ECG Interpretation — Clinical Case

DCE Long Case

Patient brief (provided to trainee)

Patient: Mr David Chen, 70 years old, retired engineer. [1]

Presenting complaint: Two episodes of rest chest pain overnight, each lasting 20 minutes and settling with sublingual glyceryl trinitrate. Now pain-free on the ward. [1]

Past history:

• Anterior STEMI 6 years ago — DES to proximal LAD
• Ischaemic cardiomyopathy, last known LVEF 32%
• Hypertension, type 2 diabetes (HbA1c 62), stage 3 CKD (eGFR 44)
• Paroxysmal atrial fibrillation [1]

Current medications:

• Aspirin 100 mg, atorvastatin 80 mg, bisoprolol 5 mg, ramipril 5 mg, spironolactone 25 mg, dapagliflozin 10 mg, apixaban 5 mg BD [1]

Examination findings (trainee elicits):

• Comfortable at rest at 45 degrees, BP 148/86, SpO₂ 97% on air
• Pulse irregularly irregular at 78/min
• JVP elevated 3 cm; apex displaced to 6th ICS, anterior axillary line, diffuse
• Soft S3 at apex; bilateral basal crackles to mid-zones; trace ankle oedema [1]

Investigations:

• ECG (the focus of the case): atrial fibrillation, ventricular rate 78, left axis deviation, QRS 134 ms with LBBB morphology, QTc 440 ms, old Q waves V1–V3, Sokolow-Lyon voltage for LVH with lateral strain
• High-sensitivity troponin: mildly elevated (2.5× upper limit of normal), with a flat trend
• Renal function and electrolytes within his baseline [1]

Candidate's structured presentation (model)

Opening statement: [1]

"Mr Chen is a 70-year-old retired engineer who presents with two episodes of rest chest pain overnight, now settled. He has a background of ischaemic cardiomyopathy from an anterior STEMI six years ago, with a last-known ejection fraction of 32 per cent, hypertension, type 2 diabetes, stage 3 chronic kidney disease, and paroxysmal atrial fibrillation." [1]

"His main problems are:

1. Possible acute coronary syndrome on a background of established ischaemic heart disease — but the ECG is confounded by LBBB
2. Heart failure with reduced ejection fraction — he has signs of mild congestion and an S3
3. Atrial fibrillation, now apparently persistent
4. Chronic kidney disease and diabetes — cardiorenal and metabolic overlap
5. Multimorbidity and polypharmacy requiring careful reconciliation"* [1]

ECG interpretation: [1]

"His ECG shows atrial fibrillation at a controlled ventricular rate of 78. The axis is leftward, consistent with left anterior fascicular block. The QRS is broad at 134 milliseconds with a left bundle branch block morphology. The QTc is normal at 440 milliseconds. There are old Q waves in V1 to V3 from his prior anterior infarction, and voltage criteria for left ventricular hypertrophy with a lateral strain pattern." [1]

"Because he has LBBB, I cannot read ischaemia in the usual way. I apply the Sgarbossa criteria: there is no concordant ST elevation or concordant ST depression in V1 to V3, and no excessively discordant ST elevation, so the score is zero — the ECG does not demonstrate an acute occlusion. I would therefore interpret his presentation as a possible non-occlusion myocardial infarction and rely on the troponin trend, symptoms, and serial ECGs, with echocardiography to look for a new wall-motion abnormality." [1]

Management plan: [1]

1. Acute coronary syndrome: continue aspirin and apixaban with cardiology input (balance ischaemic and bleeding risk), add or continue a P2Y12 inhibitor, treat as NSTEMI pathway with inpatient angiography given the high-risk features (rest pain, diabetes, CKD, prior PCI). Do NOT stress test.
2. Heart failure: confirm he is on all four GDMT pillars (he is — ARNI would be preferred over ACEi if tolerated), address congestion with loop diuretic, reassess LVEF, assess for ICD/CRT (his QRS is 134 ms — if LBBB morphology, he may qualify for CRT).
3. Atrial fibrillation: rate control, confirm anticoagulation adequacy (apixaban 5 mg BD appropriate for his renal function), consider rhythm control if symptomatic.
4. Cardiorenal-metabolic: continue SGLT2 inhibitor, monitor renal function, diabetic optimisation.
5. Communication and follow-up: medication reconciliation, cardiac rehabilitation, advance care planning appropriate to his HF trajectory. [1]

Examiner discussion questions

Q: "How do you decide whether his chest pain is ischaemic given the LBBB?" [1]

"LBBB distorts repolarisation and obscures ST analysis, so I use the Sgarbossa criteria to look for an occlusion — concordant ST change or excessively discordant ST elevation. He meets none, so there is no occlusion ECG. I then assess the clinical probability of an ACS: he has rest pain, prior ischaemia, diabetes, CKD and prior PCI — all high-risk features. The mildly elevated troponin with a flat trend is consistent with chronic myocardial injury in heart failure rather than acute infarction, but a rising trend would change that. I would manage him as a possible NSTEMI with inpatient coronary angiography and echocardiography for a new wall-motion abnormality, and avoid functional stress testing." [1]

Q: "Would his QRS of 134 ms qualify him for cardiac resynchronisation therapy?" [1]

"Current guidelines consider CRT for patients with an LVEF of 35 per cent or less who are in sinus rhythm with a QRS of 130 milliseconds or more, particularly with LBBB morphology. He has the LVEF and the QRS duration, but he is now in atrial fibrillation — CRT benefit in AF is less well established and usually requires AV nodal ablation or strict rate control to ensure a high percentage of biventricular pacing. I would first address his rhythm: if he is to receive CRT, I would consider rhythm control or AV junction ablation to guarantee biventricular capture. I would discuss this with an electrophysiologist." [1]

Q: "He is on apixaban and aspirin. Should he continue both?" [1]

"After six years from his stent, his aspirin is for secondary prevention and his apixaban is for stroke prevention in AF. Continuing both long-term increases major bleeding without a clear ischaemic benefit in most patients. The standard approach after completing the dual-therapy window following PCI is to stop the aspirin and continue oral anticoagulation alone, unless there is a separate indication for aspirin such as recent stenting. Given his chronic kidney disease and age, I would favour stopping aspirin and continuing apixaban alone, after cardiology discussion." [1]

DCE Short Case — ECG Presentation

Instruction

"Interpret this 12-lead ECG. You have 4 minutes to interpret and 6 minutes for discussion." [1]

Key findings the ECG demonstrates

• Rate and rhythm: regular narrow-complex tachycardia at 150/min
• Baseline: sawtooth flutter waves at ~300/min, with 2:1 AV conduction
• Axis: normal
• No ischaemic ST-T changes [1]

Presentation template

"This is a 12-lead ECG recorded at 25 millimetres per second and standard calibration. The rate is 150 per minute. The rhythm is regular. The QRS is narrow at 90 milliseconds. The frontal axis is normal. There are no discrete P waves; instead the baseline shows a sawtooth pattern of atrial activity at approximately 300 per minute, with two flutter waves to each QRS — a 2-to-1 atrioventricular ratio. The ST segments and T waves are normal." [1]

"In summary, this is typical atrial flutter with 2-to-1 block, conducting at 150 per minute. A regular narrow-complex tachycardia at exactly 150 is atrial flutter until proven otherwise." [1]

Discussion

1. Immediate manoeuvre: vagal manoeuvres or adenosine to transiently increase AV block and unmask the flutter waves for confirmation.
2. Management: rate control (beta-blocker or diltiazem); rhythm control (electrical or pharmacological cardioversion, or catheter ablation of the cavotricuspid isthmus — curative for typical flutter); anticoagulation per CHA₂DS₂-VASc; urgent synchronised cardioversion if haemodynamically unstable.
3. Dangerous mimic: a regular broad-complex tachycardia at 150 could be ventricular tachycardia or flutter with aberrancy/pre-excitation — never give an AV-nodal blocker to a broad-complex tachycardia of uncertain origin without a defibrillator at the bedside. [1]

Examiner: "Name three ECG patterns you must never miss because they mandate immediate reperfusion."

"First, classic ST-elevation myocardial infarction meeting the two-contiguous-lead threshold. Second, the STEMI equivalents — de Winter T waves (upsloping ST depression with tall symmetrical T waves in the precordial leads, indicating proximal LAD occlusion), Wellens syndrome (deep symmetrical or biphasic T inversion in V2–V3 in a pain-free patient, indicating critical proximal LAD stenosis), and hyperacute T waves. Third, occlusion MI in LBBB or paced rhythm meeting the Sgarbossa or modified Smith criteria. Each of these requires activation of the catheter laboratory for immediate reperfusion." [1]