Cardio Vivas · pulmonary-circulation
Pulmonary embolism — structured viva
Structured oral on acute pulmonary embolism under the 2019 ESC and 2026 AHA/ACC guidelines: the definition of high risk, reperfusion and contraindications, risk stratification, PEITHO, anticoagulant choice and duration, follow-up for chronic thromboembolic pulmonary hypertension, and THANZ duration advice.
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Practice viva. You are the cardiology registrar. The examiner describes a 64-year-old man with sudden breathlessness at home, then follows him from the emergency department to the follow-up clinic.
Branch A — Is he high risk?
Examiner: Pulmonary embolism (PE) is suspected. His blood pressure (BP) is 84/50 mmHg and has stayed there for 20 minutes despite fluids, with no new arrhythmia, hypovolaemia or sepsis. What defines high-risk PE?[1]
Strong answer:
- ESC 2019 defines high-risk PE by haemodynamic instability, i.e. one of the following at presentation: cardiac arrest; obstructive shock (systolic BP under 90 mmHg or vasopressors needed to reach 90 mmHg despite adequate filling, with end-organ hypoperfusion); or persistent hypotension (systolic BP under 90 mmHg or a drop of 40 mmHg or more, lasting longer than 15 min and not caused by new-onset arrhythmia, hypovolaemia or sepsis).[1]
- ESC 2019: in suspected high-risk PE, bedside echocardiography or emergency CT pulmonary angiography (CTPA), depending on availability and clinical circumstances, is recommended for diagnosis (Class I, level C), and intravenous (IV) unfractionated heparin (UFH) with a weight-adjusted bolus is recommended without delay (Class I, level C).[2]
Follow-up: Echocardiography shows no right ventricular (RV) overload. What does that tell you?[1]
Answer:
- In suspected high-risk PE, the absence of echocardiographic signs of RV overload or dysfunction practically excludes PE as the cause of haemodynamic instability.[1]
- Echocardiography may then help in the differential diagnosis of shock by detecting pericardial tamponade, acute valvular dysfunction, severe global or regional left ventricular dysfunction, aortic dissection or hypovolaemia.[1]
Branch B — Reperfusion
Examiner: A different patient: the same persistent hypotension (haemodynamic instability), but the RV is dilated and PE is confirmed. How do you reperfuse?[2]
Strong answer:
- Systemic thrombolytic therapy is recommended for high-risk PE (ESC 2019, Class I, level B).[2]
- ESC Table 10 gives rtPA 100 mg over 2 h; an accelerated 0.6 mg/kg over 15 min (maximum 50 mg) regimen is not officially approved but is sometimes used in extreme haemodynamic instability such as cardiac arrest.[1]
- ESC 2019, high-risk PE in whom thrombolysis is contraindicated or has failed: surgical pulmonary embolectomy is recommended (Class I, level C) and catheter-directed treatment should be considered (Class IIa, level C), if appropriate expertise and resources are available on-site.[2]
Follow-up: What are the absolute contraindications to thrombolysis?[1]
Answer:
- ESC Table 10 lists history of haemorrhagic stroke or stroke of unknown origin; ischaemic stroke in the previous 6 months; central nervous system neoplasm; major trauma, surgery or head injury in the previous 3 weeks; bleeding diathesis; and active bleeding.[1]
Branch C — Risk stratification in the stable patient
Examiner: Back to our man: suppose instead that he is normotensive, with confirmed PE. How do you stratify him?[2]
Strong answer:
- In patients without haemodynamic instability, further stratification into intermediate- and low-risk categories is recommended (ESC 2019, Class I, level B), and clinical rules integrating severity and comorbidity, preferably the Pulmonary Embolism Severity Index (PESI) or simplified PESI (sPESI), should be considered for risk assessment in the acute phase of PE (Class IIa, level B).[2]
- ESC 2019: assessment of the RV by imaging methods (transthoracic echocardiography or CTPA) or laboratory biomarkers (cardiac troponins or natriuretic peptides) should be considered, even in the presence of a low PESI or a negative sPESI (Class IIa, level B).[2]
- Within the intermediate-risk group, both RV dysfunction and a raised cardiac biomarker (particularly a positive troponin) make him intermediate-high risk; if the RV appears normal on echocardiography or CTPA, and/or cardiac biomarkers are normal, he is intermediate-low risk.[1]
Follow-up: Why check the RV if the sPESI is 0?[1]
Answer:
- In a meta-analysis of 3295 patients with PESI I–II or sPESI 0, 34% were reported to have signs of RV dysfunction on echocardiography or CTPA, and ESC 2019 says that, until the clinical implications of such discrepancies are clarified, patients with RV dysfunction or elevated cardiac biomarkers despite a low PESI or an sPESI of 0 should be classified as intermediate-low risk.[1]
Branch D — Intermediate-high risk and thrombolysis
Examiner: His sPESI is 1, and he has RV dysfunction on CTPA and a positive troponin. Will you lyse him?[2]
Strong answer:
- Not routinely: routine use of primary systemic thrombolysis is not recommended in intermediate- or low-risk PE (ESC 2019, Class III, level B; footnote: the risk-to-benefit ratios of surgical embolectomy or catheter-directed procedures have not yet been established in intermediate- or low-risk PE).[2]
- In PEITHO (normotensive intermediate-risk PE; tenecteplase vs placebo, both with heparin), death or haemodynamic decompensation within 7 days occurred in 2.6% vs 5.6%, while extracranial bleeding was 6.3% vs 1.2% and stroke 2.4% vs 0.2%.[5]
- He should be monitored over the first hours or days because of the risk of early haemodynamic decompensation and circulatory collapse (ESC 2019 text), and rescue thrombolytic therapy is recommended if he deteriorates haemodynamically on anticoagulation (ESC 2019, Class I, level B).[1][2]
Follow-up: How does the 2026 AHA/ACC guideline frame the same decision?[3]
Answer:
- It describes the PEITHO population as consistent with its categories C3–D2. In categories D1–2 with an acceptable bleeding risk, in whom advanced therapy is being considered, systemic thrombolysis and anticoagulation may be considered over anticoagulation alone to prevent further clinical deterioration (class of recommendation [COR] 2b, level of evidence [LOE] C-LD); in category C3 with acceptable bleeding risk, in whom advanced therapy is being considered, the use of systemic thrombolysis and anticoagulation over anticoagulation alone to prevent further clinical deterioration is uncertain (COR 2b, LOE C-LD); and in categories A1–C2 systemic thrombolysis should not be used over anticoagulation alone, due to increased risk of major bleeding and intracranial haemorrhage (COR 3: Harm, LOE B-R).[3]
Branch E — Anticoagulant choice
Examiner: Which anticoagulant and why?[2]
Strong answer:
- If anticoagulation is started parenterally, low-molecular-weight heparin (LMWH) or fondaparinux is recommended over UFH for most patients (ESC 2019, Class I, level A); when oral anticoagulation is started in a patient eligible for a non-vitamin K antagonist oral anticoagulant (NOAC), a NOAC is recommended in preference to a vitamin K antagonist (VKA) (Class I, level A).[2]
- The AHA/ACC text describes initiation with regimens such as apixaban 10 mg twice daily for 7 days, rivaroxaban 15 mg twice daily for 21 days, or at least 5 days of parenteral anticoagulation before dabigatran or edoxaban.[3]
Follow-up: When would you avoid a NOAC?[2]
Answer:
- NOACs are not recommended in severe renal impairment, during pregnancy and lactation, and in antiphospholipid antibody syndrome (ESC 2019, Class III, level C); the row footnote defines severe renal impairment by drug: dabigatran is not recommended with creatinine clearance (CrCl) under 30 mL/min; edoxaban 30 mg once daily at CrCl 15–50 mL/min and not recommended under 15 mL/min; rivaroxaban and apixaban with caution at 15–29 mL/min and not recommended under 15 mL/min.[2]
Branch F — Duration
Examiner: No risk factor is identified for this first PE, and he has no cancer. How long do you treat?[2]
Strong answer:
- Therapeutic anticoagulation for 3 months or more is recommended for all patients with PE (ESC 2019, Class I, level A).[2]
- ESC 2019: for a first episode of PE with no identifiable risk factor, extended oral anticoagulation of indefinite duration should be considered (Class IIa, level A); his bleeding risk should be assessed to identify and treat modifiable bleeding risk factors, and it may influence decision-making on the duration and regimen/dose of anticoagulant treatment.[2]
- ESC 2019: if extended oral anticoagulation is decided, reduced-dose apixaban 2.5 mg twice daily or rivaroxaban 10 mg once daily should be considered after 6 months of therapeutic anticoagulation in patients without cancer (Class IIa, level A); if dabigatran or edoxaban is chosen for extended anticoagulation, the dose should remain unchanged, as reduced-dose regimens were not investigated in dedicated extension trials.[2]
Follow-up: What does AHA/ACC say?[3]
Answer:
- AHA/ACC 2026: after a first PE with no major reversible risk factor, continuing anticoagulation beyond the initial 3–6 months into the extended treatment phase (anticoagulation beyond the initial 3–6 months without an anticipated stop date) is beneficial to prevent recurrent venous thromboembolism (VTE) (COR 1, LOE A), and in the extended phase half-dose apixaban or rivaroxaban is recommended to reduce bleeding (COR 1, LOE A).[3]
Branch G — Follow-up and Australia/New Zealand
Examiner: He returns at 4 months still breathless. What next?[1][2]
Strong answer:
- ESC 2019 recommends routine clinical evaluation 3–6 months after acute PE (Class I, level B), for symptoms suggesting recurrence, bleeding, malignancy, or persistent or new-onset exercise limitation, and to decide on extension of anticoagulant treatment; in persisting dyspnoea and poor physical performance, transthoracic echocardiography should be considered to assess the probability of (chronic) pulmonary hypertension and thus possible chronic thromboembolic pulmonary hypertension (CTEPH), and a ventilation/perfusion (V/Q) scan should be considered with a high echocardiographic probability of pulmonary hypertension, or intermediate probability with raised N-terminal pro B-type natriuretic peptide (NT-proBNP) or risk factors or predisposing conditions for CTEPH (ESC 2019 text). Further diagnostic evaluation should be considered in patients with persistent or new-onset dyspnoea/exercise limitation after PE (ESC 2019, Class IIa, level C), as proposed in the guideline algorithm.[1][2]
- ESC 2019: in symptomatic patients with mismatched perfusion defects persisting on V/Q scan (alternatively, dual-energy CT may be used, if appropriate expertise and resources are available on-site) beyond 3 months, referral to a pulmonary hypertension/CTEPH expert centre is recommended, after taking into account echocardiography, natriuretic peptide levels and/or cardiopulmonary exercise testing (Class I, level C).[2]
Follow-up: What does the Australian and New Zealand guideline say about duration?[8]
Answer:
- THANZ guideline summary: proximal deep vein thrombosis (DVT) or PE caused by a major surgery or trauma that is no longer present should be treated for 3 months, and proximal DVT or PE that is unprovoked or associated with a transient non-surgical risk factor for 3–6 months, and proximal DVT or PE that is recurrent (two or more) and provoked by active cancer or antiphospholipid syndrome should receive extended anticoagulation; THANZ also says most patients with acute VTE should be treated with a factor Xa inhibitor and be assessed for extended anticoagulation, and for patients continuing extended anticoagulant therapy, either therapeutic or low-dose direct oral anticoagulants can be prescribed and are preferred over warfarin in the absence of contraindications.[8]
References5ShowHide
- [1]Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS). Eur Heart J, 2020.PMID 31504429
- [2]Konstantinides SV, Meyer G, Becattini C, et al. 2019 ESC Guidelines for the diagnosis and management of acute pulmonary embolism developed in collaboration with the European Respiratory Society (ERS): The Task Force for the diagnosis and management of acute pulmonary embolism of the European Society of Cardiology (ESC). Eur Respir J, 2019.PMID 31473594
- [3]Creager MA, Barnes GD, Giri J, et al. 2026 AHA/ACC/ACCP/ACEP/CHEST/SCAI/SHM/SIR/SVM/SVN Guideline for the Evaluation and Management of Acute Pulmonary Embolism in Adults: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines. J Am Coll Cardiol, 2026.PMID 41712898
- [5]Meyer G, Vicaut E, Danays T, et al. Fibrinolysis for patients with intermediate-risk pulmonary embolism. N Engl J Med, 2014.PMID 24716681
- [8]Tran HA, Gibbs H, Merriman E, et al. New guidelines from the Thrombosis and Haemostasis Society of Australia and New Zealand for the diagnosis and management of venous thromboembolism. Med J Aust, 2019.PMID 30739331