C h a p t e r 2 3
Disorders of Ventilation and Gas Exchange
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Pathogenesis
Athough pulmonary emboli can originate from a num-
ber of sources, most arise from deep vein thrombosis
(DVT) in the large veins of the lower legs, typically origi-
nating in the popliteal vein or larger veins above it (see
Chapter 18). The presence of thrombosis in the deep veins
of the legs or pelvis often is unsuspected until embolism
occurs. Among the physiologic factors that contribute to
venous thrombosis are venous stasis, venous endothelial
injury, and hypercoagulability states. Venous stasis and
venous endothelial injury can result from prolonged bed
rest (particularly with immobilization of the legs), severe
trauma (including burns and fractures), surgery (particu-
larly orthopedic surgery of the knee or hip), childbirth,
myocardial infarction and congestive heart failure, and
spinal cord injury. Hypercoagulability is related to vari-
ous factors. Cancer cells can produce thrombin and syn-
thesize procoagulation factors, increasing the risk for
thromboembolism. Pregnancy, and hormone replacement
therapy are thought to increase the resistance to endog-
enous anticoagulants and risk of pulmonary embolism.
There is also increased risk for pulmonary embolism
among users of oral contraceptives, particularly in women
who smoke. The thrombophilias (e.g., antithrombin III
deficiency, protein C and S deficiencies, factor V Leiden
mutation) are a group of inherited disorders affecting
coagulation that make an individual prone to the devel-
opment of venous thromboemboli (see Chapter 12).
The pathophysiologic effects of thromboembolism
depend largely on the size of the embolus and degree of
pulmonary blood flow obstruction. Obstruction of pul-
monary blood flow causes reflex bronchoconstriction in
the affected area of the lung, ventilation without perfu-
sion, impaired gas exchange, and loss of alveolar sur-
factant. Pulmonary hypertension and right heart strain
may develop with large emboli or in those with poor
cardiac reserve.
Although small areas of infarction may occur, pulmo-
nary infarction is uncommon. This is because the lung
is perfused not only by the pulmonary arteries but also
by the bronchial arteries and air from the alveoli. If the
bronchial circulation is normal and adequate ventilation
is maintained, a decrease in pulmonary artery perfusion
does not usually cause infarction.
Manifestations
The clinical manifestations of pulmonary embolism
depend on the size and location of the obstruction. Small
emboli that become lodged in the peripheral branches
of the pulmonary artery are clinically silent and may go
unrecognized, especially in the elderly and acutely ill.
Persons with moderate-sized emboli often present with
breathlessness accompanied by pleuritic pain, apprehen-
sion, slight fever, andcoughproductiveofblood-streaked
sputum. Tachycardia often occurs to compensate for
decreased oxygenation, and the breathing pattern is
rapid and shallow. Patients with massive emboli usually
present with sudden collapse, crushing substernal chest
pain, shock, and sometimes loss of consciousness. The
pulse is rapid and weak, the blood pressure is low, the
neck veins are distended, and the skin is cyanotic and
diaphoretic. Massive pulmonary emboli often are fatal.
Diagnosis andTreatment
Diagnosis of pulmonary embolism is based on clinical
signs and symptoms, blood gas determinations, D-dimer
testing, lung perfusion scans, CT scans of the chest, and,
in selected cases, pulmonary angiography.
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Laboratory
studies and radiologic films are useful in ruling out other
conditions that might give rise to similar symptoms.
Because emboli can cause an increase in pulmonary vas-
cular resistance, the electrocardiogram (ECG) may be
used to detect signs of right heart strain. There has been
recent interest in combining several noninvasive methods
(lower limb compression ultrasonography, D-dimer mea-
surements, and clinical assessment measures) as a means
of establishing a diagnosis of pulmonary embolism.
Because most pulmonary emboli originate from DVT,
venous studies such as
lower limb compression ultra-
sonography, impedance plethysmography,
and
contrast
venography
are often used as initial diagnostic proce-
dures. Of these, lower limb compression ultrasonog-
raphy has become an important noninvasive means
for detecting DVT.
D-dimer testing
involves the mea-
surement of plasma D-dimer, a degradation product of
coagulation factors that have been activated as a result
of a thromboembolic event. The
ventilation–perfusion
scan
uses radiolabeled albumin, which is injected intra-
venously, and a radiolabeled gas, which is inhaled.
A scintillation (gamma) camera is used to scan the vari-
ous lung segments for blood flow and distribution of
the radiolabeled gas. Ventilation–perfusion scans are
useful only when their results are either normal or indi-
cate a high probability of pulmonary embolism.
Helical
(spiral) CT angiography
requires administration of an
intravenous radiocontrast medium. It is sensitive for the
detection of emboli in the proximal pulmonary arteries
and provides another method of diagnosis.
Pulmonary
angiography
involves the passage of a venous catheter
through the right heart and into the pulmonary artery
under fluoroscopy. Although it remains the most accu-
rate method of diagnosis, it is an invasive procedure;
therefore, its use is reserved for selected cases.
Treatment goals for pulmonary emboli include pre-
venting DVT and the development of thromboemboli,
protecting the lungs from exposure to thromboem-
boli when they occur, and in the case of large and life-threatening pulmonary emboli, sustaining life and
restoring pulmonary blood flow.
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Thrombolytic ther-
apy using streptokinase, urokinase, or recombinant tis-
sue plasminogen activator may be indicated in persons
with life-threatening pulmonary emboli. Thrombolytic
therapy is followed by anticoagulant therapy (e.g.,
heparin and then warfarin) to prevent clot reoccur-
rence but carries the risk of bleeding complications
and is contraindicated in many post-surgical patients.
Anticoagulation with unfractionated or low-molecular
weight heparin is frequently employed to prevent addi-
tional clot burden when signs of right heart strain
are absent. Surgical interruption of the vena cava or
