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ECG library

27 patterns worth recognising on sight. Each one carries a tracing, the features that identify it, the mechanism underneath, what it changes about management, and the mistake the question is usually built around.

Ischaemia and infarction

Anterior STEMI

Convex ST elevation across the anterior chest leads — the LAD occlusion you cannot afford to sit on.

78 bpm · Sinus

Inferior STEMI

ST elevation in II, III and aVF with reciprocal change in aVL — and a right ventricle you must check before giving nitrates.

52 bpm · Sinus bradycardia

Posterior myocardial infarction

Tall R waves and ST depression in V1–V3 — a STEMI viewed from behind, and easy to call NSTEMI by mistake.

84 bpm · Sinus

Wellens' syndrome

Deep or biphasic T waves in V2–V3 in a pain-free patient — critical LAD stenosis waiting to declare itself.

72 bpm · Sinus

De Winter T waves

Upsloping ST depression with tall symmetrical T waves in the chest leads — an LAD equivalent without the elevation.

88 bpm · Sinus

Acute pericarditis

Widespread concave ST elevation with PR depression — and no reciprocal change to speak of.

96 bpm · Sinus tachycardia

Tachyarrhythmias

Atrial fibrillation

Irregularly irregular narrow complexes with no P waves and a wandering baseline.

130 bpm, variable · Irregularly irregular

Atrial flutter

Sawtooth flutter waves at about 300 per minute, usually conducted 2:1 to give a ventricular rate near 150.

150 bpm · Regular, 2:1 conduction

AV nodal re-entrant tachycardia

Regular narrow complex tachycardia around 180 with P waves hidden inside or just after the QRS.

185 bpm · Regular, narrow complex

Monomorphic ventricular tachycardia

Broad, regular, identical complexes — assume VT in any broad complex tachycardia until you have proved otherwise.

165 bpm · Regular, broad complex

Torsades de pointes

Polymorphic VT twisting around the baseline, on a background of a long QT.

~250 bpm · Polymorphic, self-terminating

Ventricular fibrillation

Chaotic, irregular deflections with no identifiable complexes — a shockable cardiac arrest rhythm.

Unmeasurable · Chaotic

Conduction disease

First degree AV block

A PR interval over 200 ms with every P wave still conducted.

68 bpm · Sinus with prolonged PR

Mobitz I (Wenckebach)

The PR interval lengthens beat by beat until one P wave fails to conduct.

62 bpm · Grouped beating, 4:3 conduction

Mobitz II AV block

P waves drop without warning while the PR interval stays fixed — infranodal disease, and a pacemaker indication.

48 bpm · Sinus with intermittent 2:1 block

Complete (third degree) heart block

P waves and QRS complexes marching independently, with a slow escape rhythm keeping the patient alive.

Atrial 88, ventricular 38 · AV dissociation

Left bundle branch block

Broad QRS with a notched R in the lateral leads — and repolarisation you can no longer interpret at face value.

76 bpm · Sinus

Right bundle branch block

rSR′ in V1 with a broad terminal S in the lateral leads — often benign, occasionally the clue to something else.

74 bpm · Sinus

Chambers and pre-excitation

Wolff–Parkinson–White pattern

Short PR, delta wave and a broad QRS — an accessory pathway with a direct line to the ventricle.

70 bpm · Sinus with pre-excitation

Left ventricular hypertrophy

Towering voltages with lateral strain — sensitive to nothing, but specific enough to act on.

66 bpm · Sinus

Right heart strain and S1Q3T3

Sinus tachycardia with anterior T inversion and a right ventricle under acute load — think pulmonary embolism.

116 bpm · Sinus tachycardia

Metabolic and drug effects

Hyperkalaemia

Tall tented T waves, a flattening P wave and a widening QRS on its way to a sine wave.

58 bpm · Sinus, P waves disappearing

Hypokalaemia

Flattened T waves with prominent U waves and a long apparent QT — a substrate for torsades.

82 bpm · Sinus

Digoxin effect and toxicity

The sagging 'reverse tick' ST segment of therapeutic digoxin — and the arrhythmias that mean toxicity.

64 bpm · Sinus

Inherited and environmental

Long QT syndrome

A QTc beyond 480 ms — the substrate for torsades, whether inherited or drug-induced.

60 bpm · Sinus, QTc 520 ms

Brugada syndrome

Coved ST elevation with T inversion in V1–V2 — a sodium channelopathy that kills at night.

70 bpm · Sinus

Hypothermia and the Osborn wave

A positive deflection at the J point, with bradycardia, tremor artefact and long intervals.

42 bpm · Sinus bradycardia

Longer case write-ups

Full clinical cases built around a tracing, with the reasoning worked through end to end.

MRCP Part 2Cardiology

Atrial Flutter ECG: MRCP Part 2 Notes

A regular narrow-complex tachycardia at 150/min should always prompt the question: is this 2:1 atrial flutter?

4 min readECG / Image Case
MRCP Part 2Cardiology

Brugada Syndrome ECG: MRCP Part 2 Notes

A sodium-channelopathy causing coved ST elevation in the right precordial leads and a risk of sudden cardiac death in structurally normal hearts.

4 min readECG / Image Case

The tracings on this page are generated from a description of each rhythm rather than reproduced from a recording, so they are free of any patient identifiers and of anyone else’s copyright. They are drawn on standard paper at 25 mm/s and 10 mm/mV — the squares are real, and intervals can be measured off them. They are teaching illustrations, not diagnostic recordings.