Pulmonary embolism

Pulmonary embolism (PE) refers to embolic occlusion of the pulmonary arterial system. The majority of cases result from thrombotic occlusion, and therefore the condition is frequently termed pulmonary thromboembolism which is what this article mainly covers.

Other embolic sources include:

Clinical signs and symptoms are non-specific 14. Dyspnea, chest pain and hemoptysis have been described as a classic triad in pulmonary embolism. 

The ECG may show:

  • sinus tachycardia: the most common abnormality
  • right heart strain pattern
    • incomplete or complete right bundle branch block
    • prominent R wave in lead V1
    • right axis deviation
    • T-wave inversion in the right precordial leads +/- the inferior leads is seen in up to 34% of patients and is associated with high pulmonary artery pressures 25
      • simultaneous T-wave inversion in lead III and V1 has been repeatedly shown to have strong sensitivity (90%), specificity (97%), positive predictive value (92%), negative predictive value (96%) and an overall predictive accuracy of 95% 25,26
  • SIQIIITIII pattern: this refers to a deep S wave in lead I, Q wave and T wave inversion in lead III; this sign is seen as classical of PE but is in fact poor in terms of both sensitivity and specificity as a sign of PE

Patients may have deep vein thrombosis (usually from the lower limbs) which are the most common source of the PE.

Massive PE is suggested if the patient is hypotensive (<90 mmHg), bradycardic (<40 bpm), or pulseless 19.

Pre‐test probability scores are intended to replace empirical assessment of patients with suspected pulmonary embolism:

The right ventricular failure due to pressure overload is considered the primary cause of death in severe PE 14.

D-dimer (ELISA) is commonly used as a screening test in patients with a low and moderate probability clinical assessment, on these patients:

  • normal D-dimer has almost 100% negative predictive value (virtually excludes PE): no further testing is required
  • raised D-dimer is seen with PE but has many other causes and is, therefore, non-specific: it indicates the need for further testing if pulmonary embolism is suspected 4

On patients with a high probability clinical assessment, a D-dimer test is not helpful because a negative D-dimer result does not exclude pulmonary embolism in more than 15%. Patients are treated with anticoagulants while awaiting the outcome of diagnostic tests 4

Depends to some extent on whether it is acute or chronic. Overall, there is a predilection for the lower lobes.

Chest radiography is neither sensitive nor specific for a pulmonary embolism. It is used to assess for differential diagnostic possibilities such as pneumonia and pneumothorax rather than for the direct diagnosis of PE. 

Described chest radiographic signs include:

Sensitivity and specificity of chest x-ray signs 1:

  • Westermark sign
    • sensitivity: ~14% 
    • specificity: ~92% 
    • positive predictive value: ~38%
    • negative predictive value: ~76%
  • vascular redistribution
    • sensitivity: ~10% 
    • specificity: ~87% 
    • positive predictive value: ~21%
    • negative predictive value: ~74%
  • Hampton hump
    • sensitivity: ~22% 
    • specificity: ~82%
    • positive predictive value: ~29%
    • negative predictive value: ~76%
  • pleural effusion
    • sensitivity: ~36% 
    • specificity: ~70%
    • positive predictive value: ~28%
    • negative predictive value: ~76%
  • elevated diaphragm
    • sensitivity: ~20% 
    • specificity: ~85%
    • PPV: ~30%
    • NPV: ~76%

CT pulmonary angiography (CTPA) will show filling defects within the pulmonary vasculature with acute pulmonary emboli. When the artery is viewed in its axial plane the central filling defect from the thrombus is surrounded by a thin rim of contrast, which has been called the Polo Mint sign.

Emboli may be occlusive or non-occlusive, the latter is seen with a thin stream of contrast adjacent to the embolus. Typically the embolus makes an acute angle with the vessel, in contrast to chronic emboli. The affected vessel may also enlarge 9.

Acute pulmonary thromboemboli can rarely be detected on non-contrast chest CT as intraluminal hyperdensities 12.

Dual energy CT holds much promise for the diagnosis and prognosis of PE.

In contrast to acute pulmonary embolism, chronic thromboemboli are often complete occlusions or non-occlusive filling defects in the periphery of the affected vessel which form obtuse angles with the vessel wall 9. The thrombus may be calcified.

Features noted with chronic pulmonary emboli include:

  • webs or bands, intimal irregularities 3
  • abrupt narrowing or complete obstruction of the pulmonary arteries 3
  • pouching defects” which are defined as chronic thromboembolism organized in a concave shape that “points” toward the vessel lumen 3

Indirect signs include 7:

  • mosaic perfusion
  • vascular calcification
  • bronchial or systemic collateralisation

Bedside ultrasonography is currently not recommended for a haemodynamically stable patient with suspected pulmonary embolism. In the presence of hemodynamic compromise, echocardiography may be of value to assess for the presence of florid right ventricular dysfunction;

  • if absent, another cardiopulmonary derangement is likely responsible
  • if unequivocally present, it can establish the need for emergent treatment

Echocardiographic signs implying acute right ventricular pressure overload include:

  • a thrombus-in-transit in the inferior vena cava, right atrium, right ventricle, or pulmonary trunk
  • diastolic right ventricular diameter >30 mm
    • and/or > diastolic left ventricular diameter  
  • tricuspid annular plane systolic excursion <16 mm
  • paradoxical systolic interventricular septal motion
  • pulmonary artery acceleration time <90 ms
  • right atrioventricular pressure gradient >30 mmHg (without concomitant right ventricular hypertrophy)
  • 60/60 sign
  • McConnell sign 

Of note, transesophageal echocardiography has a reported sensitivity of 80.5% and a specificity of 97.2% for ruling in acute pulmonary embolism after the detection of right ventricular overload on transthoracic echocardiography24

Again not recommended as part of first-line work up. 

Cumulative damage from repeated embolic insults is a common cause of chronic thromboembolic pulmonary hypertension, which demonstrates a variable degree of the aforementioned signs, but with significantly higher right ventricular pressures, right ventricular hypertrophy and diastolic dysfunction, and a higher degree of tricuspid regurgitation

It is difficult to obtain technically adequate images for pulmonary embolism patients using MRI. Magnetic resonance pulmonary angiography (MRPA) should be considered only at centers that routinely perform it well and only for patients for whom standard tests are contraindicated. Technically-adequate magnetic resonance angiography has a sensitivity of 78% and a specificity of 99% 13.

A ventilation/perfusion (V/Q) scan will show ventilation-perfusion mismatches. A high probability scan is defined as showing two or more unmatched segmental perfusion defects according to the PIOPED criteria.

Providing cardiopulmonary support is the initial treatment. Anticoagulation is provided in patients without risk of active bleeding. If the emboli are large or there is a large clot burden, thrombolysis is an option. In some cases, embolectomy or placement of vena caval filters is required.

Several studies report around 80% emboli resolving at around 30 days 20,21.


  • pulmonary artery sarcoma
  • pulmonary artery vasculitis e.g. Takayasu arteritis
  • misidentification of pulmonary veins for arteries
  • arterial bifurcations (or branch-points) can mimic PE but usually easily identified on multiplanar assessment
  • artefact may cause pseudofilling defects and can be caused by
    • breathing motion
    • beam hardening
      • hyperconcentrated contrast in the superior vena cava
      • medical devices e.g. catheters, orthopedic prostheses
      • patient's arms in a down position
    • patient movement
    • transient contrast bolus interruption 16, due to Valsalva or patent foramen ovale, causing non-opacified blood to enter the right ventricle and pulmonary arteries (scanning in end expiration can reduce or eliminate this artefact)
  • chronic emboli may be mistaken for acute emboli 
    • or vice-versa
  • thromboembolic emboli may be mistaken for other embolized material
    • or vice-versa
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Article information

rID: 1937
Systems: Vascular, Chest
Tag: lung
Synonyms or Alternate Spellings:
  • Bland pulmonary embolism
  • Acute pulmonary arterial embolism
  • Acute pulmonary arterial emboli
  • Acute pulmonary embolism
  • Acute pulmonary emboli
  • Pulmonary emboli
  • Pulmonary embolus
  • Pulmonary embolism (PE)
  • Pulmonary thromboembolism
  • PE
  • PE's
  • Pulmonary thrombo-embolism
  • Pulmonary embolism - general
  • Pulmonary emboli - general
  • Pulmonary arterial thromboembolism
  • Pulmonary arterial thromboemboli
  • Pulmonary arterial embolism
  • Acute PE
  • PEs

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Cases and figures

  • Case 1: saddle pulmonary emboli
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  • Case 5: saddle embolus
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  • Case 6: adherent to vessel wall
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  • Pumonary Embolism...
    Case 7
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  • Case 8: with lung infarction
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  • Massive bilateral...
    Case 9
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  • Case 10: acute pulmonary embolism
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  • Case 11
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  • Case 12
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  • Case 13
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  • Case 14
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  • Case 15
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  • Case 16
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  • Case 17
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  • Case 18
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  • Case 19
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  • Case 20
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  • Case 21
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  • Case 22
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  • Case 23: saddle embolus
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  • Case 24: dual-energy
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  • Case 25
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  • Case 26: segmental thrombosis
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  • Case 27: complete occlusion
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  • Case 28
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  • Case 29: chronic PE
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  • Case 30: MRI
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  • Case 31: with lung infarction
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