ECGs sit across SLO3 (resuscitation) and SLO1 (the stable patient with chest pain), and they turn up in some form almost every sitting. But the exam is written at the level of a day-one consultant — the person the department turns to when the registrar isn’t sure. So the testable ECG is rarely the textbook STEMI. It’s the subtle equivalent, the toxicological clue, the channelopathy that explains the young collapse, the rhythm that looks like one thing and is another.
This guide is organised by theme. For each pattern we give the recognition features, what it means, and the consultant-level point — the reason it matters and the trap it sets. Where a pattern can be confused with something else, we say so, because that confusion is usually the question.
This list isn’t exhaustive — it’s a working set of the ECGs the exam tends to test most often. Treat it as a high-yield starting point, not the complete syllabus.
1. ACS & STEMI equivalents — the ones without obvious ST elevation
The STEMI criteria miss a meaningful number of acute coronary occlusions. The patterns below are occlusions (or critical stenoses) that don’t meet ST-elevation criteria — which is exactly why they get sent home. Recognising them is the difference between a cath lab referral and a coroner’s referral.
This ECG shows: ST elevation in aVR with widespread ST depression in the inferolateral and anterior leads (I, II, aVF, V3–V6) — the diffuse subendocardial-ischaemia pattern (here driven by demand ischaemia). · Ko W, Hurng G, Zhou R, Dai X. Cureus 2020;12(11):e11800. CC BY 4.0.
Recognise it:
- Widespread ST depression — typically in I, II and V4–6 (often 6–8 leads)
- ST elevation in aVR, with STE in aVR > V1 being the more specific pattern
- STE in aVR ≥1 mm carries the most weight; ≥0.5 mm is still significant in context
What it means: historically taught as “left main occlusion”, but that teaching has largely been overturned. The modern understanding is that this pattern usually reflects global subendocardial ischaemia from severe diffuse or triple-vessel disease (a supply–demand mismatch), rather than an acute occlusion at all. In one 2019 analysis only ~10% of these ECGs had a coronary occlusion, and none involved the LAD or left main. Where the left main is implicated it tends to be subocclusion, or a complete occlusion protected by well-developed collaterals — because a true acute total left-main occlusion presents in extremis with widespread ST elevation (and often sudden death), not this picture.
This ECG shows: broad, bulky hyperacute T waves in V2–V4, large relative to the QRS, with early ST elevation — an evolving LAD occlusion. Note: hyperacute Ts and early ST elevation often coexist; the purest pre-ST-elevation examples are fleeting. · Poyorena C, Allen C, Querin LB. Cureus 2025;17(11):e96989. CC BY 4.0.
Recognise it: broad-based, asymmetrically peaked T waves that are disproportionately large for the QRS, appearing in a coronary territory in the earliest minutes of occlusion — they often precede ST elevation and Q waves.
This ECG shows (Type A): biphasic T waves in V1–V3 (arrows) in a pain-free patient — the subtler Wellens pattern; critical proximal/ostial LAD stenosis at angiography. · Arisha MJ, Hallak A, Khan A. Case Rep Emerg Med 2019;2019:1582030. CC BY.
This ECG shows (Type B): deep, symmetric T-wave inversion in V2–V4 in a pain-free patient — the more common Wellens pattern. · James Heilman, MD, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Recognise it:
- Type A (~25%): biphasic T waves in V2–3 (initial positivity, terminal negativity)
- Type B (~75%): deep, symmetric T-wave inversion in V2–3
- Recorded in a pain-free patient with recent angina; isoelectric or minimal (<1 mm) ST elevation; preserved R-wave progression; no precordial Q waves; normal or only slightly raised troponin
What it means: critical stenosis of the proximal LAD — a warning sign of imminent extensive anterior MI over the following days to weeks.
And because the changes are dynamic, they often appear on the ambulance ECG and may have normalised by the time the patient reaches you — always pull up and review the paramedic tracing. The prehospital ECG can be the only evidence of the event.
This ECG shows: upsloping ST depression at the J point continuing into tall, symmetric T waves in V2–V5 (arrows) — the de Winter pattern of acute proximal LAD occlusion. · Hsiao C-Y, Wu K-Y. Cureus 2026;18(2):e102984. CC BY 4.0.
Recognise it:
- Upsloping ST depression >1 mm at the J point in the precordial leads (V1–6)
- Continuing into tall, prominent, symmetric T waves
- Reciprocal ST elevation (0.5–1 mm) in aVR
- No (or minimal) ST elevation in the precordials despite acute occlusion
What it means: acute proximal LAD occlusion — a recognised anterior STEMI equivalent requiring immediate reperfusion, even though it fails ST-elevation criteria. It occurs in ~2% of LAD occlusions and is frequently missed.
This ECG shows: anterior ST depression in V1–V3 (top, here on a background of RBBB — note the rSR′ in V1) which should prompt posterior leads; the lower strip shows the posterior leads V7–V9. Note: this is the RBBB variant — it illustrates “anterior ST depression → look posterior” rather than the classic tall dominant R wave. · Ramjaun A, Garg A, Klaiman M, Sibbald M, Dong JK. Cureus 2021;13(2):e13281. CC BY 4.0.
Recognise it: in the anterior leads V1–3 you see the mirror image of a posterior STEMI — horizontal ST depression, tall broad R waves (R > S in V2), and upright T waves. Confirm with posterior leads V7–9, which show the ST elevation directly (≥0.5 mm).
What it means: isolated or accompanying posterior infarction (usually circumflex or right coronary territory). Often partners an inferior or lateral STEMI.
This ECG shows: ST elevation in I, aVL and V2 with reciprocal ST depression in III (arrows, lower panel) — the South African flag sign; the upper panel superimposes the flag to show how the affected leads map onto its shape. · Luckmann J, Win S, Ajagbe T, Samarawickrama T. Cureus 2025;17(3):e81468, Fig 1. CC BY 4.0.
Recognise it:
- ST elevation in I, aVL and V2 — a non-contiguous trio
- Reciprocal ST depression in lead III (and often the other inferior leads)
- The elevated leads (I, aVL, V2) plus the depressed inferior lead map onto the 12-lead layout in a shape echoing the South African flag — a deliberate visual mnemonic
What it means: acute occlusion of the first diagonal branch (D1) of the LAD — a high (mid-anterior) lateral STEMI.
This ECG shows: a ventricular-paced rhythm meeting Sgarbossa criteria for acute MI — grossly, excessively discordant ST elevation in the inferior leads (II, III, aVF) on a deeply negative paced QRS. Note: Sgarbossa applies identically to LBBB and to paced rhythms; a clean, commercially-licensed true-LBBB example is scarce, so a paced example is shown here. · O’Rorke J, Butler G, Chandra R. Cureus 2025;17(3):e80192. CC BY 4.0.
In LBBB or a paced rhythm, the usual ST criteria don’t apply. The Sgarbossa criteria identify acute MI:
- Concordant ST elevation ≥1 mm in any lead (the most specific) — 5 points
- Concordant ST depression ≥1 mm in V1–3 — 3 points
- Excessively discordant ST elevation ≥5 mm — 2 points
A score of ≥3 is specific for MI. The modified (Smith) criterion replaces the 5 mm rule with a discordant ST/S-wave ratio ≤ −0.25, which is considerably more sensitive.
2. The ischaemia mimics — ST/T changes that aren’t coronary
Not every dramatic ST/T abnormality is an acute coronary syndrome. Two in particular catch people out — one because it sends a non-cardiac patient to the cath lab, the other because a “normal-ish” ECG falsely reassures.
This ECG shows: deep, symmetric T-wave inversions across V2–V5 (arrows) — classic “cerebral T waves” following an acute cerebrovascular event (they met the formal criterion of ≥5 mm inversion in ≥4 precordial leads, and resolved over days). · Hamilton S, Tauseen RA, Wallach SL, Kaplan AC. Cureus 2021;13(6):e16023. CC BY 4.0.
Recognise it: deep, wide, symmetric T-wave inversions — often giant and most marked in the precordial leads — frequently with QT prolongation and prominent U waves. Classically seen with raised intracranial pressure, subarachnoid haemorrhage and large ischaemic strokes (a catecholamine/autonomic surge driving repolarisation abnormality).
This ECG shows: sinus tachycardia with S1Q3T3 — an S wave in lead I (red arrow) and a Q wave with inverted T in lead III (arrows). Note: in this case the right-heart strain was caused by a massive empyema, not PE, but the S1Q3T3 pattern itself is the textbook one. · Mohammadi M, Valizadeh M, Rahmani-ju N, Khosravaninezhad Y. Clin Case Rep 2025;13(2):e70191. CC BY 4.0.
This ECG shows: deep, symmetric T-wave inversion in V1–V4 (extending to the inferior leads) in sinus rhythm — the right-heart-strain pattern of a confirmed acute PE; the more specific ECG sign and the one that matters for risk stratification. · Zhang X-Y, Li J-X, Gao M, Li X-Q, Zhang M-Y. Ann Noninvasive Electrocardiol 2025;30(2):e70049. CC BY 4.0.
Recognise it:
- Sinus tachycardia — the commonest finding by far
- T-wave inversion in V1–V4 (right ventricular strain) — the more specific sign, especially when it also involves the inferior leads
- S1Q3T3 — the “classic”, but present in only a minority and neither sensitive nor specific
- Right bundle branch block (complete or incomplete), right axis deviation, P pulmonale
3. Toxicology — the ECG as a poisoning clue
In the undifferentiated overdose, the ECG is part of the toxidrome. Three are heavily examinable because the ECG changes direct management.
Digoxin effect (expected at therapeutic levels — not a marker of toxicity): down-sloping “reverse-tick” / scooped ST depression (the “Salvador Dalí sagging”), flattened, inverted or biphasic T waves, a mildly shortened QT, prominent U waves, and mild PR prolongation. These are benign, expected changes that simply tell you the patient takes digoxin — the arrhythmia risk comes from toxicity (below), not from these repolarisation changes.
This ECG shows: down-sloping, scooped “reverse-tick” ST depression (the “Salvador Dalí sagging”), most visible in the lateral leads — the digoxin effect, an expected repolarisation change rather than a sign of toxicity. · James Heilman, MD, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Digoxin toxicity: increased automaticity plus AV block is the hallmark. Watch for frequent ventricular ectopy, paroxysmal atrial tachycardia with block, slow (regularised) AF, various AV blocks, and the near-pathognomonic bidirectional VT.
This ECG shows: bidirectional VT — beat-to-beat alternation of the QRS axis — a specific sign of digoxin toxicity (contrast the benign scooped ST “effect” above). · Aung TP, Buddhavarapu S, Park WJ, et al. Cureus 2021;13(5):e15134. CC BY 4.0.
This ECG shows: a broad QRS (~164 ms) with a rightward terminal axis and a terminal R wave in aVR — sodium-channel blockade, here from bupropion (the same mechanism as TCA toxicity). · Bruss P, Hartle R, Astacio J, Chauhdri AF. Cureus 2024;16(3):e56288. CC BY 4.0.
Recognise it:
- QRS prolongation — the key marker: >100 ms predicts seizures, >160 ms predicts ventricular arrhythmia
- Terminal R wave in aVR ≥3 mm (and a deep terminal S in I/aVL) — rightward shift of the terminal QRS axis
- Sinus tachycardia, QT prolongation, and a tendency to broad-complex arrhythmia
Seen with tricyclic antidepressants and other sodium-channel blockers (e.g. certain antiarrhythmics, quinine, some local anaesthetics).
This ECG shows: coved ST elevation in V1–V2 (a Brugada type-1 pattern) unmasked by cocaine in a severely poisoned patient — note the broad complexes and conduction delay from the sodium-channel effect; it resolved as the patient recovered. · Alraies MC, Chamsi-Pasha MAR, Baibars M, Alraiyes AH, Shaheen K. Case Rep Cardiol 2013;2013:704859. CC BY.
Recognise it: cocaine is both a sympathomimetic and a sodium-channel blocker, so the ECG can show almost anything — coronary vasospasm / ACS (ST elevation or ischaemia), QRS widening, a Brugada-type pattern, QT prolongation, LVH and tachyarrhythmias.
4. Electrolyte & metabolic patterns
The exam likes the less-drilled ones (hypokalaemia, the calcium QT changes) and likes you to act on the ECG before the bloods are back.
This ECG shows: tall, narrow, tented T waves across the precordial leads, with a serum potassium of 8.2 mmol/L. Note: this machine labels the precordial leads “U1–U6” and the augmented leads AUR/AUL/AUF (rather than V1–V6 and aVR/aVL/aVF) — the tented-T morphology is the teaching point. · Agbayani M-JF, Gonzales E, via Wikimedia Commons. CC BY 4.0.
Recognise the progression: peaked, narrow, tented T waves → P-wave flattening and loss with PR prolongation → QRS widening → sine wave → arrest. The changes track severity but unreliably — significant hyperkalaemia can present with a near-normal ECG.
This ECG shows: severe hypokalaemia (serum potassium 1.1 mmol/L) at a normal rate — prominent U waves, ST depression and T-wave flattening, giving the appearance of a long QT (really a long QU). · James Heilman, MD, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Recognise it: T-wave flattening / inversion, ST depression, and prominent U waves, giving the appearance of a long QT (really a long QU). The risk is torsades de pointes and ventricular arrhythmia.
This ECG shows (short QT — hypercalcaemia): a short QT interval (short ST segment) during hypercalcaemia. · Zhai S, Zhao Q, Wang J, Li L, Chen J, Zhang Z. Diagnostics (Basel) 2025;15(23):3034. CC BY 4.0.
This ECG shows (long QT — hypocalcaemia): marked QT prolongation (QTc ~0.52 s) from a long, flat ST segment with hypocalcaemia. · Miyao M, Aoki Y, Mizushiro N, Kitazawa R, Nakamura C. Cureus 2023;15(1):e34352. CC BY 4.0.
| Abnormality | ECG | Mechanism |
|---|---|---|
| Hypercalcaemia | Short QT (short ST segment); in severe cases Osborn-like J waves and bradyarrhythmia | Shortened repolarisation |
| Hypocalcaemia | Long QT (long, flat ST segment) — T-wave shape usually preserved | Prolonged repolarisation → TdP risk |
5. Structural disease & channelopathies — the young collapse
These are the ECGs behind the young patient with syncope, palpitations or a family history of sudden death. Recognising them changes disposition entirely — from “reassure and discharge” to “admit and refer to electrophysiology”.
This ECG shows (Type 1): coved ST elevation in V1–V2 with symmetric negative T waves (and a partial saddleback in V3) — the only diagnostic Brugada pattern. · Khan AR, Waqar S, Arif A, Ul Haq F, Shah MI. Cureus 2022;14(7):e26998. CC BY 4.0.
This ECG shows (Type 2): the “saddleback” pattern in V1–V2 (arrows) — a high take-off that dips to a saddle and rises into a positive/biphasic T wave; suggestive but not diagnostic. · Sattar Y, Ullah W, Zaidi SR, Almas T, Alraies MC. Cureus 2020;12(5):e8331. CC BY 4.0.
Recognise it: the only diagnostic pattern is Type 1 — coved ST elevation ≥2 mm in V1–V2 followed by a negative T wave. Type 2 is the “saddleback” — a high take-off in V1–V2 that dips to a saddle and rises into a positive or biphasic T wave; it is suggestive but not diagnostic, and may convert to a Type 1 with a sodium-channel-blocker challenge or by recording the leads an intercostal space higher. The pattern can be unmasked by fever, sodium-channel blockers, alcohol and electrolyte shifts, so it may be intermittent.
Know the high-risk features — a Type 1 pattern plus any of these mandates admission, cardiac monitoring and urgent cardiology/electrophysiology referral:
- Aborted sudden cardiac death, or documented VF / polymorphic VT
- Syncope — arrhythmic or unexplained (not clearly vasovagal)
- Nocturnal agonal respiration
- Family history of sudden cardiac death (especially <45 years)
- A spontaneous Type 1 pattern — higher risk than a drug- or fever-induced one
This ECG shows: deep, giant symmetric T-wave inversions across V2–V6 and the limb leads (arrows) — apical hypertrophic cardiomyopathy. Note: this is the apical (giant-TWI) variant, not the dagger-like septal Q waves of the obstructive form. · Rehman A, Chaudhary MA, Khan MY, Chishti SZ, Bibi F. Cureus 2025;17(8):e91364. CC BY 4.0.
Schematic (the dagger-Q variant): a lateral-lead complex showing a deep, narrow “dagger” septal Q wave (<0.04 s wide) followed by a tall R wave (LVH voltage) — the septal/obstructive HCM pattern, distinct from the apical giant-TWI above. Original illustration, FRCEM Mentor.
Recognise it: LVH by voltage, deep narrow (“dagger”) septal Q waves in the lateral and inferior leads, left atrial enlargement, and repolarisation changes. Apical HCM gives the striking picture of giant, deep symmetric T-wave inversions across the precordium.
This ECG shows: T-wave inversion in the right precordial leads with terminal notching after the QRS (epsilon waves) in V2–V3 — arrhythmogenic right ventricular cardiomyopathy. · Okonkwo ER, Schuetz C, Hyman B, Samuels B, Sayad D, Bower J. Cureus 2021;13(4):e14305. CC BY 4.0.
Schematic (the epsilon wave): a V1 complex showing the small terminal notch just after the QRS, on the early ST segment — the epsilon wave — with anterior T-wave inversion. Original illustration, FRCEM Mentor.
Recognise it:
- Epsilon wave — a small terminal notch/deflection at the end of the QRS in V1–V3 (the signature, though not always present)
- T-wave inversion in V1–V3 in an adult without RBBB
- Localised QRS prolongation / terminal activation delay in V1–V3
- Ventricular ectopy and VT of LBBB morphology (right-ventricular origin)
This ECG shows: sinus rhythm with a markedly prolonged QTc (~624 ms). · Ott WP, Bellamy SE, Khan M, Shahid A, Javed MT. Cureus 2023;15(4):e37263. CC BY 4.0.
Recognise it: a prolonged QTc (roughly >450 ms in men, >460 ms in women; >500 ms is high-risk), with a tendency to torsades de pointes. Causes are congenital (the LQT syndromes) or acquired — drugs (many antiarrhythmics, antipsychotics, macrolides, antiemetics), electrolyte disturbance (low K, Mg, Ca) and bradycardia.
Disposition — the structural & inherited group
In the ED your job with all of these is risk stratification. Admit, monitor and refer urgently to cardiology / electrophysiology any of these patterns when there is a red flag — syncope (especially exertional), aborted cardiac arrest, documented VT/VF, palpitations with the pattern, or a family history of sudden cardiac death. An asymptomatic, incidental finding can usually go to expedited outpatient cardiology with safety-netting and avoidance of provoking factors (QT-prolonging drugs; fever and the unmasking drugs in Brugada).
The family history is always a clue. A young relative who “died suddenly”, drowned, had an unexplained single-vehicle crash, or a “cot death” is the line the examiner has put in the stem to point you straight at a channelopathy or cardiomyopathy. And exertional syncope in a young person is a red flag until proven otherwise.
6. Tachyarrhythmias — getting the mechanism right
The exam tests the decisions that flow from the rhythm: which drug is safe, which is dangerous, and whether a broad complex is ventricular.
This ECG shows: an irregularly irregular rhythm with no P waves and uniformly broad QRS complexes (LBBB morphology) — AF with aberrant conduction, the irregular broad-complex picture that can be mistaken for VT. The giveaway remains the irregularity. · Steven Fruitsmaak, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Recognise it: irregularly irregular rhythm with no discernible P waves. When AF conducts with a bundle branch block (rate-related or pre-existing), the complexes are broad — AF with aberrancy — and can be mistaken for VT. The giveaway is the irregularity.
Schematic: the pre-excitation complex — a short PR and a delta wave, the slurred initial upstroke of the QRS. Original illustration, FRCEM Mentor.
Recognise it (sinus rhythm): short PR, a delta wave (slurred QRS upstroke) and a widened QRS — ventricular pre-excitation via an accessory pathway.
This ECG shows: sinus rhythm with a short PR interval and delta waves (slurred QRS upstrokes, clearest in the precordial leads) — the WPW pattern at normal rate. · James Heilman, MD, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
AF in WPW: an irregular, broad-complex tachycardia with varying QRS morphology. The accessory pathway has no rate-limiting properties, so the rate is often very fast (frequently >200 bpm) — and that very rapid, irregular, broad-complex picture should make you suspect pre-excited AF and look carefully for pre-excitation. Conduction can be dangerously rapid and degenerate to VF.
This ECG shows: an irregular, very fast, broad-complex tachycardia with varying QRS width and morphology (up to ~300 bpm) — pre-excited AF (AF in WPW), the dangerous picture. · Salinas-Ulloa CY, Pineda-Pineda LW, Salinas-Ulloa JC, et al. Arch Cardiol Mex 2024;95(1):119–121. CC BY.
This ECG shows (VT): a broad-complex tachycardia in every lead, with the rhythm strip (lead II, arrows) marking dissociated P waves and fusion/capture beats, and near-concordant precordial leads — the features that confirm VT. · Michael Rosengarten BEng, MD (McGill) / CardioNetworks ECGpedia, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Schematic (concordance): positive concordance — every precordial QRS (V1–V6) points the same way (all upright). Negative concordance (all downward) is equally suggestive of VT. Original illustration, FRCEM Mentor.
This ECG shows (SVT with aberrancy): a regular, broad-complex tachycardia (QRS ~166 ms, RBBB-pattern) that initially met VT criteria but was confirmed to be AVNRT with aberrancy — i.e. supraventricular — on electrophysiology study. The honest lesson: it ticked several VT boxes, which is exactly why a regular broad-complex tachycardia is treated as VT until proven otherwise. · Fahed J, Mohammad A, Afraz R, Moodie D, Georges C. Cureus 2025;17(5):e83846. CC BY 4.0.
This is the hard end of ECG reading, and the exam tests it directly — you may be shown a broad-complex trace and asked which features favour VT. So you need to be able to recognise each one on the tracing, not just recite the list:
- AV dissociation — P waves marching through at their own, independent rate (search the baseline for them). The most specific sign.
- Capture beats — an occasional narrow, normal-looking QRS interrupting the broad run (a sinus impulse briefly “captures” the ventricle).
- Fusion beats — a hybrid complex, intermediate in shape between a normal beat and the broad VT beat (sinus and ventricular impulses collide).
- Concordance — all the precordial QRS complexes (V1–V6) pointing the same way, all positive or all negative.
- Extreme (“northwest”) axis — negative in both I and aVF.
- Very broad QRS — >140 ms with RBBB-like morphology, >160 ms with LBBB-like morphology.
- Brugada-criteria features — no RS complex in any precordial lead, or an RS interval (R onset to S nadir) >100 ms in a precordial lead.
- History — known IHD, prior MI or structural disease shifts the odds heavily towards VT.
Capture and fusion beats are effectively pathognomonic of VT — if you can find one, you have your answer.
RVOT VT — a specific exception worth knowing: a monomorphic VT of LBBB morphology with an inferior axis in a structurally normal heart. It is often relatively benign and adenosine/verapamil-sensitive — the mirror image of the “treat as VT” rule, but only once it’s confidently identified.
7. Bradyarrhythmias & pacing
Two skills here: grading AV block (which decides who needs pacing), and reading the paced ECG (including when it’s malfunctioning).
This ECG shows (Mobitz I / Wenckebach): progressive PR lengthening until a beat is dropped, then the cycle resets — a 5:4 Wenckebach period (with ladder diagram). · Jer5150, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
This ECG shows (Mobitz II): a constant PR interval with an intermittent non-conducted P wave (a dropped beat) — second-degree AV block, type 2. · James Heilman, MD, via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
This ECG shows (complete heart block): AV dissociation — P waves marching independently of a slow ventricular escape rhythm. · Sande K, Diaz O, Loyola G. Cureus 2025;17(3):e80851. CC BY 4.0.
| Block | ECG | Risk |
|---|---|---|
| First-degree | Fixed prolonged PR (>200 ms), every P conducts | Benign |
| Mobitz I (Wenckebach) | Progressive PR lengthening until a beat drops, then resets | Usually benign (AV nodal) |
| Mobitz II | Constant PR, then a sudden dropped beat (often with broad QRS) | High — risk of progression to complete block; needs pacing |
| Third-degree (complete) | AV dissociation — P waves and QRS independent, escape rhythm | High — pacing |
The building blocks — recognise each on the trace:
- RBBB: QRS ≥120 ms, an rSR′ (“M-shaped” / rabbit-ears) in V1–V2, and a wide slurred S wave in I, V5–V6 (with T-wave inversion V1–V3).
- Left anterior fascicular block (LAFB): left axis deviation — qR in I and aVL, rS in II, III and aVF (QRS only mildly widened on its own).
- Left posterior fascicular block (LPFB): right axis deviation — rS in I and aVL, qR in II, III and aVF (a diagnosis of exclusion — rule out RVH and a vertical heart first).
Bifascicular block = RBBB + one fascicle:
- RBBB + LAFB → an RBBB pattern with left axis deviation (the common one)
- RBBB + LPFB → an RBBB pattern with right axis deviation (rarer)
This ECG shows (bifascicular block): an RBBB pattern (rSR′ in V1) with left axis deviation (rS in II, III, aVF) — RBBB + left anterior fascicular block; the PR here is normal, so this is bifascicular, not trifascicular. · Gubitosa JC, Xu P, Ahmed A, Pergament K. Cureus 2020;12(9):e10461. CC BY 4.0.
Trifascicular block (as the exam uses the term): the bifascicular picture plus first-degree AV block (PR >200 ms) — implying delay in the one remaining fascicle. Alternating RBBB and LBBB is another form. (Strictly, “true” trifascicular block means complete heart block arising from disease of all three fascicles.)
This ECG shows (trifascicular block): sinus rhythm with RBBB + left anterior fascicular block and a prolonged PR interval of 240 ms (first-degree AV block) — the bifascicular-plus-first-degree picture. · Siagh S, Bouali M, Amrani M, Kheyi J, Bouzelmat H. Cureus 2025;17(11):e97262. CC BY 4.0.
This ECG shows: a ventricular-paced rhythm — a sharp pacing spike before each broad, LBBB-like QRS (right-ventricular pacing). · Jason E. Roediger (Jer5150), via Wikimedia Commons. CC BY-SA 3.0 (shared unmodified).
Normal paced rhythm: a pacing spike followed by a broad, LBBB-like QRS (right-ventricular pacing). Atrial pacing gives a spike before the P wave.
The malfunctions to recognise:
- Failure to capture — a pacing spike not followed by a complex
- Failure to pace / oversensing — no spike when one is due (the device wrongly senses noise as intrinsic activity)
- Failure to sense / undersensing — spikes appearing despite the patient’s own beats (risk of an R-on-T spike)
- Pacemaker-mediated tachycardia — an endless-loop re-entrant tachycardia at around the upper rate limit
The magnet — and it differs by device:
- Magnet over a pacemaker (PPM) → asynchronous (fixed-rate) pacing — the move for pacemaker-mediated tachycardia or oversensing.
- Magnet over an ICD → suspends shock/anti-tachycardia therapy only (pacing function is unchanged) — the move for inappropriate or repeated shocks. It does not make an ICD pace asynchronously.
How the FRCEM Final actually tests ECGs
Read the history before you read the trace. In a well-written SBA there are no wasted words — the stem is doing half the diagnostic work. A dialysis patient, a young athlete with exertional syncope, an overdose, a thunderclap headache, a previously fit 30-year-old with palpitations: each one primes you for a specific ECG before you’ve looked at a single complex. Form your hypothesis from the history, then read the ECG to confirm or refute it — not the other way round. This is exactly why so many of the patterns above come down to context (hyperacute T waves vs hyperkalaemia is chest pain vs a dialysis patient).
And notice what these patterns have in common: almost none is the obvious finding. The exam is built around the second look — the ST depression that’s really a posterior STEMI, the “normal” ECG with bulky T waves, the irregular broad complex that’s pre-excited AF, the long QT hiding a stacked drug chart. The question usually rewards the candidate who acts on the subtle sign and the action that follows it (primary PCI, bicarbonate, calcium, magnesium, no AV nodal blocker), not the one who simply names the rhythm.
So when you practise ECGs, practise the decision, not just the label. For where ECGs sit in the wider revision picture, see our high-yield topics guide; and if you’re returning from a fail, start with what to do after failing FRCEM Final.
Want more detail and examples? The LITFL ECG Library is an excellent companion for further clarification, worked examples and a library of real ECGs — make regular self-testing on these part of your revision. Pattern recognition is a trained skill: the more ECGs you read, the faster the subtle ones jump out. As always, interpret any ECG within the whole clinical picture.
ECG SBAs that test the decision, not just the label
Realistic FRCEM Final ECG questions mapped to the blueprint, with explanations that teach the consultant-level call — plus coaching and support when you need it.
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