Acute pulmonary embolism (PE) is a common and often fatal
disease. Mortality can be reduced by prompt diagnosis and therapy.
Unfortunately, the clinical presentation of PE is variable and
nonspecific, making accurate diagnosis difficult.
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Definition PE refers to obstruction of the pulmonary artery or
one of its branches by material (eg, thrombus, tumor, air, or fat
). PE can be classified as acute or chronic. Patients with acute PE
typically develop symptoms and signs immediately after obstruction
of pulmonary vessels. In contrast, patients with chronic PE tend to
develop slowly progressive dyspnea over a period of years due to
pulmonary hypertension.
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Definition Massive PE causes hypotension, defined as a systolic
blood pressure 15 minutes. It should be suspected anytime there is
hypotension accompanied by an elevated central venous pressure (or
neck vein distension)
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pathophysiology Most PE arise from thrombi in the deep venous
system of the lower extremities. However, they may also originate
in the right heart or the pelvic, renal, or upper extremity veins.
Iliofemoral veins are the source of most clinically recognized PE
After traveling to the lung, large thrombi may lodge at the
bifurcation of the main pulmonary artery or the lobar branches and
cause hemodynamic compromise. Smaller thrombi continue traveling
distally and are more likely to produce pleuritic chest pain,
presumably by initiating an inflammatory response adjacent to the
parietal pleura. Only about 10 percent of emboli cause pulmonary
infarction
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pathophysiology Impaired gas exchange due to PE cannot be
explained solely on the basis of mechanical obstruction of the
vascular bed and alterations in the ventilation to perfusion ratio.
Gas exchange abnormalities are also related to the release of
inflammatory mediators, resulting in surfactant dysfunction,
atelectasis, and functional intrapulmonary shunting Hypotension is
due to diminished cardiac output (CO) which results from increased
pulmonary vascular resistance (PVR) impeding right ventricular
outflow and reducing left ventricular preload
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Prognostic factors PE is associated with a mortality rate of
approximately 30 percent without treatment. However, accurate
diagnosis followed by effective anticoagulant therapy decreases the
mortality rate to 2 to 8 percent Prognostic factors determining the
mortality and morbidity of PE includes:
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RV dysfunction RV dysfunction due to PE results in increased
PE- related mortality. This was illustrated by a meta- analysis of
seven studies (3395 normotensive or hypotensive patients with PE),
which found that RV dysfunction was associated with a two-fold
increase in PE-related mortality(determined ehocardiographically)
RV dysfunction may also predict recurrent PE or DVT
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Brain natriuretic peptides An elevated brain natriuretic
peptide (BNP) or N- terminal pro-brain natriuretic peptide (NT-
proBNP) predicts RV dysfunction and mortality In an observational
study of 73 patients diagnosed with acute PE, serum BNP levels
>90 pg/mL were associated with cardiopulmonary resuscitation,
mechanical ventilation, vasopressor therapy, thrombolysis, and
embolectomy, as well as death. Serum BNP levels
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RV thrombus Patients with PE and a right ventricular (RV)
thrombus have a higher short term and long term mortality than
patients without an RV thrombus
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Serum troponins Elevated serum troponin levels identify
patients with PE who are at increased risk for death. In a
meta-analysis of 20 observational studies (1985 patients), an
elevated troponin I or troponin T level was associated with an
increased risk of short-term mortality or death due to PE Troponin
levels can be combined with BNP levels to derive more precise
prognostic information
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Risk factors These include immobilization, surgery within the
last three months, stroke, paresis, paralysis, history of venous
thromboembolism, malignancy, central venous instrumentation within
the last three months, and chronic heart disease.Additional risk
factors identified in women include obesity (BMI 29 kg/m2), heavy
cigarette smoking (>25 cigarettes per day), and
hypertension.
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Clinical presentation Specific symptoms and signs are not
helpful diagnostically because their frequency is similar among
patients with and without PE Symptoms : -dyspnea at rest or with
exertion (73 percent) -pleurtic chest pain (44 percent ) -cough (34
percent) -orthopnea (28 percent), -calf or thigh pain (44 percent)
-calf or thigh swelling (41 percent) -wheezing (21 percent)
Diagnostic tests Many of the symptoms and signs detected in
patients with acute PE are also common among patients without PE,
emphasizing the need for additional evaluation. These include lab
tests and imaging studies
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Arterial blood gases Arterial blood gas (ABG) measurements and
pulse oximetry have a limited role in diagnosing PE.ABGs usually
reveal hypoxemia, hypocapnia, and respiratory alkalosis. Patients
with room air pulse oximetry readings
