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]