❤️ 12-Lead ECG Mastery

Read Every
Rhythm.

Real ECG images. 12-lead STEMI localization, arrhythmia recognition, conduction blocks — each with key findings, clinical pearls, and full treatment protocols.

8
STEMI Patterns
6
Arrhythmias
5
Blocks
30+
Practice Questions
12-Lead STEMI Localization
Identify the infarct territory, culprit artery, and reciprocal changes for each STEMI pattern.
🫀 Cardiac Lead Localization — Which Leads Watch Which Walls
⬇️
Inferior
II, III, aVF
RCA (80%) / LCx
➡️
Anterior
V3, V4
LAD (mid)
↗️
Anteroseptal
V1, V2, V3, V4
LAD (proximal)
↙️
Septal
V1, V2
LAD (septal branch)
↖️
High Lateral
I, aVL
LAD (diagonal) / LCx
⬅️
Low Lateral
V5, V6
LCx / LAD diagonal
🔄
Posterior
V1–V3 (mirror)
RCA / LCx
📍
RV Infarct
V4R (right-sided)
RCA proximal
1
Inferior STEMI
STEMI RCA 80% II · III · aVF RV Infarct Risk
Inferior STEMI ECG
Image: theSimTech.org — free for medical education
🔍 What You See
  • ST elevation ≥1mm in II, III, aVF
  • Reciprocal ST depression in I and aVL
  • ST III > ST II suggests RCA occlusion
  • ST II > ST III suggests LCx occlusion
  • Check for Q-wave formation (subacute stage)
⚠️ Critical Pearl
RV Infarct CheckIf ST III > ST II with hypotension + clear lungs: right-sided leads (V4R). RV infarct = preload dependent. HOLD NITRO. Give fluids instead. Up to 40% of inferior STEMIs have RV involvement.
✅ EMS Treatment
  • 1
    ASA 324mg chewed, 12-lead, IV access ×2, O2 if SpO2 <94%
  • 2
    NTG 0.4mg SL — only if BP stable and NO RV infarct suspected
  • 3
    Cath lab activation / STEMI alert — time is muscle
  • 4
    Right-sided ECG if hypotensive, bradycardic, or ST III > II
  • 5
    Atropine / pacing ready — AV block occurs in 20%
2
Anterior STEMI — The Widowmaker
STEMI Highest Mortality LAD Occlusion V1–V6 · I · aVL
Anterior STEMI ECG
Image: theSimTech.org — free for medical education
🔍 What You See
  • ST elevation in V1–V6 (full anterior: V1–V6 + I + aVL)
  • Reciprocal ST depression in II, III, aVF
  • Loss of R wave progression in precordial leads
  • Hyperacute "tombstone" T-waves (early sign)
  • STE in aVR = proximal LAD or left main occlusion
⚠️ Subtypes by Localization
Anteroseptal: V1–V4 (proximal LAD, septal branch)
Anterior: V3–V4 only (mid LAD)
Anterolateral: V1–V6 + I + aVL (proximal LAD)
High Lateral: I + aVL (first diagonal branch)
✅ EMS Treatment
  • 1
    ASA 324mg chewed, 12-lead, large-bore IV ×2
  • 2
    NTG for pain relief — watch BP closely (anterior STEMIs can drop BP fast)
  • 3
    Cath lab activation — anterior STEMI carries worst prognosis, fastest activation critical
  • 4
    Prepare for cardiogenic shock, VF, wide-complex bradycardia
  • 5
    Defibrillator ready — anterior STEMIs have highest VF risk
3
Posterior STEMI — The Hidden MI
STEMI Equivalent Often Missed RCA / LCx Mirror Image in V1–V3
Posterior STEMI ECG
Image: theSimTech.org — free for medical education
🔍 What You See (It's Backwards!)
  • ST depression in V1–V3 (NOT elevation — this is the mirror image)
  • Tall, broad R waves in V1–V2 (mirror of posterior Q waves)
  • Upright T waves in V1–V2 (mirror of T inversions)
  • R/S ratio >1 in V1 or V2 = pathologic posterior R wave
  • Confirm with posterior leads V7–V9: ST elevation >0.5mm
⚠️ Commonly MissedOnly 10% of paramedics correctly identify posterior MI on standard 12-lead. When you see ST depression maximal in V1–V3 with a tall R wave, flip the ECG upside down — if it looks like a STEMI, it probably is one.
✅ EMS Treatment
  • 1
    Treat as STEMI — cath lab activation
  • 2
    Obtain posterior leads V7–V9 if available
  • 3
    Often associated with inferior STEMI — check II, III, aVF too
  • 4
    ASA, IV, monitoring, NTG if BP allows
4
High Lateral STEMI
STEMI LAD Diagonal / LCx Leads I · aVL Reciprocal: II · III · aVF
❤️High Lateral STEMI
ST↑ in I and aVL
ST↓ in II, III, aVF
🔍 Key Findings
  • ST elevation in Lead I and aVL
  • Reciprocal ST depression in II, III, aVF (inferior leads)
  • Often isolated to I and aVL — "lateral without precordials"
  • Can be subtle — even 1mm STE in aVL with inferior reciprocal changes is significant
  • Caused by first diagonal (D1) branch of LAD or obtuse marginal of LCx
💡 Clinical Pearl
aVL is the most sensitive lead for subtle inferior STEMI — ST depression in aVL is often the FIRST sign of inferior MI. High lateral is the opposite: STE in aVL = high lateral STEMI with inferior reciprocal changes.
✅ EMS Treatment
  • 1
    Treat as STEMI — cath lab activation
  • 2
    ASA 324mg, IV access, continuous monitoring
  • 3
    Often a smaller infarct than anterior — but still time-critical
5
Septal, Low Lateral & Anteroseptal — Lead Reference
Septal: V1–V2 Low Lateral: V5–V6 Anteroseptal: V1–V4
TerritoryElevated LeadsReciprocal ChangesCulprit Artery
SeptalV1, V2None typicalLAD septal perforators
AnteroseptalV1, V2, V3, V4Sometimes II/III/aVFProximal LAD
AnteriorV3, V4Sometimes II/III/aVFMid LAD
High LateralI, aVLII, III, aVFD1 branch / LCx OM
Low LateralV5, V6V1–V2 (sometimes)LCx / LAD diagonal
Extensive AnteriorV1–V6, I, aVLII, III, aVFProximal LAD / LMCA
InferiorII, III, aVFI, aVLRCA (80%) / LCx
PosteriorNone (ST depress V1–V3)Tall R + upright T in V1–V2RCA / LCx
🧠 Memory Trick — Contiguous LeadsSTEMI requires ST elevation in 2+ contiguous leads. Contiguous means electrically adjacent: V1–V6 are contiguous with each other. I and aVL are contiguous with each other. II, III, aVF are contiguous with each other. A single isolated lead elevation is not a STEMI.
Arrhythmia Recognition & Treatment
Real 12-lead and rhythm strip images with complete prehospital treatment protocols.
A
Atrial Fibrillation (A-Fib)
Unstable = Cardiovert Irregularly Irregular No P Waves
Atrial Fibrillation ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • No identifiable P waves — replaced by fibrillatory baseline
  • Irregularly irregular R-R intervals — no pattern whatsoever
  • Ventricular rate can be slow, normal, or fast (RVR)
  • QRS usually narrow (unless aberrant conduction or WPW)
✅ Stable A-Fib (BP stable, no serious signs)
  • 1
    Monitor, IV access, 12-lead ECG
  • 2
    Rate control per protocol (usually hospital-based: metoprolol, diltiazem)
  • 3
    Transport — cardioversion decision usually made in-hospital
🚨 Unstable A-Fib (Hypotensive, Altered, Pulmonary Edema)
  • 1
    Synchronized cardioversion — 120–200J biphasic
  • 2
    Sedate first if conscious — Versed 1–2mg IV + fentanyl
  • 3
    Reassess rhythm and BP after each attempt
⚠️ WPW + A-FibWide complex A-Fib with very rapid rate (>250 bpm) = suspect WPW. DO NOT give AV-nodal blockers (adenosine, diltiazem, metoprolol). Electrical cardioversion only.
B
Supraventricular Tachycardia (SVT)
Rate 150–250 bpm Adenosine First-Line Regular Narrow Complex AV Node Reentry
SVT ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • Rate typically 150–250 bpm
  • Regular rhythm — perfectly consistent R-R intervals
  • Narrow QRS (<0.12s) unless aberrant conduction
  • P waves often hidden in T waves or retrograde (inverted in II, III, aVF)
  • Abrupt onset and termination ("paroxysmal")
✅ Stable SVT Treatment
  • 1
    Vagal maneuvers — Modified Valsalva (most effective): bear down hard × 15 sec, supine, legs raised immediately after
  • 2
    Adenosine 6mg rapid IV push — largest proximal vein + immediate 20mL saline flush
  • 3
    Adenosine 12mg if no conversion after 2 min
  • 4
    Adenosine 12mg again if still no conversion
  • 5
    Warn patient: chest tightness, doom feeling, brief asystole — all expected
🚨 Unstable SVT
  • 1
    Synchronized cardioversion — 50–100J biphasic (start low for narrow complex)
  • 2
    Sedate if time allows
💎 Adenosine Technique TipUse antecubital or more proximal vein. Slow/distal push = metabolized before reaching the AV node. You only get a few seconds — be fast.
C
Sinus Bradycardia
Rate <60 bpm Normal P:QRS Atropine First-Line
Sinus Bradycardia ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • Rate <60 bpm
  • Normal upright P wave before every QRS — normal sinus morphology
  • Regular rhythm — consistent R-R intervals
  • Normal PR interval (0.12–0.20s) and QRS (<0.12s)
💡 Is it Symptomatic?
Only treat if symptomatic: hypotension, altered mentation, chest pain, pulmonary edema, syncope. Athletes and sleeping patients often have heart rates in the 40s — normal for them. Ask: "Have you always had a slow pulse?"
✅ Symptomatic Sinus Bradycardia
  • 1
    Atropine 0.5mg IV — minimum dose. Repeat q3–5 min, max 3mg total
  • 2
    If no response: Dopamine 2–10 mcg/kg/min IV infusion
  • 3
    Transcutaneous pacing — if medications fail or patient is severely compromised
  • 4
    Consider inferior STEMI — bradycardia + chest pain = check 12-lead!
D
Torsades de Pointes
Life-Threatening VT Prolonged QT Mag Sulfate 2g Twisting QRS Axis
Torsades de Pointes ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • Polymorphic VT with twisting QRS axis around the isoelectric line
  • Rate 150–300 bpm — chaotic, waxing-waning amplitude
  • Preceded by prolonged QT interval on baseline ECG (QTc >500ms)
  • Often triggered by "short-long-short" sequence
  • Can degenerate into VF — always potentially fatal
⚡ Causes (AEIOU)
Antiarrhythmics (amiodarone, sotalol) · Electrolyte abnormalities (↓Mg, ↓K) · Ischemia · QT-prolonging drugs (antipsychotics, antibiotics) · Underlying congenital long QT
✅ Torsades Treatment
  • 1
    Magnesium Sulfate 2g IV over 5–10 min — even if Mg levels are normal. This is the drug of choice.
  • 2
    If pulseless → defibrillate immediately (unsynchronized)
  • 3
    If recurrent: correct electrolytes (K+, Mg), increase heart rate to shorten QT (atropine or pacing at 90–100 bpm)
  • 4
    Discontinue all QT-prolonging drugs
⚠️ Do NOT use amiodaroneAmiodarone prolongs the QT interval — it can worsen Torsades. Mag sulfate is the antidote.
E
Ventricular Fibrillation (V-Fib)
Cardiac Arrest Shock Immediately No Output
V-Fib ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • Completely chaotic, irregular waveform — no identifiable P, QRS, or T
  • Amplitude varies — coarse VF has larger waveforms (more responsive to shock)
  • Fine VF has small-amplitude waves (harder to defibrillate)
  • Patient is pulseless and unresponsive
✅ VF / Pulseless VT Protocol
  • 1
    CPR immediately — high quality, minimal interruptions
  • 2
    Defibrillate 200J biphasic — resume CPR immediately after shock
  • 3
    Epinephrine 1mg IV/IO q3–5 min
  • 4
    After 2nd shock with no conversion: Amiodarone 300mg IV/IO
  • 5
    Search for reversible causes: Hs and Ts
F
Ventricular Tachycardia (V-Tach)
Wide Complex Rate >100 bpm Assume VT Until Proven Otherwise
Ventricular Tachycardia ECG
Image: theSimTech.org — free for medical education
🔍 Recognition
  • Rate >100 bpm, wide QRS (>0.12s)
  • Regular or slightly irregular rhythm
  • AV dissociation = VT (P waves marching independently)
  • Fusion beats and capture beats = pathognomonic for VT
  • Concordance in precordial leads (all positive or all negative = VT)
💡 Rule: Assume VTAny wide complex tachycardia in a patient >35 with structural heart disease = VT until proven otherwise. Treating SVT-with-aberrancy as VT is safe. Treating VT as SVT with verapamil or diltiazem can be fatal.
✅ VT Treatment
  • 1
    Pulseless VT: CPR + defibrillate 200J — same as VF protocol
  • 2
    Stable VT with pulse: Amiodarone 150mg IV over 10 min
  • 3
    Unstable VT with pulse (hypotensive/altered): Synchronized cardioversion 100J
  • 4
    Correct reversible causes: electrolytes, ischemia
Conduction Blocks
AV blocks and bundle branch blocks — recognition, clinical significance, and treatment.
1°
1st Degree AV Block
BenignPR >0.20sUsually No Tx
1st Degree AV Block
Image: theSimTech.org — free for medical education
  • PR interval >0.20s (5 small boxes)
  • Every P wave is followed by a QRS — 1:1 conduction
  • Regular rhythm — just delayed conduction
✅ Treatment
  • 1
    Usually none required — monitor
  • 2
    Treat if symptomatic (rare) or associated with inferior STEMI
W
2nd Degree — Mobitz I (Wenckebach)
Vagally MediatedUsually BenignAtropine Responsive
Wenckebach Block
Image: theSimTech.org — free for medical education
  • PR interval progressively lengthens until a P wave is dropped (no QRS)
  • Cycle then resets — grouped beating pattern
  • Supranodal (AV node) — responsive to atropine
✅ Treatment
  • 1
    Usually monitor only unless symptomatic
  • 2
    If symptomatic: Atropine 0.5mg IV (responds well)
  • 3
    Associated with inferior MI — get 12-lead
3°
3rd Degree — Complete Heart Block
Life-ThreateningAV DissociationPacing Required
3rd Degree Heart Block
Image: theSimTech.org — free for medical education
  • P waves and QRS complexes march independently — no relationship
  • Atrial rate faster than ventricular escape rate
  • Wide QRS escape rhythm = infranodal (more dangerous)
  • Narrow QRS escape = junctional (more stable)
⚠️ Atropine Does NOT Work3rd degree block is structural/infranodal. Atropine can paradoxically increase atrial rate without improving ventricular rate. Go straight to pacing.
✅ Treatment
  • 1
    Transcutaneous pacing immediately — don't waste time on atropine
  • 2
    Dopamine 2–10 mcg/kg/min as bridge if pacing unavailable
  • 3
    Consider inferior STEMI — 3rd degree block + chest pain = STEMI until proven otherwise
L
Left Bundle Branch Block (LBBB)
WiLLiaM patternAlways PathologicalSTEMI Masker
LBBB ECG
Image: theSimTech.org — free for medical education
  • QRS ≥0.12s (3 small boxes wide)
  • WiLLiaM pattern: W shape in V1, M shape in V6
  • Broad notched R waves in lateral leads (I, aVL, V5–V6)
  • Deep QS complex in V1–V3
  • Appropriate discordance: ST/T wave opposite to QRS direction
  • LBBB always indicates cardiac pathology — never a normal finding
🔍 Sgarbossa Criteria for STEMI in LBBBConcordant STE ≥1mm (same direction as QRS) OR Concordant STD ≥1mm in V1–V3 OR Excessive discordant STE ≥5mm = activate cath lab
R
Right Bundle Branch Block (RBBB)
MaRRoW patternCan be NormalRSR' in V1
RBBB ECG
Image: theSimTech.org — free for medical education
  • QRS ≥0.12s
  • MaRRoW pattern: M shape in V1 (rSR'), W shape in V6
  • Prominent terminal S wave in leads I, V5, V6
  • ST depression + T wave inversion in V1–V3 (appropriate discordance)
  • Can be incidental — less always pathological than LBBB
💡 RBBB Mnemonic
WiLLiaM MaRRoW:
W-I-LLiam = LBBB: W in V1, M in V6
Ma-RR-oW = RBBB: M (rSR') in V1, W in V6
Practice Mode
Real ECG images. Identify the rhythm, STEMI territory, or block. Immediate feedback with clinical rationale.
0
Correct
0
Answered
—
Accuracy
ECG to identify
Loading question...
Question 1 of 30+
Quick Reference Tables
Everything you need to read any 12-lead or rhythm strip — in one place.
AV Block Decision Guide
Block TypePR / PatternTreatment
1st DegreePR >0.20s, all QRS presentMonitor only
2nd Deg Mobitz IPR lengthens → dropped QRSAtropine if symptomatic
2nd Deg Mobitz IIConstant PR → sudden dropped QRSPacing (not atropine)
3rd Degree (CHB)P and QRS completely dissociatedTCP immediately
Tachycardia Treatment Summary
RhythmStableUnstable
SVTVagal → AdenosineSync cardiovert 50J
A-Fib/FlutterRate control, monitorSync cardiovert 120J
Stable VTAmiodarone 150mgSync cardiovert 100J
Pulseless VT/VFN/A (no pulse)CPR + Defib 200J
TorsadesMag 2g IVUnsync defib
6-Step Systematic ECG Interpretation
1. Rate
300 ÷ large boxes between R waves. Or: 300–150–100–75–60–50 (1–6 boxes)
2. Rhythm
Regular or irregular? Is every R-R interval the same? March out P waves.
3. P Waves
Present? Upright in II? One P per QRS? PR interval normal (0.12–0.20s)?
4. QRS Width
Narrow (<0.12s) = supraventricular origin. Wide (≥0.12s) = BBB, VT, or aberrant.
5. ST Segment
Elevated? Depressed? Which leads? Are there reciprocal changes? STEMI pattern?
6. T Waves / QT
Hyperacute? Inverted? QT prolonged (QTc >440ms men, >460ms women)?
Hs and Ts — Reversible Arrest Causes
H's
Hypovolemia · Hypoxia · Hydrogen ion (Acidosis) · Hypo/Hyperkalemia · Hypothermia · Hypoglycemia
T's
Tension pneumothorax · Tamponade · Toxins · Thrombosis (PE) · Thrombosis (MI)