ECG Interpretation — Written Clinical Reasoning

SAQ 1 — Integrated ECG Interpretation and Management (20 marks, 30 minutes)

Prompt: Interpret this ECG systematically using the five-step approach, state the most likely diagnosis and the immediate, definitive and surveillance management, and justify each decision. Identify the key exam trap and how you would avoid it. [1]

Model Answer

Systematic five-step interpretation (5 marks): [1]

1. Rate: 88 per minute (300 ÷ 3.4 large squares) — normal.
2. Rhythm: Sinus — every P followed by a QRS, P axis normal (upright in II, inverted in aVR), PR constant, R–R regular.
3. Axis: Normal (positive QRS in I and aVF).
4. Intervals: PR normal, QRS < 120 ms, QTc 460 ms (borderline-long; Bazett formula).
5. Morphology: Two coexisting abnormalities — (a) deep symmetrical T-wave inversion in V2–V3 with preserved R waves; (b) Sokolow-Lyon voltage for LVH (SV1 + RV5 ≥ 35 mm) with lateral strain pattern (asymmetric ST depression and T inversion in I, aVL, V5–V6). [1]

Diagnosis (3 marks): [1]

The dominant acute finding is Wellens syndrome — deep symmetrical T-wave inversion in V2–V3 during a pain-free period, with preserved R waves and only a mildly elevated troponin. This indicates a critical stenosis high in the proximal LAD (de Zwaan, Bär and Wellens, 1982; PMID 6121481). The coexisting LVH with strain reflects his chronic hypertensive heart disease and is a chronic, not acute, change. [1]

Key exam trap (2 marks): The danger is treating this as a low-risk NSTEMI (because the patient is pain-free and the troponin is only mildly raised) and arranging functional testing. Wellens is specifically a pain-free phenomenon, and the ECG is most abnormal when the patient feels best. A stress test is contraindicated — provoking demand ischaemia in a critical proximal LAD stenosis risks occlusion and extensive anterior infarction. [1]

Immediate management (4 marks): [1]

1. Antiplatelet and antithrombotic therapy: Aspirin 300 mg loading then 100 mg daily, plus a P2Y12 inhibitor (ticagrelor 180 mg load then 90 mg BD, or clopidogrel if high bleeding risk), plus parenteral anticoagulation (unfractionated heparin or fondaparinux).
2. Urgent coronary angiography — NOT a routine NSTEMI 72-hour pathway, and NOT an outpatient stress test. The aim is to identify and revascularise the critical proximal LAD lesion (PCI with drug-eluting stent, or CABG if complex anatomy).
3. Secondary prevention: High-intensity statin (atorvastatin 80 mg), beta-blocker, and an ACE inhibitor or ARB (cautious dosing given CKD; monitor renal function and potassium).
4. Glucose control and smoking cessation counselling as part of secondary prevention. [1]

Definitive and longitudinal management (3 marks): [1]

• Post-revascularisation: dual antiplatelet therapy for 12 months (longer if stent-specific guidance), high-intensity statin, beta-blocker, RAAS blocker, SGLT2 inhibitor (cardiovascular + renal benefit in diabetes with CKD).
• Optimise blood pressure to < 130/80 with the above regimen; address the LVH substrate.
• Echocardiography to assess left ventricular function and wall motion; if LVEF is reduced, institute GDMT for HFrEF.
• Cardiac rehabilitation, diabetic optimisation, nephrology co-management for CKD. [1]

Surveillance and communication (2 marks): [1]

• Serial ECGs during the admission to detect evolution (development of pathologic Q waves, persistent T inversion).
• Explain to the patient in plain language: "You have a severe narrowing in the main artery on the front of your heart. We need to look with a coronary angiogram and likely open it with a stent today or tomorrow to prevent a major heart attack."
• Document the Wellens pattern explicitly in the chart so the catheter-lab team understands the urgency. [1]

High-yield discriminating question the examiner will ask (1 mark): [1]

"How do you distinguish Wellens from other causes of deep anterior T-wave inversion?" Answer: Wellens is characterised by (1) the pain-free timing, (2) preserved R waves (no infarction yet), (3) minimal/no troponin rise, and (4) a critical proximal LAD stenosis at angiography. Other causes of deep anterior T inversion — evolving STEMI (which has ST elevation or Q waves), apical HCM (giant T inversion with LVH voltage), pulmonary embolism (S1Q3T3, sinus tachycardia, right-heart strain), and stress (takotsubo) cardiomyopathy — do not share this combination. [1]

SAQ 2 — Wide-Complex Tachycardia: Diagnostic Reasoning (20 marks, 30 minutes)

Prompt: A 72-year-old woman with a prior anterior STEMI (stented LAD 4 years ago) and an LVEF of 35% presents with sudden-onset palpitations and presyncope. Her ECG shows a regular broad-complex tachycardia at 170/min with a QRS of 160 ms, a leftward (northwest) frontal axis, and positive concordance of the QRS across the precordial leads (all positive V1–V6). Blood pressure is 90/60. Outline your systematic approach to diagnosis, the immediate management, and the reasoning that distinguishes VT from SVT with aberrancy. [1]

Model Answer

Diagnosis: ventricular tachycardia (3 marks). [1]

The default diagnosis for any regular broad-complex tachycardia in a patient with structural heart disease (prior infarction, LVEF 35%) is ventricular tachycardia until proven otherwise. Multiple features here confirm VT: positive precordial concordance (highly specific for VT), extreme axis deviation, very broad QRS, and the substrate of prior infarction. AV dissociation, if present, would be pathognomonic. [1]

Immediate management (5 marks): [1]

1. Assess haemodynamic stability. This patient is hypotensive with presyncope — she is unstable.
2. Synchronised direct current cardioversion (sedated) is first-line for an unstable VT. Begin with 150–200 J biphasic.
3. If pulseless VT → defibrillation (unsynchronised) and commence the ALS cardiac-arrest algorithm.
4. If she were stable, pharmacological management would be IV amiodarone 300 mg over 20–60 minutes, or procainamide.
5. Correct reversible contributors: electrolytes (K+, Mg2+), ischaemia (check troponin, repeat ECG after cardioversion), and drug effect. [1]

Diagnostic reasoning — VT versus SVT with aberrancy (6 marks): [1]

The Brugada algorithm applies these stepwise: if there is AV dissociation, or a morphology criterion for VT, the diagnosis is VT. [1]

The safety-critical rule (3 marks): [1]

A regular broad-complex tachycardia should be treated as VT when in doubt. Giving an AV-nodal blocker (verapamil, diltiazem, adenosine) to VT can cause cardiovascular collapse and VF — this is a classic and dangerous error. Adenosine is acceptable only as a diagnostic challenge in a stable, monitored patient with a clear narrow-complex differential, and even then with defibrillation pads on. [1]

Long-term management after cardioversion (3 marks): [1]

• Search for the trigger: ischaemia (the prior stent may have re-stenosed), electrolyte disturbance, scar-related re-entry.
• Implantable cardioverter-defibrillator for secondary prevention of sustained VT (if not already in situ), provided survival expectancy exceeds one year.
• Beta-blocker (maximally tolerated), and consideration of amiodarone or catheter ablation for scar-related VT.
• Optimise HFrEF guideline-directed therapy (ARNI, beta-blocker, MRA, SGLT2i) — improving the substrate reduces arrhythmia risk. [1]

Key examiner discriminator (1 mark): "Why default to VT?" — Because in adults with structural heart disease, over 90% of regular broad-complex tachycardias are VT, and mistaking VT for SVT and giving verapamil is potentially fatal. The cost of treating VT as VT when it is actually SVT is small (a cardioversion or amiodarone); the cost of treating VT as SVT is death. [1]