Massive pulmonary embolism and reperfusion

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

Acute RV pressure overload causes septal shift, reduced LV filling and obstructive shock. Hypotension is a late, dangerous sign; deterioration can be abrupt.

The central decision is whether the mortality risk from untreated obstruction exceeds the major-bleeding risk from reperfusion. That balance is usually clear in arrest or persistent shock and much less favourable in stable intermediate-risk PE.

Reperfusion is a system decision: systemic thrombolysis is widely available; catheter thrombectomy and surgical embolectomy require an immediately contactable multidisciplinary pathway.

Post-reperfusion care includes anticoagulation, bleeding surveillance, neurological checks, RV/organ recovery and a later decision about long-term VTE treatment.

Key points

Prefer the term high-risk PE: risk is defined by haemodynamic instability, not by 'saddle' position or clot size on CT.
Recognise cardiac arrest, obstructive shock or persistent hypotension (commonly systolic BP below 90 mmHg or a fall of at least 40 mmHg for more than 15 minutes not explained by another cause).
Start ABCDE/ALS, controlled oxygen, monitoring, IV/IO access and immediate critical-care/PE-team input; treat competing reversible causes in parallel.
Avoid uncritical large fluid loads: a small 250–500 mL crystalloid challenge may help selected underfilled patients, but RV distension can worsen output; reassess after every bolus.
If stable enough, CTPA confirms PE. If too unstable to transfer, focused echocardiography can show RV failure and exclude major alternatives, but RV strain alone is not diagnostic in a stable patient.
NICE recommends considering systemic thrombolysis for PE with haemodynamic instability and not offering it routinely to haemodynamically stable PE, even with RV dysfunction.
A licensed alteplase regimen for massive PE in adults at least 65 kg is 10 mg IV over 1–2 minutes then 90 mg over 2 hours; below 65 kg, do not exceed 1.5 mg/kg and follow the product schedule.
When thrombolysis is contraindicated or fails, urgently consider surgical embolectomy or catheter-directed/mechanical treatment according to expertise and availability.
In cardiac arrest from suspected PE, RCUK recommends fibrinolysis; consider continuing CPR for 60–90 minutes after thrombolytic administration.
Use UFH when immediate reperfusion/procedures are anticipated because it is rapidly adjustable; record bolus, infusion, APTT/anti-Xa plan and thrombolytic timing.

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

Proximal venous thrombosis

A large clot arising in deep leg or pelvic veins can embolise and abruptly obstruct a substantial proportion of the pulmonary arterial circulation.

Strong provoking factors

Recent surgery, trauma, immobility, pregnancy, oestrogen exposure and active cancer promote venous stasis or hypercoagulability and increase the risk of a high-burden event.

Persistent thrombophilia

Previous venous thromboembolism, antiphospholipid syndrome and selected inherited thrombophilias increase recurrence risk, though the acute presentation remains defined by haemodynamic effect.

Limited cardiopulmonary reserve

A smaller embolic burden may cause shock in people with severe pulmonary or cardiac disease because the right ventricle cannot tolerate even a moderate rise in afterload.

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

1
Pulmonary arterial obstruction
Embolic material blocks the pulmonary circulation while hypoxic vasoconstriction further raises pulmonary vascular resistance, which links the underlying lesion to the observed respiratory dysfunction.
2
Acute right-ventricular strain
The thin-walled right ventricle dilates against the sudden afterload, increasing wall stress and oxygen demand while reducing efficient forward flow.
3
Falling left-heart preload
Reduced pulmonary flow and septal shift limit left-ventricular filling, causing low cardiac output, hypotension and impaired coronary perfusion.
4
Obstructive shock
A self-reinforcing cycle of right-ventricular ischaemia, worsening contractility and systemic hypoperfusion can progress rapidly to pulseless electrical activity arrest.

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

Cardiac arrestRed flag

PE commonly presents with pulseless electrical activity; very low ETCO2 despite a confirmed airway, appropriate ventilation and high-quality compressions may support but does not prove the diagnosis.

Obstructive shockRed flag

Hypotension plus altered mental state, cool peripheries, oliguria or raised lactate with signs of RV strain/venous congestion indicates critical circulatory failure.

Persistent hypotensionRed flag

Systolic BP below 90 mmHg or a sustained fall of at least 40 mmHg without arrhythmia, hypovolaemia or sepsis strongly supports the high-risk category.

Impending collapseRed flag

Syncope, escalating tachycardia, rising lactate, increasing oxygen need, severe RV dysfunction or recurrent near-arrest requires a monitored critical-care setting and an agreed rescue plan.

Stable RV strain is different

CT/echo RV dysfunction and biomarker elevation in a normotensive patient indicate increased risk and close monitoring, but NICE advises against routine systemic thrombolysis while haemodynamically stable.

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
Continuous ECG, BP, SpO2 and capnography when intubatedFirst step
Why
Track shock and detect peri-arrest deterioration.
Interpretation and limitations
Trend physiology continuously; a single preserved BP does not guarantee stability.
02
Arterial/venous gas and lactate
Why
Quantify gas exchange, acidosis and tissue hypoperfusion.
Interpretation and limitations
Rising lactate or worsening metabolic acidosis despite treatment signals failure; hypocapnia is common before fatigue/arrest.
03
Focused bedside echocardiography
Why
Assess RV size/function and look for alternative causes of shock without unsafe transfer.
Interpretation and limitations
RV dilatation/poor function supports high-risk PE in context; absence does not absolutely exclude PE, and chronic pulmonary hypertension can mimic acute strain.
04
CT pulmonary angiography
Why
Confirm clot and provide anatomical/procedural planning when transfer is safe.
Interpretation and limitations
Do not delay life-saving treatment in an arrest or patient too unstable for CT solely to obtain anatomical confirmation.
05
FBC, platelets, PT/APTT, fibrinogen, renal/liver function and group-and-save
Why
Prepare for anticoagulation, thrombolysis/procedure and haemorrhage management.
Interpretation and limitations
Major coagulopathy, thrombocytopenia or recent bleeding changes reperfusion choice but results must be integrated at resuscitation speed.
06
Troponin and natriuretic peptide
Why
Support myocardial/RV injury assessment after immediate stabilisation.
Interpretation and limitations
Elevations indicate stress and prognosis but are non-specific and do not independently mandate thrombolysis.
07
Contraindication screen
Why
Identify intracranial haemorrhage, recent stroke/surgery, active bleeding or other major hazards.
Interpretation and limitations
In cardiac arrest, contraindications become relative because death without reperfusion is imminent; make and document a senior risk decision.

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

Acute coronary syndrome

Chest pain, shock and biomarker elevation overlap, but coronary-pattern electrocardiographic or imaging findings and absence of right-heart pressure overload favour primary myocardial ischaemia.

Cardiac tamponade

Raised venous pressure, hypotension and obstructive shock with pericardial fluid and chamber collapse on focused imaging indicate tamponade.

Tension pneumothorax

Unilateral absent breath sounds, pleural air and rapid improvement after decompression distinguish tension physiology; urgent treatment takes priority over imaging when clinically evident.

Aortic catastrophe

Abrupt tearing pain, pulse or neurological asymmetry and aortic imaging abnormalities suggest dissection or rupture, which materially changes anticoagulation and reperfusion decisions.

Septic or cardiogenic shock

Infection features or primary left-ventricular failure may explain hypotension, but bedside echocardiography and the overall clinical context help distinguish mixed causes.

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

01ShockHigh-risk PE with a pulseFirst stepObstructive shock or persistent hypotension with PE confirmed or overwhelmingly likely.

1Start ABCDE, controlled oxygen, continuous monitoring, 2 IV/IO lines and immediate critical-care/PE-team activation. Take reperfusion bloods without delaying treatment.
2Use cautious 250–500 mL crystalloid only if clinically underfilled and reassess; avoid repeated large boluses that distend the failing RV. Start vasoactive support in critical care when hypotension persists.
3If safe, obtain urgent CTPA. If too unstable, use bedside echo/ultrasound to support PE and exclude tamponade, tension pneumothorax and profound hypovolaemia.
4If bleeding risk is acceptable, give systemic thrombolysis. If contraindicated, unavailable to succeed or failed, move urgently to surgical embolectomy or catheter-directed/mechanical therapy.
5Continue UFH/anticoagulation according to thrombolytic/procedural timing, then monitor for bleeding and RV/organ recovery in critical care.

02ArrestCardiac arrest probably caused by PECardiac arrest with PE known or strongly suspected.

1Run standard ALS with high-quality CPR, 100% oxygen, waveform capnography and immediate treatment of reversible causes; obtain ultrasound only without prolonged compression interruption.
2Administer a fibrinolytic when PE is suspected as the cause; if PE is known, fibrinolysis, surgical embolectomy or percutaneous mechanical thrombectomy are options according to immediate capability.
3After thrombolysis, consider continuing CPR for 60–90 minutes. Consider ECPR for selected patients in an established system.
4DefinitiveAfter ROSC, proceed to definitive imaging/intervention, anticoagulation planning and critical-care bleeding/neurological monitoring.

03Stable RV injuryIntermediate-risk PE surveillanceNormotensive PE with RV dysfunction and/or myocardial injury but no shock.

1Admit to a closely monitored setting, start therapeutic anticoagulation and trend BP, perfusion, oxygen need and mental state.
2Do not offer routine systemic thrombolysis while haemodynamically stable under NICE NG158.
3Document a rescue-reperfusion plan and activate it if persistent hypotension, shock or arrest develops; re-evaluate bleeding contraindications before deterioration if possible.

04Thrombolysis unsuitableMechanical or surgical reperfusionHigh-risk PE with prohibitive bleeding risk, failed thrombolysis or rapid deterioration despite therapy.

1Contact the on-call interventional and cardiothoracic pathways immediately; share physiology, clot imaging, contraindications and last anticoagulant dose.
2Choose catheter thrombectomy/direct treatment or surgical embolectomy based on anatomy, expertise, bleeding risk and time to treatment; use ECMO only as a bridge/rescue in a capable service.
3Do not let referral conversations leave the patient without ongoing resuscitation, UFH planning and an explicit fallback if transfer fails.

Key medicines and prescribing safety3 treatments · regimens, roles and cautions

Systemic reperfusion for acute high-risk/massive PE with haemodynamic instability when benefit outweighs bleeding risk.

Alteplase for massive PE

Body weight at least 65 kg: 10 mg IV over 1–2 minutes, then 90 mg by IV infusion over 2 hours (total 100 mg). Below 65 kg: total dose must not exceed 1.5 mg/kg; follow the current Actilyse PE dosing table.

Major bleeding and intracranial haemorrhage; screen urgently for active bleeding, prior haemorrhagic stroke, recent major surgery/trauma and uncontrolled hypertension. Arrest may change the risk balance. Use only the PE-licensed vial/regimen and coordinate anticoagulation timing.

Rapidly adjustable anticoagulation when reperfusion, invasive procedures or severe instability are anticipated.

Unfractionated heparin

RCUK 2025 gives 80 units/kg IV during the diagnostic process unless bleeding or an absolute contraindication is present; continue with a specialist-prescribed IV infusion titrated to the service's APTT or anti-Xa target rather than an unmonitored fixed rate.

Active bleeding, HIT history and dosing errors. Check platelets/coagulation; the infusion target and post-thrombolysis restart must be explicitly prescribed and monitored.

Corrects hypoxaemia while obstruction and RV failure are treated.

Controlled oxygen

During peri-arrest/arrest use high-concentration oxygen; after ROSC or when reliable readings return, titrate usually to 94–98%, or 88–92% if at risk of hypercapnic respiratory failure pending gases.

Do not allow oxygen delivery or intubation attempts to delay reperfusion/ALS. Positive-pressure ventilation can reduce venous return and precipitate collapse; involve an experienced airway/critical-care clinician.

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

Cardiac arrest

Profound obstruction can eliminate effective pulmonary flow, commonly producing pulseless electrical activity and severe hypoxic injury.

Right-ventricular failure

Persistent pressure overload may cause ongoing low output, hepatic and renal congestion and difficulty recovering despite restoration of systemic pressure.

Major bleeding

Reperfusion and anticoagulation expose vulnerable sites to haemorrhage, particularly after recent surgery, trauma or intracranial disease.

Recurrent embolism

Ongoing thrombus formation or interruption of effective anticoagulation can produce further obstruction during an already unstable period.

Chronic thromboembolic disease

Failure of clot resolution and vascular remodelling may later cause persistent dyspnoea and pulmonary hypertension after apparent acute recovery.

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

Continuous ECG, SpO2 and frequent or invasive BP monitoring; trend consciousness, urine output, skin perfusion and lactate.
After thrombolysis, perform frequent neurological and bleeding checks; inspect lines, urine, stool, access sites and serial haemoglobin/fibrinogen according to the critical-care protocol.
Trend RV function, vasopressor requirement, lactate and end-organ function rather than judging success only from oxygen saturation.
Monitor UFH with the prescribed APTT/anti-Xa schedule and platelet count; document the precise restart time after thrombolysis/procedure.
After stabilisation, transition to a complete minimum-three-month anticoagulation plan and investigate ongoing dyspnoea/RV dysfunction at follow-up.

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

'Massive' describes physiology

A dramatic CT appearance without hypotension is not automatically a systemic-thrombolysis indication; shock can occur with less visually striking clot burden.

The RV dislikes indiscriminate fluid

A small, reassessed bolus can restore preload, but repeated litres increase RV wall tension and septal shift, reducing LV output.

Echo answers the unstable question

In shock it can support an immediate working diagnosis and reveal alternatives; in stability, isolated RV strain is a prognostic marker rather than proof of PE.

Thrombolysis changes the clock

In PE arrest, RCUK specifically supports prolonged CPR for 60–90 minutes after fibrinolysis because reperfusion is not instantaneous.

A rescue plan belongs before collapse

A stable patient with RV injury should have monitoring location, contraindication review and escalation contacts defined before hypotension occurs.

11Common pitfallsFrequent interpretation and management errors.

01
Calling a stable saddle embolus 'massive' and giving thrombolysis based on anatomy alone.
02
Sending a patient in obstructive shock to CT without resuscitation and a deterioration plan.
03
Giving repeated large fluid boluses to a distended failing RV.
04
Using bedside RV strain as definitive proof of PE when chronic pulmonary hypertension or another cause is plausible.
05
Stopping CPR shortly after fibrinolysis in suspected PE arrest.
06
Giving alteplase without confirming the PE regimen, weight cap, contraindication screen and post-dose anticoagulation plan.