
in the intrathoracic pressure compared with airway
pressure. The resistance that air encounters as it moves
out of the lungs causes a further drop in airway pres-
sure. If this drop in airway pressure is sufficiently great,
the surrounding intrathoracic pressure will compress
the collapsible airways that lack cartilaginous support,
causing airflow to be interrupted and air to be trapped
in the terminal airways (Fig. 21-14).
Although this type of airway compression usually is
seen only during forced expiration in persons with nor-
mal respiratory function, it may occur during normal
breathing in persons with lung diseases. For example,
in conditions that increase airway resistance, such as
asthma or chronic obstructive lung disease, the pres-
sure drop along the smaller airways is magnified, and an
increase in intra-airway pressure is needed to maintain
airway patency. Measures such as pursed-lip breathing
increase airway pressure and improve expiratory flow
rates in persons with obstructive lung diseases (discussed
in Chapter 23). This is also the rationale for using posi-
tive end-expiratory pressure in persons who are being
mechanically ventilated. Infants who are having trouble
breathing often grunt to increase their expiratory air-
way pressures and keep their airways open.
Lung Volumes and Pulmonary
Function Studies
Lung volumes, or the amount of air exchanged during
ventilation, can be subdivided into three components:
(1) the tidal volume, (2) the inspiratory reserve volume,
and (3) the expiratory reserve volume. The tidal volume
(TV), usually about 500 mL, is the amount of air that
moves into and out of the lungs during a normal breath
(Fig. 21-15). The inspiratory reserve volume (IRV) is the
maximum amount of air that can be inspired in excess
of the normal TV, and the expiratory reserve volume
(ERV) is the maximum amount that can be exhaled in
excess of the normal TV. Approximately 1200 mL of
air remains in the lungs after forced expiration; this air
is the
residual volume
(RV). The RV increases with age
because there is more trapping of air in the lungs at the
end of expiration.
Nonrigid
airways
Oral airway pressure
Area of airway collapse
Forced
expiration
Intrapleural
pressure
Airway pressure
Airway
resistance
A
B
FIGURE 21-14.
Mechanism that
limits maximal expiratory flow rate.
(A)
Airway patency and airflow in the
nonrigid airways of the lungs rely on
a transpulmonary pressure gradient
in which airway pressure is greater
than intrapleural pressure.
(B)
Airway
resistance normally produces a drop
in airway pressure as air moves out of
the lungs.The increased intrapleural
pressure that occurs with forced
expiration produces airway collapse in
the nonrigid airways at the point where
intrapleural pressure exceeds airway
pressure.
