ECG Interpretation Viva

Long Case Viva Defence

Candidate's opening statement (model answer)

"This 12-lead ECG shows atrial fibrillation with a controlled ventricular rate of approximately 78 per minute. The frontal QRS axis is leftward, consistent with left anterior fascicular block. The QRS is widened at 132 milliseconds with a left bundle branch block morphology. The QTc is 440 milliseconds, within normal limits. There are voltage criteria for left ventricular hypertrophy with lateral strain pattern, and pathological Q waves in V1 to V3 consistent with an old anterior infarction." [1]

"In summary, the ECG demonstrates established ischaemic cardiomyopathy with left bundle branch block, left ventricular hypertrophy, and evidence of prior anterior myocardial infarction, complicated by atrial fibrillation." [1]

Examiner probing questions and model answers

Q1: "How confident can you be about ischaemia in the presence of left bundle branch block?" [1]

"Left bundle branch block produces secondary repolarisation changes — discordant ST depression and T inversion opposite the dominant QRS — so I cannot read ischaemia in the usual way. To diagnose an occlusion infarction in LBBB, or in a paced rhythm, I apply the Sgarbossa criteria. Concordant ST elevation of at least one millimetre in a lead with a positive QRS scores five points; concordant ST depression of at least one millimetre in V1 to V3 scores three; and excessively discordant ST elevation of at least five millimetres scores two. A score of three or more is highly specific for occlusion MI, though sensitivity is modest. The modified Smith criteria replace the third rule with a proportional ST-to-S ratio of at least 25 per cent, which improves sensitivity while preserving specificity. In this patient there is no concordant ST change meeting Sgarbossa, so I have no ECG evidence of an acute occlusion — I would rely on troponin trend, symptoms, and serial ECGs, and consider echocardiography for new wall motion abnormality." [1]

Q2: "The QTc is 440 ms. What would change your concern about long QT, and how do you score it?" [1]

"A QTc above 470 milliseconds in men or 480 in women is prolonged, and above 500 milliseconds is high risk for torsades. I apply the Schwartz diagnostic score, which awards points for QTc — three points for 480 or more — plus points for torsades, T-wave alternans, notched T waves, syncope with or without stress, congenital deafness, and family history. A score of 3.5 or more is high probability of congenital long QT. Crucially, I would first exclude acquired causes — QT-prolonging drugs such as macrolides, fluoroquinolones, antipsychotics and methadone, hypokalaemia, hypomagnesaemia, hypocalcaemia, hypothyroidism and hypothermia — before attributing a long QT to a congenital channelopathy." [1]

Q3: "He develops a regular broad-complex tachycardia at 170. What is it, and what do you do?" [1]

"In a patient with ischaemic cardiomyopathy and left bundle branch block, a regular broad-complex tachycardia is ventricular tachycardia until proven otherwise — scar-related re-entry is the mechanism in most post-infarction patients. I would assess stability immediately. If he is pulseless, I defibrillate. If hypotensive but with a pulse, I perform synchronised cardioversion. If stable, I give intravenous amiodarone. I would not give verapamil or adenosine as a first move in a broad-complex tachycardia of uncertain origin — an AV-nodal blocker given to VT can precipitate cardiovascular collapse. After cardioversion I would search for a reversible trigger — ischaemia, electrolyte disturbance, drug effect — and arrange ICD therapy for secondary prevention if sustained VT is confirmed." [1]

Q4: "His potassium comes back at 6.8. Describe what you expect on the ECG and your immediate action." [1]

"Severe hyperkalaemia produces a recognisable ladder: tall peaked tented T waves, then flattening or loss of the P wave with PR prolongation, then widening of the QRS, and finally a sine-wave pattern merging the QRS and T wave that can progress to ventricular fibrillation or asystole. The immediate treatment is intravenous calcium gluconate — 10 millilitres of 10 per cent — to stabilise the myocardial membrane within minutes. Calcium does not lower the potassium, so I follow immediately with an insulin-dextrose infusion to shift potassium into cells, a beta-agonist such as salbutamol, and then definitive removal with a potassium binder or, if refractory, haemodialysis." [1]

Q5: "Why does the strain pattern of LVH look like ischaemia, and how do you tell them apart?" [1]

"Left ventricular hypertrophy produces a 'strain' repolarisation abnormality — asymmetric ST depression with T-wave inversion in the lateral leads I, aVL and V5 to V6 — because the thickened muscle repolarises abnormally. It mimics ischaemic ST depression. I distinguish them by context: the strain pattern is chronic and stable on serial ECGs, conforms to the LVH voltage distribution rather than an ischaemic territory, and is accompanied by voltage criteria. Ischaemic ST depression is dynamic, territory-related, and accompanied by symptoms and a troponin rise. When in doubt I compare with prior ECGs and trend troponin." [1]

Short Case Discussion

Scenario: "Interpret this ECG"

Candidate presentation (model): [1]

"I will interpret this ECG systematically. The rate is 150 per minute. The rhythm is regular. There is a narrow QRS at 90 milliseconds, and no discrete P waves are visible preceding the QRS — instead there is a sawtooth baseline, with around 300 flutter waves per minute, giving a 2-to-1 atrioventricular conduction. The axis is normal. The intervals that I can measure are normal. There are no ischaemic ST-T changes." [1]

"In summary, this is atrial flutter with 2-to-1 block conducting at 150 per minute — a classic regular narrow-complex tachycardia at this rate. The immediate manoeuvre would be vagal manoeuvres or adenosine to transiently increase AV block and unmask the flutter waves, then rate or rhythm control and anticoagulation assessment." [1]

Examiner: "Why 150 rather than sinus tachycardia or SVT?" [1]

"A regular narrow-complex tachycardia at exactly 150 per minute is atrial flutter with 2-to-1 block until proven otherwise, because the typical flutter rate is 300 per minute and the most common conduction ratio is 2-to-1. Sinus tachycardia would show discrete upright P waves in lead II with a 1-to-1 relationship, and AV-nodal re-entry tachycardia usually runs faster, at 170 to 220, with P waves buried in or just after the QRS. Adenosine is both diagnostic and therapeutic here: it will transiently block the AV node, expose the sawtooth flutter waves, and confirm the diagnosis." [1]

Examiner: "How would you decide between rate and rhythm control?" [1]

"For most patients presenting with atrial flutter, initial rate control with an AV-nodal agent — a beta-blocker or diltiazem — is reasonable and safe, with consideration of rhythm control by pharmacological cardioversion, electrical cardioversion, or catheter ablation. Ablation of the cavotricuspid isthmus is highly effective and curative for typical flutter. Anticoagulation follows the same stroke-risk logic as atrial fibrillation — I calculate the CHA₂DS₂-VASc score and recommend a direct oral anticoagulant if the score indicates. If the patient is haemodynamically unstable, I perform urgent synchronised cardioversion." [1]

Examiner: "What is the most dangerous mimic of flutter?" [1]

"A regular broad-complex tachycardia at 150 could be ventricular tachycardia with 2-to-1 or 1-to-1 conduction, or atrial flutter with aberrancy or pre-excitation. The width of the QRS and the morphology — concordance, fusion beats, AV dissociation — determine whether I treat it as VT or flutter with aberrancy. I would never give an AV-nodal blocker to a broad-complex tachycardia of uncertain origin without a defibrillator at the bedside." [1]