690
Chapter 19
arterial blood vessels, thereby depriving vital organs of oxygen
and nutrients and preventing the removal of toxic waste prod-
ucts. If this occurs in the cerebral arterial circulation, it can lead
to a stroke. If this occurs in the coronary arteries, it can lead to
a heart attack.
Physiological Integration
The presence of hypoxemia and hyperventilation (the cause of
the acute respiratory alkalosis), and the history and symptoms,
suggest that the patient is suffering from an acute decrease in
pulmonary blood fl ow to some parts of the lung. This results
in a clinically signifi cant ventilation/perfusion inequality (see
Table 13–11). The hyperventilation is only partly due to the
mild hypoxemia, because the arterial
P
O
2
of 60 mmHg in our
patient, although low, is just at the threshold oxygen level that
stimulates the peripheral chemoreceptors (see Figures 13–33
and 13–34). Other causes of hyperventilation may be anxiety
and pain, which may also explain the increased heart rate ob-
served in the patient at the emergency room.
The ventilation/perfusion inequality means that the pa-
tient is ventilating areas of the lung to which blood is not fl ow-
ing, leading to increased alveolar dead space (see Figure 13–19).
The extra blood fl ows to other nearby lung regions leading to a
local decrease in the ratio of ventilation to perfusion (physiologic
shunt). This results in some blood leaving the lung without ad-
equate oxygenation. Remember that disruption of the delicate
balance between regional ventilation and perfusion throughout
the lung results in a failure to fully oxygenate the blood leaving
the lung. In addition, hypoxia within the pulmonary circulation
leads to vasoconstriction of the arterioles in the lungs and an
increase in pulmonary artery pressure (see Figure 13–24).
We know that the respiratory alkalosis was acute and not
a long-standing problem because the arterial pH was still alka-
line from the hyperventilation. This indicates that the kidneys
did not have time to respond to the change in pH by increas-
ing bicarbonate excretion in the urine (see Table 14–7).
Why did the pulmonary embolism cause a decrease in
arterial
P
O
2
but did not increase and, in fact, decreased arte-
rial
P
CO
2
? Remember from Chapter 13 that the relationship
between partial pressure and content is sigmoid for oxygen but
relatively linear for CO
2
. Because of the plateau of O
2
content
as
P
O
2
increases above 60 mmHg (see Figure 13–26), increas-
ing alveolar O
2
in over-ventilated regions of the lung does not
signifi cantly increase O
2
content of the blood leaving that re-
gion. Therefore, although hyperventilation does increase O
2
in some alveoli, it does not compensate for the decrease in
O
2
content in some pulmonary capillaries due to ventilation-
perfusion inequalities. Increasing ventilation can decrease the
CO
2
content of blood due to the linearity of the relationship
between
P
CO
2
and CO
2
content of the blood. The overall net
effect is acute respiratory alkalosis due to decreased arterial
P
CO
2
. Interestingly, the hypoxemia can be partially overcome
if the patient breathes gas that is enriched in oxygen because,
although ventilation and perfusion are not well matched, there
is not complete shunting of blood in the lungs. Thus, increas-
ing alveolar
P
O
2
can still increase oxygenation of some areas
of the lung with ventilation-perfusion mismatching, at least
somewhat. The arterial
P
CO
2
may have increased a little and pH
decreased a little on supplemental O
2
because the improved ar-
terial
P
O
2
decreased peripheral chemoreceptor stimulation and
the degree of hyperventilation lessened (see Figure 13–34).
Our patient’s initial complaint was chest pain, which made
him think he was having a heart attack. He was actually fortunate
to have chest pain because it caused him to go to the emergency
room, and that may have saved his life. Although the exact rea-
sons for chest pain in pulmonary embolism are uncertain, one
possibility is that the clots result in an acute increase in pulmo-
nary artery pressure, which can result in pain.
Why did this man have a pulmonary embolism? There are
several risk factors for the development of deep vein thrombosis
that can result in pulmonary embolism. Prolonged sitting often
causes a stagnant pooling of blood in the lower legs (see Fig-
ures 12–45 and 12–60). That is why it is highly recommended
that we avoid sitting for extended periods of time. Even just
sitting at a computer for hours is discouraged. Contraction of
the leg skeletal muscles compresses the leg veins. This results
in intermittent emptying of the veins, decreasing the chances
for clot formation. Obesity also increased the risk of deep vein
thrombosis in our patient by further increasing the pooling of
blood in the leg veins, increasing the amount of certain clot-
ting factors in the blood, and changing platelet function.
There are also a number of gene defects that can lead to
an increased tendency to form clots, a condition called inherited
hypercoagulability
. The most common is resistance to activated
protein C (see Figure 12–78), which can occur in up to 3 per-
cent of healthy adults in the United States. In fact, our patient
was tested and found to have resistance to activated protein C.
Therefore, the combination of obesity, sitting for a prolonged
period of time, and hypercoagulability is the likely cause of deep
vein thrombosis and pulmonary embolism in our patient.
Therapy
As soon as the diagnosis of pulmonary embolism was made,
our patient was immediately started on intravenous heparin
and
recombinant tissue plasminogen activator
(
rec-tPA
)
.
Heparin is an anticlotting factor that counteracts the hyperco-
agulability. Rec-tPA is a synthetic form of a naturally occurring
molecule that helps dissolve clots. The ventilation-perfusion
scan was repeated a few days later and lung blood fl ow was al-
most normal. Supplemental oxygen was reduced over this time
and then stopped when blood gases normalized.
Considering that this patient now has a proven inherited
cause of hypercoagulability, he has an increased probability to
have another deep vein thrombosis and even pulmonary em-
bolism in the near future. It is also possible that some of his
family members have the same defect, for which they should
be tested and adequately counseled. Our patient was sent home
and continued to receive oral anticoagulants for 6 months (see
description of anticlotting drugs in Chapter 12, Section F),
and was actively followed by his primary care physician. He
was encouraged to lose weight because obesity increases the
risk of a deep vein thrombosis occurring again. Some phy-
sicians even advocate life-long anticoagulation therapy for a
patient such as ours.
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