Ganong's Review of Medical Physiology, 23rd Edition

602 SECTION VII Respiratory Physiology
this latter term is close to zero, so it can be ignored and the
equation becomes:
DLCO = V• CO
PACO
The normal value of DLCO at rest is about 25 mL/min/mm
Hg. It increases up to threefold during exercise because of
capillary dilation and an increase in the number of active capillaries.
The PO 2 of alveolar air is normally 100 mm Hg (Figure 35–18),
and the PO 2 of the blood entering the pulmonary capillaries is
40 mm Hg. The diffusing capacity for O 2 , like that for CO at
rest, is about 25 mL/min/mm Hg, and the PO 2 of blood is raised
to 97 mm Hg, a value just under the alveolar PO 2. This falls to
95 mm Hg in the aorta because of the physiologic shunt. DLO 2
increases to 65 mL/min/mm Hg or more during exercise and is
reduced in diseases such as sarcoidosis and beryllium poisoning
(berylliosis) that cause fibrosis of the alveolar walls.
The PCO 2 of venous blood is 46 mm Hg, whereas that of
alveolar air is 40 mm Hg, and CO 2 diffuses from the blood
into the alveoli along this gradient. The PCO 2 of blood leaving
the lungs is 40 mm Hg. CO 2 passes through all biological
membranes with ease, and the diffusing capacity of the lung
for CO 2 is much greater than the capacity for O 2 . It is for this
reason that CO 2 retention is rarely a problem in patients with
alveolar fibrosis even when the reduction in diffusing capacity
for O 2 is severe.
PULMONARY CIRCULATION
PULMONARY BLOOD VESSELS
The pulmonary vascular bed resembles the systemic one, except
that the walls of the pulmonary artery and its large branches
are about 30% as thick as the wall of the aorta, and the small
arterial vessels, unlike the systemic arterioles, are endothelial
tubes with relatively little muscle in their walls. The walls of the
postcapillary vessels also contain some smooth muscle. The
pulmonary capillaries are large, and there are multiple anastomoses,
so that each alveolus sits in a capillary basket.
PRESSURE, VOLUME, & FLOW
With two quantitatively minor exceptions, the blood put out
by the left ventricle returns to the right atrium and is ejected
by the right ventricle, making the pulmonary vasculature
unique in that it accommodates a blood flow that is almost
equal to that of all the other organs in the body. One of the exceptions
is part of the bronchial blood flow. As shown in Figure
35–5, there are anastomoses between the bronchial
capillaries and the pulmonary capillaries and veins, and although
some of the bronchial blood enters the bronchial
veins, some enters the pulmonary capillaries and veins, bypassing
the right ventricle. The other exception is blood that
flows from the coronary arteries into the chambers of the left
side of the heart. Because of the small physiologic shunt created
by those two exceptions, the blood in systemic arteries
has a PO 2 about 2 mm Hg lower than that of blood that has
equilibrated with alveolar air, and the saturation of hemoglobin
is 0.5% less.
The pressure in the various parts of the pulmonary portion
of the pulmonary circulation is shown in Figure 35–4. The
pressure gradient in the pulmonary system is about 7 mm Hg,
compared with a gradient of about 90 mm Hg in the systemic
circulation. Pulmonary capillary pressure is about 10 mm Hg,
whereas the oncotic pressure is 25 mm Hg, so that an inwarddirected
pressure gradient of about 15 mm Hg keeps the alveoli
free of all but a thin film of fluid. When the pulmonary
capillary pressure is more than 25 mm Hg—as it may be, for
example, in “backward failure” of the left ventricle—pulmonary
congestion and edema result.
The volume of blood in the pulmonary vessels at any one
time is about 1 L, of which less than 100 mL is in the capillaries.
The mean velocity of the blood in the root of the pulmonary
artery is the same as that in the aorta (about 40 cm/s). It
falls off rapidly, then rises slightly again in the larger pulmonary
veins. It takes a red cell about 0.75 s to traverse the pulmonary
capillaries at rest and 0.3 s or less during exercise.
EFFECT OF GRAVITY
Gravity has a relatively marked effect on the pulmonary circulation.
In the upright position, the upper portions of the lungs
are well above the level of the heart, and the bases are at or below
it. Consequently, in the upper part of the lungs, the blood
flow is less, the alveoli are larger, and ventilation is less than at
the base (Figure 35–20). The pressure in the capillaries at the
top of the lungs is close to the atmospheric pressure in the alveoli.
Pulmonary arterial pressure is normally just sufficient to
maintain perfusion, but if it is reduced or if alveolar pressure
is increased, some of the capillaries collapse. Under these circumstances,
no gas exchange takes place in the affected alveoli
and they become part of the physiologic dead space.
In the middle portions of the lungs, the pulmonary arterial
and capillary pressure exceeds alveolar pressure, but the pressure
in the pulmonary venules may be lower than alveolar
pressure during normal expiration, so they are collapsed.
Under these circumstances, blood flow is determined by the
pulmonary artery–alveolar pressure difference rather than the
pulmonary artery–pulmonary vein difference. Beyond the
constriction, blood “falls” into the pulmonary veins, which are
compliant and take whatever amount of blood the constriction
lets flow into them. This has been called the waterfall effect.
Obviously, the compression of vessels produced by alveolar
pressure decreases and pulmonary blood flow increases as the
arterial pressure increases toward the base of the lung.
In the lower portions of the lungs, alveolar pressure is lower
than the pressure in all parts of the pulmonary circulation and
blood flow is determined by the arterial–venous pressure