2. Definition
Pulmonary embolism is a sudden blockage in a
lung artery. The blockage usually is caused by
a blood clot that travels to the lung from a vein
in the leg.
3. Etiology of emboli
Thrombus, usually formed in the systemic veins or rarely in the
right heart (<10% of cases), may dislodge and embolize into
the pulmonary arterial system.
Source of thrombi include
Pelvic and abdominal veins
DVT
Hypercoagulable states
Amniotic emboli
Fat emboli from long bones
4. Pathophysiology
As a thrombus clogs pulmonary vessels, there is a decline in
perfusion of the lung tissue but ventilation remains intact which
results in increased intrapulmonary dead space and impaired
gaseous exchange through alveoli.
After some hours the non-perfused lung no longer produces
surfactant. Alveolar collapse occurs and exacerbates
hypoxaemia.
The primary haemodynamic consequence of pulmonary embolism
is a reduction in the cross-sectional area of the pulmonary arterial
bed which results in an elevation of pulmonary arterial pressure and
a reduction in cardiac output. The zone of lung that is no longer
perfused by the pulmonary artery may infarct, but often does not
do so because oxygen continues to be supplied by the bronchial
circulation and the airways.
5. Clinical features
Sudden onset of unexplained dyspnea (most common)
Pleuritic chest pain and hemoptysis (if infarct occurs)
On basis of clinical symptoms emboli can be classified as
Small/medium pulmonary embolism
Massive pulmonary embolism
Multiple recurrent pulmonary emboli
6. Small/medium pulmonary embolism
In this situation an embolus has impacted in a terminal pulmonary
vessel.
Symptoms are
pleuritic chest pain and breathlessness.
Haemoptysis occurs in 30%, often ≥3 days after the initial event.
On examination
tachypnoeic with a localized pleural rub and often coarse
crackles over the area involved.
An exudative pleural effusion (occasionally blood-stained) can
develop. The patient may have a fever, and cardiovascular
examination is normal.
7. Massive pulmonary embolism
This is a much rarer condition where sudden collapse occurs
because of an acute obstruction of the right ventricular outflow
tract.
Severe central chest pain (cardiac ischaemia due to lack of
coronary blood flow) and becomes shocked, pale and sweaty.
Syncope may result if the cardiac output is transiently but
dramatically reduced, and death may occur.
On examination the patient is tachypnoeic, has a tachycardia with
hypotension
The jugular venous pressure (JVP) is raised with a prominent ‘a’
wave. There is a right ventricular heave, a gallop rhythm and a
widely split second heart sound.
8. Multiple recurrent pulmonary emboli
Increased breathlessness, often over weeks or months accompanied by
Weakness
syncope on exertion and occasionally angina.
The physical signs are due to the pulmonary hypertension that has
developed from multiple occlusions of the pulmonary vasculature.
On examination
Right ventricular heave
Loud pulmonary second sound.
9. Investigation
Small/medium pulmonary emboli
Chest X-ray is often normal, but linear atelectasis or blunting of a costophrenic
angle (due to a small effusion) is not uncommon. These features develop only
after some time. A raised hemidiaphragm is present in some patients. Previous
infarcts may be seen as opaque linear
ECG is usually normal, except for sinus tachycardia, but sometimes atrial
fibrillation or another tachyarrhythmia occurs. There may be evidence of right
ventricular strain.
Blood tests. Pulmonary infarction results in a polymorphonuclear leucocytosis,
an elevated ESR and increased lactate dehydrogenase levels in the serum.
Immediately prior to commencing anticoagulants a thrombophilia screen
should be checked.
Plasma D-dimer – if this is undetectable, it excludes a diagnosis of pulmonary
embolism.
10.
Radionuclide ventilation/perfusion scanning (V̇/Q̇ scan) is a good and widely
available diagnostic investigation. Pulmonary 99mTc scintigraphy demonstrates
underperfused areas which, if not accompanied by a ventilation defect on a
ventilation scintigram performed after inhalation of radioactive xenon gas , is highly
suggestive of a pulmonary embolus. There are limitations to the test, however. For
example, a matched defect may arise with a pulmonary embolus which causes an
infarct, or from emphysematous bullae. This test is therefore conventionally reported
as a probability (low, medium or high) of pulmonary embolus and should be
interpreted in the context of the history, examination and other investigations.
Ultrasound scanning can be performed for the detection of clots in pelvic or
iliofemoral veins
CT scans. Contrast-enhanced multidetector CT angiograms (CTA) , have a sensitivity
of 83% and specificity of 96%, with a positive predictive value of 92%. These values
will increase with the use of 64-multislice scanners.
MR imaging gives similar results and is used if CT angiography is contraindicated.
11.
Massive pulmonary emboli
Chest X-ray may show pulmonary oligaemia, sometimes with
dilatation of the pulmonary artery in the hila. Often there are no
changes.
ECG shows right atrial dilatation with tall peaked P waves in lead II.
Right ventricular strain and dilatation give rise to right axis
deviation, some degree of right bundle branch block, and T wave
inversion in the right precordial leads . The ‘classic’ ECG pattern
with an S wave in lead I, and a Q wave and inverted T waves in
lead III (S1, Q3, T3), is rare.
12.
Blood gases show arterial hypoxaemia with a low arterial CO2 level,
i.e. type I respiratory failure pattern.
Echocardiography shows a vigorously contracting left ventricle,
and occasionally a dilated right ventricle and a clot in the right
ventricular outflow tract.
Pulmonary angiography has now been replaced by CT and MR
angiography.
13.
14.
15.
Multiple recurrent pulmonary emboli
Chest X-ray may be normal. Enlarged pulmonary arterioles with oligaemic
lung fields indicate advanced disease.
ECG can be normal or show signs of pulmonary hypertension
Leg imaging with ultrasound and venography may show thrombi.
V̇/Q̇ scan may show evidence of pulmonary infarcts.
Multidetector CT scans can detect small emboli.
Further tests looking for exercise-induced hypoxaemia and catheter
studies to estimate pulmonary artery pressures are sometimes required.
16. Diagnosis
The symptoms and signs of small and medium-sized
pulmonary emboli are often subtle and nonspecific, so the
diagnosis is often delayed or even completely missed.
Pulmonary embolism should be considered if patients
present with symptoms of unexplained cough, chest pain,
haemoptysis, new-onset atrial fibrillation (or other
tachycardia), or signs of pulmonary hypertension
17.
High clinical probability patients should proceed to multi-detector
contrast-enhanced CT angiography (CTA) . A positive test confirms
the diagnosis. A negative test but with an elevated D-dimer may
require venous ultrasonography. (Patients with renal failure or
contrast allergy can have ventilation/perfusion V̇/Q̇ scanning).
Low or intermediate clinical risk patients should have a D-dimer
assay performed. A negative D-dimer rules out a pulmonary
embolism. A positive D-dimer requires further investigation with CTA.
18.
Patients who are haemodynamically unstable (shock,
systolic blood pressure <90 mmHg, drop in pressure of
≥40 mmHg) may require urgent CTA or if critically ill with
a high clinical probability, an echocardiogram should
be performed – right ventricular dysfunction is highly
suggestive of a pulmonary embolism – a normal right
ventricle should suggest alternative diagnoses.
19.
20. Treatment
Acute management
All patients should receive high-flow oxygen (60–100%) unless they have
significant chronic lung disease. Patients with pulmonary infarcts require
bed rest and analgesia.
Patients should be anticoagulated initially with subcutaneous lowmolecular-weight heparin or fondaparinux or intravenous unfractionated
heparin followed by warfarin therapy.
Massive pulmonary emboli. Intravenous fluids and even inotropic agents
to improve the pumping of the right heart are sometimes required, and
very ill patients will require care on the intensive therapy unit
21.
Fibrinolytic therapy such as streptokinase (250 000 units by i.v.
infusion over 30 min, followed by streptokinase 100 000 units i.v.
hourly for up to 12–72 hours, according to manufacturer’s
instructions) has been shown in controlled trials to clear pulmonary
emboli more rapidly and to confer a survival benefit in massive PE.
It should be used in unstable patients and in some stable patients
with adverse features, e.g. right ventricular dysfunction.
Surgical embolectomy is rarely necessary, but there may be no
alternative when the haemodynamic circumstances are very
severe
22.
Prevention of further emboli
Patients should be anticoagulated with vitamin K antagonists for a period
of 3–6 months with a target INR of 2.0–3.0.
Patients with cancer or pregnant women should be treated with longterm low-molecular-weight heparin. Occasionally, physical methods are
required to prevent further emboli. This is usually because recurrent emboli
occur despite adequate anticoagulation, but it is also indicated in highrisk patients in whom anticoagulation is absolutely contraindicated.
The most common method by which pulmonary embolism is treated in this
situation is by insertion of a filter in the inferior vena cava via the femoral
vein to above the level of the renal veins.
