CHAPTER 35Pulmonary Function 603difference. Examples of diseases affecting pulmonary circula-
tion are given in Clinical Box 35–3.
VENTILATION/PERFUSION RATIOS
The ratio of pulmonary ventilation to pulmonary blood flow
for the whole lung at rest is about 0.8 (4.2 L/min ventilation di-
vided by 5.5 L/min blood flow). However, relatively marked
differences occur in this ventilation/perfusion ratio in vari-
ous parts of the normal lung as a result of the effect of gravity,
and local changes in the ventilation/perfusion ratio are com-
mon in disease. If the ventilation to an alveolus is reduced rel-
ative to its perfusion, the PO 2 in the alveolus falls because less
O 2 is delivered to it and the PCO 2 rises because less CO 2 is ex-
pired. Conversely, if perfusion is reduced relative to ventila-
tion, the PCO 2 falls because less CO 2 is delivered and the PO 2
rises because less O 2 enters the blood. These effects are sum-
marized in Figure 35–21.
As noted above, ventilation, as well as perfusion in the
upright position, declines in a linear fashion from the bases to
the apices of the lungs. However, the ventilation/perfusion
ratios are high in the upper portions of the lungs. When wide-
spread, nonuniformity of ventilation and perfusion in the
lungs can cause CO 2 retention and declines in systemic arte-
rial PO 2.
PULMONARY RESERVOIR
Because of their distensibility, the pulmonary veins are an im-
portant blood reservoir. When a normal individual lies down,
the pulmonary blood volume increases by up to 400 mL, and
when the person stands up this blood is discharged into the
general circulation. This shift is the cause of the decrease in vi-
tal capacity in the supine position and is responsible for the
occurrence of orthopnea in heart failure.REGULATION OF PULMONARY
BLOOD FLOWIt is unsettled whether pulmonary veins and pulmonary arter-
ies are regulated separately, although constriction of the veins
increases pulmonary capillary pressure and constriction of
pulmonary arteries increases the load on the right side of the
heart.
Pulmonary blood flow is affected by both active and passive
factors. There is an extensive autonomic innervation of the
pulmonary vessels, and stimulation of the cervical sympatheticFIGURE 35–20 Diagram of normal differences in ventilation
and perfusion of the lung in the upright position. Outlined areas
are representative of changes in alveolar size (not actual size). Note the
gradual change in alveolar size from top (apex) to bottom. Character-
istic differences of alveoli at the apex of the lung are stated. (Modified
from Levitsky, MG: Pulmonary Physiology, 6th ed. McGraw-Hill, 2003).
At apex
Intrapleural pressure
more negative
Greater transmural
pressure
Large alveoli
Lower intravascular
pressure
Less blood flow
So less ventilation
and perfusionCLINICAL BOX 35–3
Diseases Affecting the Pulmonary CirculationPulmonary Hypertension
Sustained primary pulmonary hypertension can occur at any
age. Like systemic arterial hypertension, it is a syndrome with
multiple causes. However, the causes are different from
those causing systemic hypertension. They include hypoxia,
inhalation of cocaine, treatment with dexfenfluramine and
related appetite-suppressing drugs that increase extracellu-
lar serotonin, and systemic lupus erythematosus. Some cases
are familial and appear to be related to mutations that in-
crease the sensitivity of pulmonary vessels to growth factors
or cause deformations in the pulmonary vascular system.
All these conditions lead to increased pulmonary vascu-
lar resistance. If appropriate therapy is not initiated, the in-
creased right ventricular afterload can lead eventually to
right heart failure and death. Treatment with vasodilators
such as prostacyclin and prostacyclin analogs is effective.
Until recently, these had to be administered by continuous
intravenous infusion, but aerosolized preparations that ap-
pear to be effective are now available.
Pulmonary Embolization
One of the normal functions of the lungs is to filter out
small blood clots, and this occurs without any symptoms.
When emboli block larger branches of the pulmonary ar-
tery, they provoke a rise in pulmonary arterial pressure and
rapid, shallow respiration (tachypnea). The rise in pulmo-
nary arterial pressure may be due to reflex vasoconstriction
via the sympathetic nerve fibers, but reflex vasoconstric-
tion appears to be absent when large branches of the pul-
monary artery are blocked. The tachypnea is a reflex re-
sponse to activation of vagally innervated pulmonary
receptors close to the vessel walls. These appear to be acti-
vated at the site of the embolization.