EDAITUTOR
ED Reference · ECG v0.1 · illustrated Educational use only

How to Read a
12-Lead ECG

A systematic approach for the emergency department — work the same 10 steps every time, then step back and read the ECG in the clinical context.

LookThinkDon't miss

🔴 Clinical pearl — read it in context

Always interpret the ECG with the patient in front of you. Confirm ID & clinical context, check calibration (25 mm/s, 10 mm/mV) and the standardisation mark, and look for artefact or lead misplacement. Compare with old ECGs whenever possible. When in doubt, ask for help — don't sit on it.

Getting started
  • Confirm patient ID & clinical context
  • Check calibration & standardisation mark
  • Look for artefact / lead misplacement
  • Scan all 12 leads systematically
⚪ habitSame order every time: rate → rhythm → axis → intervals → morphology.
🟢 LITFL · EM Cases
The grid
  • Paper speed 25 mm/s · gain 10 mm/mV
  • Small box = 1 mm = 0.04 s (40 ms) · 0.1 mV
  • Large box = 5 mm = 0.20 s (200 ms) · 0.5 mV
  • Calibration pulse = 10 mm = 1 mV
⚠ checkA miscalibrated trace mimics LVH or low voltage — always verify the standardisation mark.
🟢 LITFL ECG Library
12-lead layout
  • Limb leads: I, II, III, aVR, aVL, aVF
  • Precordial: V1–V6
  • V1: 4th ICS, right sternal border
  • V2: 4th ICS, left sternal border
  • V4: 5th ICS, mid-clavicular line
  • V6: 5th ICS, mid-axillary line
⚪ tipV3 sits midway between V2 and V4; V5 between V4 and V6.
🟢 LITFL · EM Cases
Normal values
Rate60–100 bpm
PR interval120–200 ms
QRS duration<120 ms
QTc<440 (M) / <460 (F)
P wave<120 ms · <2.5 mm
Axis−30° to +90°
⚪ noteQTc = QT / √RR (Bazett). Watch QTc with bradycardia & drugs.
🟢 LITFL · Dr Smith's ECG Blog
How to read it well — look · think · don't miss

Be systematic

Work the same 10 steps in the same order, every single ECG — speed comes from routine, misses come from skipping.

🟢 EM Cases

Compare with old

An old ECG turns "abnormal" into "new vs chronic". Always hunt for a prior trace before you commit.

🟢 Dr Smith's ECG Blog

Correlate clinically

The same trace means different things in chest pain, syncope or a well patient. Read the ECG with the story.

🟢 EM Cases

Hunt the killers

Actively look for the can't-miss patterns — STEMI, hyperkalaemia, WPW, Brugada, PE/RV strain, pericarditis.

🟢 LITFL

The systematic approach — 10 steps
1

Rate

  • 300 / large boxes between R waves
  • Irregular → count QRS in 6 s × 10
normal 60–100
2

Rhythm

  • Regular or irregular?
  • P before every QRS · constant PR?
find the P waves
3

Axis

  • Look at QRS in I and aVF
  • Both positive → normal axis
−30° to +90°
4

Intervals

  • PR 120–200 · QRS <120 ms
  • QTc <440 (M) / <460 (F)
measure, don't eyeball
5

P wave

  • Best seen in lead II
  • Tall = P pulmonale · notched = P mitrale
<2.5 mm · <120 ms
6

QRS morphology

  • Pathological Q · bundle branch block
  • R-wave progression V1→V6 · voltage
wide = think BBB
7

ST segment

  • Compare to the PR baseline
  • ≥2 contiguous leads → think STEMI
limb ≥1 · chest ≥2 mm
8

T wave

  • Polarity, amplitude, symmetry
  • Inverted · peaked · flattened?
peaked → K⁺
9

U wave

  • Best seen in V2–V4
  • Prominent → low K⁺ · bradycardia · drugs
prominent → low K⁺
10

Put it together

  • Normal? If not, what's the rhythm?
  • Ischaemia / STEMI? Other pathology?
synthesise + clinical picture
Coronary territories — which leads, which wall
Leads & walls · localise the ischaemia
II · III · aVFinferior I · aVLV5–V6 lateral V1–V2septal V3–V4anterior
Territory map
WallLeadsVessel
InferiorII, III, aVFRCA
LateralI, aVL, V5–V6LCx
SeptalV1–V2LAD
AnteriorV3–V4LAD
ExtensiveV1–V6, I, aVLprox LAD
⚠ reciprocalLook for reciprocal change in the opposite territory (e.g. inferior STEMI → ST depression in I/aVL). Check posterior (tall R + ST depression V1–V3) and right-sided leads in inferior infarcts.
Common patterns — recognise at a glance

STEMI

  • ST elevation in ≥2 contiguous leads
  • Reciprocal change opposite

Ischaemia

  • ST depression · T-wave inversion
  • Dynamic with symptoms

Pericarditis

  • Widespread concave ST elevation
  • PR depression (PR elevation in aVR)

Hyperkalaemia

  • Tall, peaked, narrow T waves
  • → wide QRS → sine wave
⚪ rememberPatterns are clues, not diagnoses — confirm with the clinical picture, serial ECGs and (where relevant) troponin & electrolytes.
STEMI equivalents — occlusion without classic ST elevation
critical proximal LAD

Wellens

Biphasic (type A) or deep symmetric (type B) T-wave inversion in V2–V3, typically when pain-free. Heralds imminent anterior MI — don't stress test.

discuss cardiology
acute LAD occlusion

De Winter T-waves

Upsloping ST depression at the J point with tall, symmetric T waves across the precordial leads (± STE in aVR).

treat as occlusion → cath
circumflex / RCA

Posterior MI

Horizontal ST depression V1–V3 + tall R (dominant R) + upright T. Confirm with posterior leads V7–V9 (STE).

do posterior leads
LBBB / paced rhythm

Modified Sgarbossa

Concordant STE ≥1 mm · concordant STD ≥1 mm in V1–V3 · or discordant STE ≥25% of the S/R wave (Smith).

occlusion in LBBB
left main / triple-vessel

aVR elevation

STE in aVR (& V1) with widespread ST depression → left main / proximal LAD / severe 3-vessel disease.

high-risk — urgent
very early occlusion

Hyperacute T

Broad, tall, symmetric T waves — an early sign that precedes ST elevation. Repeat the ECG.

serial ECGs
⚠ occlusion MI (OMI)These are acute coronary occlusion patterns that miss classic STEMI criteria — easy to overlook and time-critical. Discuss early with cardiology, compare with old ECGs and repeat serial ECGs if the clinical story fits.
STEMI mimics — ST elevation isn't always infarct

LBBB / paced

Discordant ST changes — apply Sgarbossa / modified Sgarbossa criteria.

LVH

High voltage with discordant ST/T (strain); STE in V1–V3.

Early repolarisation

Young patient, concave STE, notched J point, widespread, no reciprocal change.

Pericarditis

Widespread concave STE + PR depression; PR elevation in aVR.

Brugada

Coved STE in V1–V2 (type 1), RBBB-like morphology.

LV aneurysm

Persistent STE with well-formed Q waves after old anterior MI.

Takotsubo

Anterior STE mimicking LAD; apical ballooning; emotional / physical stress trigger.

Other

Hyperkalaemia · raised ICP / SAH · hypothermia (Osborn / J waves).

⚠ decide on the whole pictureSeparate mimics from infarct using morphology, reciprocal change, an old ECG and the clinical story — never ST elevation alone. Use Sgarbossa for LBBB / paced rhythms; when unsure in chest pain, get serial ECGs and senior review.
Toxicology & the ECG — drugs that change the trace
TCA · cocaine · local anaesthetic · flecainide

Na-channel block

Wide QRS + tall terminal R in aVR (≥3 mm). QRS >100 ms → seizure risk; >160 ms → ventricular arrhythmia risk.

IV sodium bicarbonate
antipsychotics · methadone · antiarrhythmics · some antihistamines

QT → Torsades

Prolonged QTc → risk of polymorphic VT (Torsades de Pointes).

magnesium · correct K⁺/Mg²⁺
digoxin

Digoxin

Effect: scooped "reverse-tick" ST depression. Toxicity: almost any arrhythmia — classically atrial tachy with block; bidirectional VT.

level · digoxin-specific Fab
β-blocker · calcium-channel blocker

Brady / blocks

Bradycardia, AV block, hypotension; QRS usually narrow.

brady → think BB / CCB
cocaine · amphetamines

Sympathomimetic

Sinus tachycardia; ischaemia / STE (cocaine vasospasm); wide QRS with cocaine (Na-channel block).

benzodiazepines first-line
K⁺-sparing diuretics · ACEi · renal failure

Hyperkalaemia

Peaked T → wide QRS → sine wave; flattening / loss of P waves.

calcium · shift K⁺
⚪ the ECG is a tox toolQRS width and QTc drive management in the poisoned patient — sodium bicarbonate for sodium-channel blockade, magnesium for Torsades. Always correlate with the agent, dose, time since ingestion and clinical state.
Don't miss
  • STEMIST elevation ≥2 contiguous leads + reciprocal change
  • Hyperkalaemiapeaked T → wide QRS → sine wave
  • WPWshort PR + delta wave + wide QRS
  • Brugadacoved ST elevation V1–V2 (type 1)
  • Pericarditiswidespread ST elevation + PR depression
  • PE / RV strainS1Q3T3, RBBB, T inversion V1–V3, sinus tachy
🔴 alsoLong QT · complete heart block · ventricular tachycardia.
🟢 LITFL · Dr Smith's ECG Blog
Quick rules
  • Rate: 300 / large boxes (regular)
  • Rate: QRS in 6 s × 10 (irregular)
  • Axis: I & aVF both up = normal
  • QTc: roughly < half the RR (if HR ~60)
  • STEMI: limb ≥1 mm · chest ≥2 mm
  • Q wave: >1 box wide or >25% of R
  • R progression: transition by V3–V4
🟢 LITFL · EM Cases
Paediatric notes
  • Use age-specific normals — rate, PR & QRS all change with age
  • Right-axis & dominant R in V1 are normal in newborns (RV dominance)
  • T inversion V1–V3 ("juvenile T waves") is normal in children
  • Faster rates: newborn ~110–160, falling through childhood
Approx. resting rate
Agebpm
Newborn110–160
1–3 yr90–150
3–8 yr80–120
>8 yr60–100

Guide only — always use age-based reference ranges (RCH).

🟢 RCH Clinical Practice Guidelines

ED AI Tutor — ED Reference Series · v0.1 · For clinician education only. Not a substitute for clinical judgment, formal ECG reporting, local guidelines or senior oversight. ECG interpretation must always be correlated with the clinical context.