Pulmonary Embolism Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"Mrs Patel is a 74-year-old retired teacher who presented two days ago with acute pleuritic chest pain, dyspnoea, and presyncope. She has a background of stage 3 chronic kidney disease (eGFR 45), hypertension, and osteoarthritis. [1]

CT pulmonary angiography confirmed a large right lower lobe pulmonary embolus with right ventricular dilation. Her Wells score is 6 (PE likely). Troponin is mildly elevated at 0.05. Bedside echo shows RV dilation with preserved systolic function. Her sPESI is 2 (age over 80 not met, but pulse 110 and saturation 88 percent on room air). [1]

Her main problems are:

1. Unprovoked intermediate-high-risk pulmonary embolism on anticoagulation, requiring monitoring for decompensation
2. Right ventricular strain (echo RV dilation, mild troponin elevation)
3. Moderate chronic kidney disease (eGFR 45) — relevant to drug choice
4. An unprovoked event — needs malignancy and thrombophilia screening, and a decision on long-term anticoagulation" [1]

Examiner probing questions and model answers

Q1: "Walk me through how you arrived at the diagnosis and your immediate management." [1]

"My first step was a structured pre-test probability — I calculated the Wells score at 6, which is PE likely. In a PE-likely patient, a D-dimer has no role, because even a negative result does not lower the probability below the treatment threshold. I proceeded directly to CT pulmonary angiography, which confirmed a large pulmonary embolus with right ventricular dilation. In parallel, I commenced therapeutic anticoagulation immediately — you should not delay anticoagulation for imaging in a high-probability patient when there is no bleeding contraindication, because the disease risk exceeds the bleeding risk of a single day of treatment. I gave her a loading dose of apixaban, started high-flow oxygen for her hypoxaemia, established cardiac monitoring, and arranged bedside echocardiography to assess right ventricular function." [1]

Q2: "Her troponin is mildly elevated and her echo shows RV dilation. Is she a candidate for thrombolysis?" [1]

"She is intermediate-HIGH risk — normotensive but with right ventricular dysfunction on imaging AND a positive biomarker. The answer is NO, not as prophylactic (upfront) therapy. The PEITHO trial randomised intermediate-risk PE patients to tenecteplase versus placebo on top of anticoagulation. Lysis reduced the composite of death or decompensation, but at the cost of significantly increased major bleeding and an intracranial haemorrhage rate of around 2 percent. The net mortality benefit was absent. So my plan is anticoagulation plus close monitoring with a low threshold for RESCUE thrombolysis — I would give alteplase 100 mg over 2 hours the moment she becomes hypotensive or develops signs of shock. Catheter-directed thrombolysis is an option in a centre with interventional capability, delivering a fraction of the systemic lytic dose directly into the clot, but it is not mandatory." [1]

Q3: "She has an eGFR of 45. How does that affect your anticoagulation choice?" [1]

"Apixaban remains a valid choice at eGFR 45 — the AMPLIFY trial and subsequent renal sub-group analyses support its use in moderate renal impairment without dose adjustment at 5 mg twice daily. I would monitor her renal function closely, because a further decline below 30 would force a re-evaluation. Rivaroxaban can also be used at eGFR above 30, but I would avoid dabigatran, which is predominantly renally cleared and contraindicated in severe renal impairment. The 2.5 mg twice-daily apixaban dose reduction is NOT indicated here — it requires any two of age at least 80, weight at most 60 kg, or creatinine at least 133 micromol/L, and she does not meet two of these. If her renal function deteriorated significantly or she needed thrombolysis, I would switch to an unfractionated heparin infusion, which is rapidly reversible and dialysis-filterable." [1]

Q4: "This is an unprovoked PE. How long would you anticoagulate her?" [1]

"For a first unprovoked pulmonary embolism in a patient with a low bleeding risk, the recommendation is indefinite anticoagulation with periodic reassessment. The rationale is that the annual recurrence rate off anticoagulation after an unprovoked VTE is around 10 percent, and recurrent PE is frequently fatal. Before committing to indefinite therapy, I would complete two pieces of work: a focused malignancy screen — history and examination, age-appropriate screening (colonoscopy, mammography if applicable), and basic bloods — because around 10 to 20 percent of unprovoked PEs have an underlying cancer diagnosed within a year. And selective thrombophilia testing, though in a 74-year-old with a first event, the yield is low and the result would not change my plan unless antiphospholipid syndrome is found. I would discuss the trade-off with her: a small annual bleeding risk in exchange for a large reduction in recurrence, and review it annually." [1]

Q5: "What would you do if she became hypotensive during your shift?" [1]

"That converts her to high-risk (massive) PE, in which systemic thrombolysis is unequivocally indicated and immediately life-saving. I would give alteplase 100 mg intravenously over 2 hours alongside haemodynamic support — cautious IV fluids (no more than 250 mL boluses, because volume overload worsens right ventricular failure), noradrenaline for vasoplegia, and dobutamine if cardiac output is low. If thrombolysis was absolutely contraindicated — for example, recent intracranial haemorrhage or neurosurgery — I would arrange surgical pulmonary embolectomy or catheter-directed thrombectomy in a centre with that capability. In cardiac arrest, I would give a 50 mg intravenous bolus of alteplase and continue resuscitation, provided PE was the most likely cause." [1]

Q6: "What is the risk of CTEPH and how would you detect it?" [1]

"The cumulative incidence of chronic thromboembolic pulmonary hypertension after a symptomatic pulmonary embolism is around 0.4 to 4 percent over two years, as shown by Pengo et al. in the New England Journal in 2004. The patients at highest risk are those with recurrent PE, a large perfusion defect, younger age, and an idiopathic event. I would screen any patient who returns with persistent or new dyspnoea at three to six months. The screening test of choice is a ventilation-perfusion (V/Q) lung scan — a normal perfusion scan effectively excludes CTEPH, and it is more sensitive than CTPA for organised segmental thrombus. If the V/Q is abnormal, I would proceed to right heart catheterisation and pulmonary angiography to define anatomy, and refer operable disease for pulmonary endarterectomy, which is potentially curative." [1]

Short Case Discussion

Scenario: "Examine this patient's cardiovascular system"

Candidate presentation (model): [1]

"I examined Mrs Patel's cardiovascular system. She is comfortable at rest on room air with a respiratory rate of 16. She is not clubbed. The pulse is 92 and regular. The blood pressure is 132/82. The JVP is elevated 3 cm with a normal waveform. There is no peripheral oedema. [1]

On palpation there is a subtle right ventricular heave at the lower left sternal edge. The pulmonary component of the second heart sound is marginally accentuated. Heart sounds are otherwise normal with no murmurs. The chest is clear to auscultation. There is no hepatomegaly or ascites. The calves are symmetrical with no tenderness or swelling. [1]

In summary, these findings are consistent with a recent pulmonary embolism with residual mild right ventricular involvement, and no evidence of established pulmonary hypertension or right heart failure at this stage." [1]

Examiner: "Why is her JVP normal if she had right ventricular strain?" [1]

"The JVP reflects right atrial pressure. In the acute phase of a pulmonary embolism, right ventricular dilation raises right-sided filling pressures and the JVP rises. Now that she is two days into treatment and the clot burden is being lysed by her endogenous fibrinolytic system and protected by anticoagulation from extension, her right ventricular pressures have begun to normalise, and the JVP has fallen. A normal JVP at this stage is reassuring but does not mean the right heart is fully recovered — I would continue to monitor her with serial troponin and a repeat echocardiogram at 48 to 72 hours." [1]

Examiner: "What would change your mind about her risk?" [1]

"Two things would upgrade her to high-risk and trigger thrombolysis: a sustained fall in systolic blood pressure below 90, or signs of end-organ hypoperfusion — a rising lactate, falling urine output, or altered consciousness. A rising troponin or worsening right ventricular function on repeat echocardiography without haemodynamic change would keep her at intermediate-high risk but would lower my threshold for catheter-directed thrombolysis if a centre with that capability were available." [1]

Examiner: "Explain the loud P2 to a medical student." [1]

"The second heart sound is made of two components — the aortic valve closing (A2) and the pulmonary valve closing (P2). Normally A2 is louder and precedes P2 slightly, and P2 is soft. When pulmonary artery pressure rises — as it does when a pulmonary embolus obstructs the pulmonary bed — the pulmonary valve closes more forcefully, making P2 louder. A loud or palpable P2 is therefore a sign of pulmonary hypertension. Combined with a right ventricular heave, it indicates that the right heart is pumping against increased afterload, which is the haemodynamic signature of a significant pulmonary embolus." [1]