Pulmonary embolism

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Pulmonary embolism spans small incidental clot to sudden obstructive shock. Symptoms and routine observations are individually unreliable. Probability-led testing prevents both missed PE and harmful over-imaging. If suspicion is genuinely low and another diagnosis is feasible, PERC may identify patients needing no further testing. Otherwise, the two-level PE Wells score separates likely disease above 4 from unlikely disease at 4 or below. D-dimer belongs to the unlikely branch; imaging belongs first in the likely branch.

CT pulmonary angiography usually confirms clot and shows alternative thoracic diagnoses. V/Q imaging is useful when iodinated contrast is unsuitable or radiation distribution is preferable, especially with a normal chest radiograph. Pregnancy requires a shared local radiology and obstetric pathway rather than avoiding definitive testing. When imaging is delayed, interim therapeutic anticoagulation reduces risk; draw FBC, renal and liver tests, PT and APTT first when doing so causes no delay.

Severity is haemodynamic, not simply anatomical. Persistent hypotension and tissue hypoperfusion mean high-risk PE and require reperfusion consideration. Right-ventricular dysfunction and positive troponin in a stable patient identify closer-monitoring need but do not alone justify routine systemic thrombolysis because major and intracranial bleeding increase. If shock makes transport unsafe, bedside echocardiography can demonstrate acute RV pressure overload and exclude alternatives, but a normal study cannot exclude stable PE.

Stable PE is treated like proximal DVT with at least three months of anticoagulation. Agent choice incorporates kidney and liver function, active cancer, APS, pregnancy, weight, interactions and adherence. At three months, major transient provocation may support stopping, while unprovoked or persistent-risk disease may merit extended prevention. Follow-up must also ask about breathlessness and exercise tolerance; unresolved symptoms after three months trigger echocardiography, perfusion imaging or a CTEPH pathway rather than reassurance from completed anticoagulation.

Key points

PE presents with acute dyspnoea, pleuritic pain, tachypnoea, tachycardia, syncope, haemoptysis or DVT signs, but normal oxygen saturation, chest radiograph or ECG does not exclude it.
If overall clinical suspicion is low and another diagnosis is feasible, consider the PERC rule; otherwise calculate the two-level PE Wells score rather than ordering D-dimer indiscriminately.
PE likely means Wells score above 4: arrange immediate CTPA and give interim therapeutic anticoagulation if imaging cannot occur promptly unless contraindicated.
PE unlikely means Wells score 4 or less: obtain D-dimer first; a negative validated result excludes PE, while a positive result requires CTPA or a suitable alternative scan.
CTPA is the usual confirmatory test. Use V/Q SPECT or planar scanning when contrast allergy, severe renal impairment, pregnancy radiation balance or a normal chest radiograph makes it preferable through the local imaging pathway.
For haemodynamically stable confirmed PE, offer apixaban or rivaroxaban first-line when suitable, with the same mandatory acute loading phases as DVT and at least 3 months of treatment.
For haemodynamically unstable PE, start continuous UFH and consider systemic thrombolysis; do not routinely thrombolyse stable PE solely because troponin or right-ventricular imaging is abnormal.
At three months, review provocation, cancer, APS, recurrence and bleeding, and investigate persistent limitation for post-PE syndrome or CTEPH rather than repeating D-dimer as surveillance.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Embolisation from venous thrombosis

Most PE arises when fibrin-rich clot from proximal leg or pelvic veins detaches and lodges within progressively smaller pulmonary arteries.

Provoked systemic risk

Surgery, trauma, immobility, pregnancy, puerperium, oestrogen, hospitalisation and long travel transiently increase stasis and coagulation activation.

Persistent thrombotic drivers

Cancer, APS, previous VTE, inflammatory disease, obesity, nephrotic syndrome, myeloproliferative disease and rare inherited thrombophilia sustain recurrence risk.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Pulmonary vascular obstruction
Mechanical clot and vasoconstrictor release abruptly increase pulmonary resistance, raising right-ventricular afterload and diverting perfusion away from ventilated lung.
2
Right-ventricular failure
The thin-walled right ventricle dilates, wall tension and oxygen demand increase, septal shift reduces left filling and coronary perfusion falls, creating shock and ischaemia.
3
Gas-exchange disturbance
Ventilation-perfusion mismatch, reduced mixed venous oxygen, atelectasis and occasionally right-to-left shunting cause hypoxaemia; PaCO2 is often low from tachypnoea.
4
Organisation or resolution
Anticoagulation prevents propagation while endogenous fibrinolysis clears thrombus; incomplete resolution and vascular remodelling rarely progress to chronic thromboembolic pulmonary hypertension.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Common presentation

Sudden breathlessness, pleuritic chest pain, tachypnoea, tachycardia, mild hypoxaemia, haemoptysis or unilateral leg findings should prompt structured probability assessment.

High-risk physiology

Hypotension, syncope, cool peripheries, confusion, oliguria and rising lactate indicate inadequate right-heart output and immediate reperfusion need.

Pulmonary infarction

Peripheral pleuritic pain, small-volume haemoptysis, fever and a wedge-shaped opacity can mimic pneumonia while representing distal occlusion.

Subtle or incidental disease

Older adults and cancer patients may present with unexplained tachycardia, functional decline or an incidental clot that still needs clinical significance assessment.

Cardiac arrestRed flag

Pulseless electrical activity with preceding dyspnoea, DVT risk or bedside RV dilatation should trigger the RCUK suspected-PE arrest pathway.

Red flags requiring action

Persistent systolic hypotension, cool peripheries, confusion, oliguria, rising lactate or cardiac arrest indicates obstructive shock and overrides the routine D-dimer and outpatient pathway.
Major active bleeding, recent intracranial haemorrhage, recent brain or spinal surgery or suspected aortic dissection materially changes thrombolysis and anticoagulation decisions and requires immediate expert balance.
Pregnancy, severe kidney impairment, active cancer, triple-positive APS or platelets falling after heparin alters imaging or anticoagulant selection but must not produce untreated suspected PE.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
First-line: two-level PE Wells scoreFirst stepFirst line
Why
Select imaging-first or D-dimer-first diagnosis in a haemodynamically stable patient.
Interpretation and limitations
More than 4 is PE likely and prompts CTPA; 4 or less is PE unlikely and prompts D-dimer. Clinical signs of DVT and whether PE is likelier than alternatives carry major weight.
02
First-line in unlikely PE: D-dimerFirst line
Why
Exclude PE without imaging when probability is low.
Interpretation and limitations
A negative validated assay ends the pathway; a positive result is non-specific and requires imaging. Consider an age-adjusted threshold above age 50 when supported by the local assay.
03
Confirmatory CTPAConfirmatory
Why
Directly demonstrate intraluminal pulmonary arterial filling defects and assess RV size and alternative chest pathology.
Interpretation and limitations
A positive scan confirms PE. If negative despite high continuing suspicion, review scan quality and seek radiology or specialist advice rather than repeating tests reflexively.
04
Alternative V/Q imaging
Why
Diagnose perfusion obstruction when iodinated contrast or CTPA radiation distribution is unsuitable.
Interpretation and limitations
A normal perfusion scan excludes clinically important PE; a non-diagnostic result requires integration with chest radiograph, probability and further imaging.
05
Severity and treatment baseline
Why
Identify RV strain, myocardial injury, competing diagnoses and anticoagulant safety.
Interpretation and limitations
Use ECG, troponin, BNP, blood gas, FBC, renal and liver tests and echocardiography according to severity. Biomarkers stratify risk after diagnosis and do not replace imaging in stable patients.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

Acute coronary syndrome

Central pressure, ischaemic ECG change and troponin rise can occur in both; coronary phenotype, imaging and right-heart findings guide parallel urgent assessment.

Pneumonia or pleural disease

Fever, focal crackles, consolidation, pneumothorax and pleuritis can mimic PE, while infection itself increases VTE risk and may coexist.

Acute aortic syndrome

Abrupt tearing pain, pulse or neurological deficit and aortic imaging features make anticoagulation or thrombolysis dangerous until dissection is excluded.

Heart failure or arrhythmia

Pulmonary oedema, atrial arrhythmia and decompensated right or left heart disease cause dyspnoea, tachycardia and biomarkers without pulmonary arterial clot.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Stable suspected PEUse probability before testingFirst stepPE is possible but there is no persistent hypotension, shock or cardiac arrest.

1If clinical suspicion is low and another diagnosis is feasible, consider PERC; otherwise calculate the two-level PE Wells score.
2For a score above 4, arrange immediate CTPA; for 4 or below, use D-dimer and image only when positive.
3Give interim therapeutic anticoagulation if the indicated D-dimer or imaging is delayed, unless a bleeding contraindication outweighs benefit.

02High-risk PEReperfuse obstructive shockConfirmed or strongly suspected PE causes persistent hypotension, tissue hypoperfusion or rapidly failing right ventricle.

1Call critical care and senior PE expertise, support oxygenation and perfusion cautiously and use bedside echo when transport to CT is unsafe.
2Start UFH when suitable and give systemic thrombolysis if haemodynamic instability persists and bleeding risk does not prohibit it.
3If lysis is contraindicated or ineffective, arrange surgical embolectomy or catheter-directed treatment according to immediate expertise and anatomy.

03PE cardiac arrestContinue reperfusion resuscitationCardiac arrest is caused by known PE or PE is strongly suspected from context and ultrasound.

1Follow advanced life support, seek reversible causes and give fibrinolytic treatment when suspected PE is the cause unless a decisive contraindication exists.
2After thrombolysis, consider continuing CPR for 60–90 minutes in selected patients because clot dissolution and right-heart recovery may be delayed.
3Use extracorporeal CPR, surgical embolectomy or percutaneous thrombectomy where immediately available and appropriate to the arrest system.

04Stable confirmed PEAnticoagulate and select place of careImaging confirms PE without haemodynamic instability.

1Assess RV strain, biomarkers, bleeding, comorbidity and a validated outpatient tool plus social ability to obtain and take treatment safely.
2First lineAlternativeUse apixaban or rivaroxaban first-line when suitable, or a renal, cancer, APS, pregnancy or interaction-adjusted alternative, for at least 3 months.
3Book the three-month recurrence and duration review and give a route for new bleeding, dyspnoea, syncope or persistent exercise limitation.

Key medicines and prescribing safety4 treatments · regimens, roles and cautions

NICE first-line treatment for haemodynamically stable PE in suitable adults and a continuing option for secondary prevention.

Apixaban

Give 10 mg orally twice daily for 7 days, then 5 mg twice daily for at least the remainder of the first 3 months; if extended prevention is selected after 6 months, 2.5 mg twice daily is the licensed reduced-intensity dose.

Review renal and hepatic function, active bleeding, pregnancy, APS and strong CYP3A4 or P-gp interactions. Do not omit the 7-day loading phase or use atrial-fibrillation reduction criteria for acute PE.

Provides rapidly adjustable anticoagulation around systemic thrombolysis, embolectomy, shock, severe renal failure or an imminent invasive procedure.

Unfractionated heparin for unstable PE

Use the local weight-based intravenous UFH protocol, commonly an 80 units/kg bolus followed by 18 units/kg/hour, with bolus modification when bleeding risk is high and rapid titration by the validated anti-Xa or APTT method.

Baseline lupus anticoagulant or severe acute-phase change can make APTT unreliable, favouring anti-Xa monitoring. Review active bleeding, recent surgery, neuraxial intervention and HIT, and coordinate stopping and restarting around thrombolysis.

Systemic fibrinolysis rapidly reduces thrombotic obstruction in haemodynamically unstable high-risk PE when expected survival benefit exceeds bleeding risk.

Alteplase for massive pulmonary embolism

For adults at least 65 kg, give 100 mg intravenously over 2 hours using the licensed massive-PE schedule; in adults below 65 kg, do not exceed a total dose of 1.5 mg/kg. Use the cardiac-arrest protocol when arrest is ongoing.

Assess intracranial disease, recent surgery or trauma, active bleeding, severe hypertension and aortic dissection, but avoid paralysing delay during life-threatening shock. Monitor for intracranial and systemic haemorrhage and have a rescue plan.

Single-drug NICE first-line anticoagulation for stable PE when oral therapy and organ function are suitable.

Rivaroxaban

Give 15 mg orally twice daily with food for 21 days, then 20 mg once daily with food; selected extended prevention after at least 6 months may use 10 mg once daily, while high recurrence risk can justify 20 mg.

Record the day-22 transition and food requirement. Review renal and hepatic impairment, pregnancy, APS, cancer bleeding, weight and strong CYP3A4 or P-gp interactions.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Obstructive shock and arrest

Severe right-ventricular outflow obstruction reduces left-heart preload and coronary perfusion, causing pulseless electrical activity, shock and multiorgan failure.

Pulmonary infarction and bleeding

Peripheral occlusion can cause pleuritic pain, haemoptysis and effusion; anticoagulation usually continues because mild infarct haemoptysis is not uncontrolled haemorrhage.

Recurrent VTE

Recurrence follows undertreatment, premature discontinuation, cancer, APS or ongoing risk and may present during apparently therapeutic anticoagulation through non-adherence or interaction.

Post-PE syndrome and CTEPH

Persistent breathlessness may reflect deconditioning, anxiety, cardiac or pulmonary disease, residual obstruction or chronic thromboembolic pulmonary hypertension requiring specialist evaluation.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During high-risk PE, continuously follow blood pressure, perfusion, oxygenation, rhythm, lactate, urine output and bleeding, with serial right-heart assessment and an explicit rescue-reperfusion threshold.
During oral treatment, confirm completion of the loading phase, adherence, renal and liver function, bleeding, interactions and recovery of breathlessness at an early review.
At three months, decide whether anticoagulation stops, continues at full dose or moves to extended prevention using provocation, recurrence, cancer, APS, bleeding and preference.
Investigate persistent breathlessness, syncope, exercise limitation or right-heart signs after at least three months with echocardiography and perfusion-focused CTEPH assessment rather than attributing all symptoms to anxiety.
For indefinite therapy, review at least annually and after acute illness for renal or liver change, anaemia, bleeding, drug interactions, pregnancy plans, adherence and whether benefit remains greater than harm.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Haemodynamics define emergency

A small measured clot can destabilise limited cardiopulmonary reserve, while anatomically extensive emboli may remain normotensive; shock determines reperfusion urgency.

Troponin is not a lysis order

Myocardial injury and RV dysfunction in a stable patient justify observation and rescue readiness, not automatic systemic thrombolysis.

Normal oxygen does not exclude

Gas exchange depends on clot burden and reserve, so a patient with proven PE can have normal saturation and blood gases.

Mild haemoptysis may be infarction

Small-volume blood from pulmonary infarction does not automatically outweigh the need for anticoagulation, although major bleeding requires reassessment.

Recovery has a differential

Persistent limitation may reflect deconditioning, cardiac disease, lung disease, residual clot or CTEPH and deserves structured review.

11Common pitfallsFrequent interpretation and management errors.

01
Ordering D-dimer after declaring PE likely and delaying imaging.
02
Excluding PE because oxygen saturation or chest radiograph is normal.
03
Transporting a shocked patient to CT without a resuscitation plan.
04
Thrombolysing a stable patient solely for raised troponin.
05
Omitting the acute loading phase of a DOAC.
06
Stopping follow-up despite persistent breathlessness after treatment.