Pulmonary embolism

Last updated: September 21, 2023

Summarytoggle arrow icon

Pulmonary embolism (PE) is the obstruction of one or more pulmonary arteries by an embolic solid, fluid, or gas. In the majority of cases, PE is caused by a venous thrombus that originated in the legs or pelvis and embolized to the lungs via the inferior vena cava. Risk factors include immobility, inherited hypercoagulability disorders, pregnancy, postpartum period, and recent surgery. The clinical presentation can range from asymptomatic to obstructive shock, depending on the extent of pulmonary artery obstruction. Because symptoms are often nonspecific (e.g., chest pain, coughing, shortness of breath, and tachycardia), PE should be considered in all patients with acute dyspnea. A tentative diagnosis of PE is usually based on history and clinical suspicion, then confirmed with CT pulmonary angiography (CTPA). Arterial blood gas analysis (ABG) may be normal or show low partial oxygen pressure and respiratory alkalosis. Serum D-dimer test is highly sensitive for PE and can help rule out the diagnosis. Therapeutic anticoagulation is initiated to prevent further embolic events and to promote the gradual dissolution of the embolism and any underlying thrombosis. Treatment for massive PE with hemodynamic instability additionally involves restoring pulmonary perfusion with thrombolytic agents and/or embolectomy.

See also “Nonthrombotic embolism” and “Deep vein thrombosis.”

Definitiontoggle arrow icon

Epidemiologytoggle arrow icon

Epidemiological data refers to the US, unless otherwise specified.

Etiologytoggle arrow icon

PE is FATAL: PE caused by Fat, Air, Thrombus, Amniotic fluid, and Less common, i.e., bacterial, tumor, and cement.

Pathophysiologytoggle arrow icon

Clinical featurestoggle arrow icon

Most patients with PE have a grossly normal physical examination; abnormalities heard on lung auscultation (e.g., wheezes or bilateral rales) often suggest a different cause for the symptoms. [5]

Consider PE as a differential diagnosis in recurring or progressive dyspnea of uncertain etiology.

Pretest probability of pulmonary embolismtoggle arrow icon

Overview [11][12]

Estimate pretest probability (PTP) using validated tools and/or clinician gestalt to guide diagnostic testing. [11][12][13]

Wells criteria for pulmonary embolism [14]

The Wells score is a diagnostic algorithm for assessing the probability of PE and has been validated in inpatient and outpatient settings. Use “Wells criteria for DVT” to calculate the PTP of deep vein thrombosis.

Wells criteria for PE [15][16]
Criteria Points
Clinical symptoms of DVT 3
PE more likely than other diagnoses 3
Previous PE/DVT 1.5
Tachycardia (heart rate > 100/min) 1.5
Surgery or immobilization in the past 4 weeks 1.5


Malignancy 1
Original Wells score (clinical probability) [15]

Modified Wells score (simplified clinical probability) [16]

  • Total score ≤ 4: PE unlikely (8%)
  • Total score > 4: PE likely (34%)

Revised Geneva score [17]

The revised Geneva score utilizes objective clinical variables. It has been externally validated and was initially studied in emergency department outpatients.

Revised Geneva score [15]
Criteria Points
Age > 65 years 1
Prior history of DVT or PE 3
Recent surgery or fracture of the lower limbs 2
Personal history of cancer 2
Unilateral lower limb pain 3
Hemoptysis 2
Heart rate 75–94/min 3
Heart rate ≥ 95/min 5
Pain on palpation of lower limb and unilateral edema 4

Clinical pretest probability

Pulmonary embolism rule-out criteria (PERC) [12][18][19]

Patients with a low PTP of PE and a PERC score of zero have a very low probability of PE and require no further testing.

Pulmonary embolism rule-out criteria (PERC)
Criteria Points
Age > 50 years 1
Heart rate > 100/min 1
Oxygen saturation < 95% 1
Hemoptysis 1
Estrogen use 1
Prior history of DVT or PE 1
Recent surgery or trauma in the past 4 weeks 1
Unilateral lower limb edema 1

Clinical pretest probability

  • Total score 0: pretest probability < 1%; no further testing needed
  • Total score ≥ 1: PE is not ruled out; further testing needed

PERC should only be used in patients with a previously determined low PTP of PE.

The presence of any PERC criteria in a patient with suspected PE necessitates further testing.

Diagnosticstoggle arrow icon

Approach [5][12][20]

Initial evaluation

The initial evaluation of patients with dyspnea and/or chest pain typically includes laboratory studies, CXR, and ECG. Findings may suggest but do not confirm PE. [5]

D-dimer [12][21]

Normal D-dimer values usually rule out PE or DVT in patients with a low PTP. A positive D-dimer is nonspecific, since it may be elevated in any situation in which there is increased fibrinolysis.

Additional laboratory studies [12]

A normal oxygen saturation and/or normal PaO2 do not rule out PE. [5][28]

Chest x-ray [22]

Electrocardiography (ECG)

Confirmatory imaging

CT pulmonary angiography (CTPA) [12][22][31]

CTPA is the preferred test for the diagnosis of acute PE. [22]

A wedge-shaped infarction with pleural effusion is almost pathognomonic for PE. [22]

Ventilation/perfusion scintigraphy (V/Q scan) [12][22]

CTPA and V/Q scans have similar sensitivities and specificities for PE, but CTPA is faster and more readily available. [22]

Pulmonary angiography [22][31]

  • Technique: selective injection of contrast dye into the pulmonary arteries during fluoroscopic examination
  • Indications
    • Inconclusive CTPA findings and high level of suspicion for PE
    • Candidates for concomitant endovascular treatment, e.g., embolectomy
  • Findings: intraluminal filling defects in pulmonary arteries

Adjunctive imaging

The absence of a DVT does not rule out PE, but the presence of a DVT can justify starting empiric anticoagulation for PE. [38]

Severity assessment [21][40][41]

Signs of RV dysfunction that predict adverse outcomes (e.g., hemodynamic collapse or death) can be identified clinically, electrically, biochemically, and radiologically (e.g., on echocardiography or CTPA). [21][23][41]

ECG and cardiac biomarkers

BNP is nonspecific but can predict early adverse outcomes in patients with PE. [21]


  • Goal: mostly used for prognosis; can be used as a diagnostic tool in patients too unstable for confirmatory imaging
  • Indications
    • Suspected right-heart strain or RV dysfunction
    • Critically ill patients with suspected PE
  • Findings [21][22][41]

The presence or absence of RV dysfunction guides the risk stratification and subsequent management of hemodynamically stable patients with PE. [23][46]

Identification of underlying pathology

Classificationtoggle arrow icon

Classification by PE severity [48]

This system guides management using hemodynamic parameters and markers of RV dysfunction.

Classification by overall PE prognosis [49][50]

This system guides disposition using prognostic risk stratification scores (e.g., PESI or sPESI).

Pulmonary embolism severity index (PESI) and simplified PESI (sPESI) [49][50]

The PESI and sPESI stratify the 30-day risk of mortality or adverse outcomes based on patient demographics, comorbidities, and degree of clinical stability.

Criteria Points
PESI [49] sPESI [50]
Age 1 per year 1 if > 80 years
History of cancer 30 1
Systolic blood pressure < 100 mm Hg 30 1
Heart rate ≥ 110/min 20 1
O2 saturation on room air < 90% 20 1
Heart failure 10 1
Chronic lung disease 10
Altered mental status 60 Not considered
Temperature < 96.8°F (< 37°C) 20
Respiratory rate ≥ 30/min 20

Male: 10

Female: 0

PESI interpretation (30-day mortality rate, inpatient mortality) [49]

  • < 66 points: class I, very low risk (0–1.6%, ≤ 1.1%)
  • 66–85 points: class II, low risk (1.7–3.5%, ≤ 1.9%)
  • 86–105 points: class III, intermediate risk (3.2–7.1%, ≤ 4.7%)
  • 106–125 points: class IV, high risk (4.0–11.4%, ≤ 7.0%)
  • > 125 points: class V, very high risk (10.0–23.9%, ≤ 17.2%)

sPESI interpretation (30-day mortality) [50]

  • 0 points: low risk (1%)
  • ≥ 1 point: high risk (10.9%)

Managementtoggle arrow icon

General principles [21][46][51]

Start empiric anticoagulation for PE if clinical suspicion is high unless there is a high risk of bleeding (e.g., recent surgery, hemorrhagic stroke, active bleeding). [46]

Overview of treatment options by severity

Pulmonary embolism treatment by severity and bleeding risk [23][46][51]
Bleeding risk
Low High
Nonmassive PE
Submassive PE
Massive PE

Unstable patients

Management of massive PE [21][46][51]

Avoid volume overload during resuscitation. Aggressive fluid administration can worsen impaired RV function and further decrease cardiac output. [21]

Management of cardiac arrest due to PE [53]

Stable patients [21][23][51]

Disposition [21][23][51]

PESI and sPESI score can be used to help guide disposition.

  • Low-risk PE (PESI class I–II or sPESI score = 0)
    • Consider outpatient management in consultation with specialists.
    • Criteria for outpatient management include:
      • Hemodynamic stability and adequate room air oxygenation
      • Opiates are not required for pain relief.
      • Availability of family or social support, easy access to health care
      • No other major comorbidities or reasons for hospitalization
  • Intermediate-risk PE or high-risk PE (PESI class ≥ III or sPESI score ≥ 1)
    • Hospitalization is required; consult PERT if available.
    • ICU admission: commonly necessary for massive PE or patients with severe RV dysfunction [5]

Anticoagulationtoggle arrow icon

Bleeding risk assessment [23][51][59]

Evaluate a patient's risk for major bleeding and identify contraindications before initiating anticoagulation. [46]

The benefits of anticoagulation in PE outweigh the bleeding risks in most patients who do not have an absolute contraindication to anticoagulation. [63]

Empiric anticoagulation for PE [21][23][51][59]

Empiric anticoagulation may be started while waiting for a definitive diagnosis, depending on the risk of bleeding, the PTP of PE, and the expected timing of the diagnostic study.

Initial anticoagulation (first 5–10 days) [23][51][57][64]

The selection of the initial anticoagulant depends on the severity of the PE, patient comorbidities, and/or planned concurrent treatment. [46]

Long-term anticoagulation (up to 3 months) [23][51][64]

Extended anticoagulation (> 3 months) [23][51][57]

  • Reassess the need for anticoagulation after 3 months, then annually.
  • Indications for extended anticoagulation

Reperfusion therapytoggle arrow icon

Bleeding risk assessment [46]

Evaluate a patient's risk for major bleeding and identify contraindications before initiating thrombolytics.

Thrombolysis for PE is associated with a high risk of major bleeding.

Thrombolysis for PE [23][46]

Follow local protocols in consultation with a thrombosis specialist.

Systemic thrombolysis [51][57]

Catheter-directed thrombolysis [70]


Contraindications to thrombolysis for pulmonary embolism [21][46][57]
Absolute contraindications
Relative contraindications

Embolectomy for PE [46]

Acute management checklisttoggle arrow icon

Initial management

Nonmassive PE

  • Low bleeding risk: Start anticoagulation with a DOAC or heparin.
  • High bleeding risk: Consider IVC filter placement.
  • Consider outpatient management; see “Risk stratification and disposition.”

Submassive PE

Massive PE

Cardiac arrest due to suspected PE

  • Start ACLS.
  • Consider administration of a reduced dose of tPA.

Complicationstoggle arrow icon

We list the most important complications. The selection is not exhaustive.

Pathologytoggle arrow icon

  • Purpose: distinguishing cause of embolism (See “Etiology”.)
  • Histological findings [71]
    • Lines of Zahn: alternating layers of platelets mixed with fibrin (light pink layers) and red blood cells (dark red layers)
    • Only appear premortally (help distinguish a premortal thrombus from a postmortem one)

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Referencestoggle arrow icon

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