706
Appendix A
in oxygen saturation for the same change in
P
O
2
occurs at the steepest part of the curve—between a
P
O
2
of 40 and 60 mmHg.
13-6 b
Increases in blood temperature, decreases in blood
pH, and increases in DPG shifts the oxygen-
hemoglobin curve downward, leading to a lower
oxygen saturation at the same
P
O
2
.
13-7 b
There are forms of asthma that are not primarily due
to the presence of allergens. Examples are exercise-
or cold-air-induced asthma.
13-8 e
Respiratory acidosis (increase in blood
P
CO
2
and
decrease in pH) is a major stimulus to ventilation—
this is mediated both by afferents from the
peripheral chemoreceptors and by an increase in
central chemoreceptor activity.
13-9 c
Because of the shape of the oxygen-hemoglobin
dissociation curve, small increases in
P
O
2
due
to increases in ventilation cannot fully saturate
hemoglobin. When the desaturated blood mixes
with saturated blood, the average is still hypoxemic.
13-10 c
Remember that a lung capacity is the sum of at least
two volumes. Inspiratory capacity is the sum of tidal
volume and inspiratory reserve volume.
Quantitative and Thought Questions
13-1
200 ml/mmHg.
Lung compliance =
lung volume/
(
P
alv
P
ip
)
= 800 ml/[0 – (–8)] mmHg–
[0 – (–4)] mmHg
= 800 ml/4 mmHg = 200 ml/mmHg
13-2
More subatmospheric than normal. A decreased
surfactant level causes the lungs to be less compliant
(i.e., more diffi cult to expand). Therefore, a greater
transpulmonary pressure (
P
alv
P
ip
) is required to
expand them a given amount.
13-3
No.
Alveolar
ventilation = (tidal volume – dead space)
×
breathing rate
= (250 ml – 150 ml)
×
20 breaths/min
= 2 ml/min
whereas normal alveolar ventilation is approximately
4 ml/min.
13-4
The volume of the snorkel constitutes an additional
dead space, so total pulmonary ventilation must be
increased if alveolar ventilation is to remain constant.
13-5
The alveolar
P
O
2
will be higher than normal, and the
alveolar
P
CO
2
will be lower. If you do not understand
why, review the factors that determine the alveolar
gas pressures.
13-6
No. Hypoventilation reduces arterial
P
O
2
but
only because it reduces alveolar
P
O
2
. That is, in
hypoventilation,
both
alveolar and arterial
P
O
2
are
decreased to essentially the same degree. In this
problem, alveolar
P
O
2
is normal, and so the person
is not hypoventilating. The low arterial
P
O
2
must
therefore represent a defect that causes a discrepancy
between alveolar
P
O
2
and arterial
P
O
2
. Possibilities
include impaired diffusion, a shunting of blood from
the right side of the heart to the left through a hole in
the heart wall, and a mismatch between air fl ow and
blood fl ow in the alveoli.
13-7
Not at rest, if the defect is not too severe. Recall that
equilibration of alveolar air and pulmonary capillary
blood is normally so rapid that it occurs well before
the end of the capillaries. Therefore, even though
diffusion may be retarded, as in this problem, there
may still be enough time for equilibration to be
reached. In contrast, the time for equilibration is
decreased during exercise, and failure to equilibrate
is much more likely to occur, resulting in a lowered
arterial
P
O
2
.
13-8
Only a few percent (specifi cally, from approximately
200 ml O
2
/L blood to approximately 215 ml O
2
/L
blood). The reason the increase is so small is that
almost all the oxygen in blood is carried bound to
hemoglobin, and hemoglobin is almost 100 percent
saturated at the arterial
P
O
2
achieved by breathing
room air. The high arterial
P
O
2
achieved by breathing
100 percent oxygen does cause a directly proportional
increase in the amount of oxygen
dissolved
in the
blood (the additional 15 ml), but this still remains
a small fraction of the total oxygen in the blood.
Review the numbers given in the chapter.
13-9
All. The reasons are all given in the chapter.
13-10
It would cease. Respiration depends on descending
input from the medulla to the nerves supplying the
diaphragm and the inspiratory intercostal muscles.
13-11
(a) The combination of hypercapnia (elevated
P
CO
2
due to increased inspired CO
2
) and hypoxia (due to
decreased inspired O
2
) greatly augments ventilation
by stimulating central and peripheral chemoreceptors.
Although CO decreases O
2
content, chemoreceptors
are not stimulated and ventilation does not increase.
13-12
These patients have profound hyperventilation,
with marked increases in both the depth and rate of
ventilation. The stimulus, mainly via the peripheral
chemoreceptors, is the marked increase in their
arterial hydrogen ion concentration due to the acids
produced. The hyperventilation causes an increase in
their arterial
P
O
2
and a decrease in their arterial
P
CO
2
.
13-13
In pure anatomical shunt, blood passes through the
lung without exposure to any alveolar air. Therefore,
increases in alveolar
P
O
2
caused by increased inspired
O
2
will not affect the
P
O
2
of the shunt blood. By
contrast, there is still some blood fl owing through
a region of the lung with a ventilation-perfusion
mismatch. Therefore, an increase in
P
O
2
in the alveoli
can increase the
P
O
2
in this blood, which, when
mixing with blood leaving other areas of the lung, can
increase the blood in the pulmonary vein and hence
the arterial circulation.
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