Here is your complete ECG masterclass, built from Harrison's Principles of Internal Medicine (22nd ed., 2025) and Fuster & Hurst's The Heart (15th ed.).
ECG Mastery: Basics to Advanced
MODULE 1 - Why ECG? The Big Picture
The ECG records electrical activity of the heart from the body surface using 12 leads. It is the single most used diagnostic test in medicine - cheap, instant, non-invasive, and packed with information. Every clinical doctor must be able to read one confidently.
What the ECG tells you:
- Rhythm and rate
- Conduction system integrity
- Chamber size (hypertrophy)
- Ischemia and infarction (location, age, extent)
- Metabolic/electrolyte status
- Drug effects
- Pericardial disease
MODULE 2 - The Cardiac Conduction System
Before reading any ECG you must understand what generates the signals.
SA Node (right atrium)
↓ (atrial depolarization = P wave)
AV Node (PR delay = AV node slowing)
↓
Bundle of His
↓
Right Bundle Branch + Left Bundle Branch
↙ ↘
Left Anterior Left Posterior
Fascicle Fascicle
↓
Purkinje Fibers → Ventricular myocardium (= QRS)
Key points:
- SA node fires at 60-100/min (dominant pacemaker)
- AV node fires at 40-60/min if SA fails (junctional escape)
- Purkinje / ventricle fires at 20-40/min (ventricular escape)
- Ventricular repolarization = ST segment + T wave
MODULE 3 - ECG Paper and Calibration
Always check calibration before reading any ECG.
| Parameter | Value |
|---|
| Paper speed | 25 mm/s (standard) |
| 1 small square (1 mm) | 0.04 s (40 ms) |
| 1 large square (5 mm) | 0.20 s (200 ms) |
| Standard voltage | 1 mV = 10 mm (2 large squares tall) |
| Half-standard | 1 mV = 5 mm (written on trace) |
MODULE 4 - ECG Waveforms and Intervals
(Harrison's Principles of Internal Medicine 22E, Fig. 247-2)
The Waves
| Wave | Represents | Normal |
|---|
| P wave | Atrial depolarization | <120 ms wide, <2.5 mm tall; upright in II, inverted in aVR |
| QRS complex | Ventricular depolarization | <100-110 ms (2.5 small squares) |
| Q wave | Septal depolarization (normal) or infarction (pathological) | Normal: <0.04 s, <25% of R height |
| ST segment | Plateau of action potential (phase 2) | Isoelectric (flat) |
| T wave | Ventricular repolarization | Upright in I, II, V3-V6; inverted in aVR normal |
| U wave | After-depolarization / Purkinje repolarization | Same direction as T, low amplitude |
The Intervals
| Interval | Normal Range | Meaning |
|---|
| PR | 120-200 ms (3-5 small squares) | AV conduction time |
| QRS | <100-110 ms | Ventricular conduction |
| QT | <450 ms men, <460 ms women (rate-corrected) | Total ventricular repolarization |
| RR | Depends on rate | Used to calculate heart rate |
Heart Rate Calculation:
- Regular rhythm: HR = 300 ÷ (number of large squares between R-R)
- Or: HR = 1500 ÷ (number of small squares between R-R)
- Irregular: count QRS complexes in 10-second strip × 6
Memorize the 300 rule:
1 large square = 300 bpm | 2 = 150 | 3 = 100 | 4 = 75 | 5 = 60 | 6 = 50
MODULE 5 - The 12 Leads (Understanding the "Camera Angles")
Each lead is like a camera viewing the heart from a different direction. A positive (upright) deflection means electrical activity is moving toward that lead's positive pole.
Limb Leads (Frontal Plane)
| Lead | Looks at | Positive Pole Direction |
|---|
| I | Lateral | 0° (left) |
| II | Inferior | +60° |
| III | Inferior | +120° |
| aVR | Cavity (right shoulder) | -150° |
| aVL | Lateral (left shoulder) | -30° |
| aVF | Inferior (feet) | +90° |
Memory trick for limb lead placement: RA, LA, RL, LL (Red Arm, Yellow Arm, Green Leg, Black Leg - "Ride Your Green Bike")
Precordial Leads (Horizontal Plane)
| Lead | Position | Looks at |
|---|
| V1 | 4th ICS, right sternal border | Septal / RV |
| V2 | 4th ICS, left sternal border | Septal |
| V3 | Between V2 and V4 | Anterior |
| V4 | 5th ICS, midclavicular line | Anterior |
| V5 | Anterior axillary line | Lateral |
| V6 | Midaxillary line | Lateral |
Grouping Leads by Territory
| Territory | Leads | Coronary Artery |
|---|
| Inferior | II, III, aVF | RCA (right coronary) |
| Anteroseptal | V1, V2, V3, V4 | LAD (left anterior descending) |
| Lateral | I, aVL, V5, V6 | LCx (left circumflex) |
| Posterior | Reciprocal changes in V1, V2 | RCA / LCx |
| Right ventricle | V3R, V4R (right leads) | RCA proximal |
MODULE 6 - The Normal ECG (What to Expect)
Normal Sinus Rhythm Checklist
- Rate: 60-100 bpm
- P wave before every QRS; QRS after every P
- PR interval: 120-200 ms
- P wave: upright in I, II; inverted in aVR
- QRS: <110 ms, normal axis (-30° to +90°)
- R-wave progression in V1-V6 (R grows from V1 to V5)
P Wave Morphology
- Right atrial enlargement (P pulmonale): P wave >2.5 mm tall in II (peaked)
- Left atrial enlargement (P mitrale): P wave >120 ms wide, notched in II; terminal negative deflection in V1 >1 mm² (>1 small square wide AND deep)
QRS Axis
(Harrison's Principles of Internal Medicine 22E, Fig. 247-4)
| Axis | Degrees | Leads |
|---|
| Normal | -30° to +90° | QRS upright in I and aVF |
| Left axis deviation (LAD) | -30° to -90° | QRS upright in I, negative in aVF |
| Right axis deviation (RAD) | +90° to +180° | QRS negative in I, positive in aVF |
| Extreme ("Northwest") axis | -90° to +/-180° | QRS negative in both I and aVF |
Quick axis trick: Look at I and aVF.
- Both upright → Normal
- I up, aVF down → Left axis
- I down, aVF up → Right axis
- Both down → Extreme axis
Causes of LAD: LBBB, left anterior fascicular block, inferior MI, LVH, WPW (right-sided accessory pathway)
Causes of RAD: RVH, RBBB, left posterior fascicular block, PE, lateral MI, WPW (left-sided accessory pathway), normal variant in tall thin adults
MODULE 7 - Chamber Enlargement / Hypertrophy
Left Ventricular Hypertrophy (LVH)
Most used criteria (Sokolow-Lyon):
- S in V1 + R in V5 or V6 ≥ 35 mm
- R in aVL ≥ 11 mm (Cornell criteria)
- Associated with: LV strain pattern (ST depression + T wave inversion in lateral leads I, aVL, V5, V6)
Causes: Hypertension (most common), aortic stenosis, HCM, coarctation
Right Ventricular Hypertrophy (RVH)
- R ≥ S in V1 (dominant R in V1)
- RAD (axis >+90°)
- rSR' in V1 is NOT RVH - that is RBBB
- ST depression + T wave inversion in V1-V3 (RV strain)
Causes: Pulmonary hypertension, mitral stenosis, cor pulmonale, Tetralogy of Fallot
MODULE 8 - Bundle Branch Blocks
Right Bundle Branch Block (RBBB)
Criteria:
- QRS ≥ 120 ms
- RSR' ("M-shaped" or "rabbit ears") in V1
- Wide, slurred S wave in I, V5, V6
- T wave inverted in V1 (secondary change - normal with RBBB)
Memory: "William Marrow" - RBBB: W in V1 (rSR'), M in V6... wait, it's actually simpler:
RBBB = bunny ears in V1 (rSR' = ears of a rabbit)
Causes: Normal variant, RV pressure overload, PE, anterior MI, post-cardiac surgery
Left Bundle Branch Block (LBBB)
Criteria:
- QRS ≥ 120 ms
- Broad, notched R (no Q, no S) in I, aVL, V5, V6
- rS or QS (deep S) in V1, V2
- T wave opposite to main QRS deflection (secondary change)
CRITICAL clinical point: New LBBB with chest pain = treat as STEMI equivalent (Sgarbossa criteria needed)
Memory: "WiLLiaM MaRRow"
- LBBB: W in V1, M in V6
- RBBB: M in V1, W in V6
Causes: IHD, HTN, cardiomyopathy, aortic valve disease
Fascicular Blocks (Hemiblocks)
| Block | Axis | QRS duration | Pattern |
|---|
| Left Anterior Fascicular Block (LAFB) | LAD > -45° | Normal or slightly prolonged | Small Q in I, aVL; small R in II, III, aVF |
| Left Posterior Fascicular Block (LPFB) | RAD > +120° | Normal | Small R in I, aVL; small Q in II, III, aVF; must exclude other RAD causes |
Bifascicular block: RBBB + LAFB (most common) = wide QRS with RBBB pattern + LAD
Trifascicular block: Bifascicular + prolonged PR = one step away from complete heart block
MODULE 9 - AV Blocks
First Degree AV Block
- PR interval > 200 ms (>1 large square)
- Every P conducts to QRS (just slowly)
- Usually benign; can be normal in athletes
Second Degree AV Block
Mobitz Type I (Wenckebach):
- Progressive PR lengthening until a P wave is blocked (QRS dropped)
- "Longer, longer, longer, DROP - then you have a Wenckebach"
- PR after the dropped beat is shortest
- Usually at AV node level; generally benign
- Can be normal in athletes (vagal tone)
Mobitz Type II:
- Fixed PR interval; sudden non-conducted P wave (QRS drops without warning)
- Below AV node (His-Purkinje level) - more serious
- Often associated with wide QRS
- High risk of progressing to complete heart block → needs pacemaker
Third Degree (Complete) AV Block
- Complete dissociation: P waves and QRS complexes march independently
- P rate > QRS rate
- QRS escape rhythm: narrow (junctional, 40-60/min) or wide (ventricular, 20-40/min)
- Wide-complex escape = more severe (infranodal block)
- Emergency: Atropine (for narrow-complex), transcutaneous pacing, then permanent pacemaker
Memory for 2nd degree blocks:
Wenckebach = Increasing PR before drop (I = Increasing)
Mobitz II = Suddenly drops (II = abrupt, Sudden)
MODULE 10 - Ischemia and Infarction
This is the most clinically critical section.
Spectrum of Ischemic ECG Changes
Hyperacute T waves (earliest change, minutes):
- Tall, broad, peaked T waves over ischemic zone
- First sign of complete coronary occlusion
ST Elevation (STEMI - transmural ischemia):
- ST elevation in ≥2 contiguous leads
- Threshold: ≥1 mm (most leads), ≥2 mm (V1-V3 men), ≥1.5 mm (V1-V3 women)
- Represents full-thickness (transmural) injury
- Mechanism: epicardial injury current shifts ST vector outward
ST Depression (subendocardial ischemia/NSTEMI):
- Horizontal or downsloping ST depression ≥0.5-1 mm
- Mechanism: ischemia confined to subendocardium; ST vector shifts inward
T wave inversion (ischemia or evolving MI):
- Symmetric, deep T wave inversions
- Wellens' syndrome: deep T inversions in V2-V3 = critical proximal LAD stenosis (do NOT stress test - risk of VF)
Pathological Q waves (established infarction, hours-days):
- Width ≥ 40 ms (1 small square)
- Depth ≥ 25% of R wave height in same lead
- Represent electrically dead (necrotic) myocardium
- Q waves in II, III, aVF = inferior MI; V1-V4 = anterior MI; I, aVL = lateral MI
Localization of STEMI
| Location | ST Elevation In | Reciprocal ST Depression In | Culprit Artery |
|---|
| Inferior | II, III, aVF | I, aVL | RCA (80%), LCx (20%) |
| Anterior | V1-V4 | II, III, aVF (sometimes) | LAD |
| Anteroseptal | V1-V3 | - | LAD proximal |
| Apical/Extensive | V1-V6 | - | LAD proximal (widow maker) |
| Lateral | I, aVL, V5-V6 | V1-V2 | LCx |
| Posterior | Tall R + ST depression V1-V2 | ST elevation in V7-V9 | RCA or LCx |
| Right Ventricular | V1 + V4R elevation | - | Proximal RCA |
Posterior MI pearl: Tall broad R in V1 + ST depression in V1-V2 - the mirror image of anterior ST elevation. Always do V7-V9 leads if inferior MI to check for posterior extension.
RV MI pearl: Inferior STEMI + RV MI = hypotension + clear lungs - DO NOT give nitrates (will drop BP catastrophically). Give IV fluids instead.
Evolution of STEMI Over Time
Minutes: Hyperacute T waves (peaked, tall)
Hours: ST elevation (convex/"tombstone" shape)
6-24h: ST elevation + Q waves appear + T inversion begins
Days: ST returns to baseline + T waves inverted + Q waves persist
Weeks-mos: ST and T normalize; Q waves often persist permanently
MODULE 11 - Arrhythmias
Approach to Any Arrhythmia (systematic)
- Rate: Fast / slow / normal?
- Regular or irregular?
- QRS wide or narrow?
- P waves present? What is the relationship to QRS?
Narrow Complex Tachycardias (QRS < 120 ms)
| Arrhythmia | Rate | Rhythm | P waves | Key feature |
|---|
| Sinus tachycardia | 100-160 | Regular | Present, normal | Gradual onset/offset |
| Atrial flutter | 250-350 atrial; 150 ventricular (2:1) | Regular | Sawtooth in II, III, aVF | 150 bpm = think flutter |
| Atrial fibrillation | 100-160 ventricular | Irregularly irregular | No discrete P waves (fibrillatory baseline) | Most common sustained arrhythmia |
| AVNRT | 140-280 | Regular | P buried in QRS or just after | Pseudo-R' in V1, pseudo-S in II |
| AVRT (WPW) | 150-250 | Regular | Retrograde P after QRS | Delta wave in sinus rhythm |
| Atrial tachycardia | 150-250 | Regular | Abnormal P before QRS | Different P morphology |
| Multifocal atrial tachycardia | Variable >100 | Irregular | ≥3 different P wave morphologies | COPD patients |
Wide Complex Tachycardias (QRS ≥ 120 ms) - THE HIGH-STAKES AREA
Causes:
- VT (ventricular tachycardia) - most dangerous, assume this first
- SVT with aberrant conduction (LBBB/RBBB)
- SVT with pre-excitation (WPW with AF = most dangerous SVT)
- Pacemaker-mediated tachycardia
Rules:
If in doubt, treat wide complex tachycardia as VT until proven otherwise
Never give adenosine or verapamil to pre-excited AF (WPW+AF) - can precipitate VF
Features favoring VT over SVT with aberrancy (Brugada criteria):
- AV dissociation (P waves marching independently) = definitive VT
- Capture beats (narrow QRS among wide) = definitive VT
- Fusion beats = definitive VT
- QRS duration > 160 ms
- Concordance (all precordial leads all-positive or all-negative)
- NW (extreme) axis deviation
Bradyarrhythmias
| Arrhythmia | ECG Feature | Management |
|---|
| Sinus bradycardia | Regular rhythm <60, P before each QRS | Treat if symptomatic: atropine, pacing |
| Sick Sinus Syndrome | SA dysfunction: Brady-tachy, sinus pauses, sinus arrest | PPM if symptomatic |
| Junctional escape | Narrow QRS, rate 40-60, P absent/inverted/retrograde | Treat underlying cause |
| Ventricular escape | Wide QRS, rate 20-40 | Emergency pacing |
Ventricular Arrhythmias
Premature Ventricular Complexes (PVCs):
- Wide (>120 ms), bizarre QRS
- No preceding P wave
- Compensatory pause
- Bigeminy (every other beat), trigeminy (every third)
Ventricular Tachycardia (VT):
- ≥3 consecutive wide QRS complexes at ≥100 bpm
- Sustained (>30 s) vs non-sustained (<30 s)
- Monomorphic (uniform QRS) vs polymorphic (varying QRS)
Torsades de Pointes:
- Polymorphic VT with twisting QRS axis around baseline
- Occurs with long QT (congenital or acquired)
- Triggers: hypokalemia, hypomagnesemia, drugs (class IA/III antiarrhythmics, antipsychotics, antibiotics like azithromycin)
- Treatment: IV magnesium sulfate; correct electrolytes; stop offending drug
Ventricular Fibrillation (VF):
- Chaotic, irregular deflections, no organized QRS
- No cardiac output = cardiac arrest
- Immediate defibrillation + CPR
MODULE 12 - Pre-excitation (WPW Syndrome)
ECG features (in sinus rhythm):
- Short PR interval (<120 ms) - bypass of AV node
- Delta wave - slurred upstroke of QRS
- Wide QRS (>110 ms) - fusion of normal and accessory pathway conduction
- ST-T changes secondary to abnormal depolarization
Accessory pathway location by delta wave polarity:
- Positive delta in V1-V3, negative in aVL = left-sided pathway (most common)
- Negative delta in II, III, aVF = posterior/inferior pathway
Danger: AF with pre-excitation. Very rapid ventricular response via accessory pathway (can conduct at >250 bpm) → VF. ECG shows irregular wide complex tachycardia with varying QRS. NEVER use digoxin, verapamil, diltiazem, adenosine (enhance accessory conduction or drop AVN without blocking AP). Use: DC cardioversion (if unstable) or procainamide / ibutilide.
MODULE 13 - Metabolic and Drug Effects
Hyperkalemia (sequential changes as K+ rises)
| K+ level (approx) | ECG change |
|---|
| 5.5-6.5 mEq/L | Peaked ("tented"), narrow T waves |
| 6.5-7.5 mEq/L | Prolonged PR, flattened P waves |
| 7.5-8.0 mEq/L | Wide QRS |
| >8.0 mEq/L | Sine-wave pattern → asystole |
Treatment: Calcium gluconate (membrane stabilization, immediate), insulin+dextrose, sodium bicarbonate, furosemide, kayexalate, dialysis.
Hypokalemia
- Flattened T waves
- Prominent U waves (U > T wave height = significant)
- Apparent QT prolongation (actually QU prolongation)
- Risk of Torsades
Hypercalcemia
- Shortened QT interval
- Short ST segment or absent ST
Hypocalcemia
- Prolonged QT (prolonged ST segment)
- T wave remains normal
Digoxin
- "Reverse tick" or "Salvador Dali mustache" ST depression (scooping)
- Shortened QT
- T wave flattening or inversion
- Digoxin toxicity: PAT with block, ventricular bigeminy, PVCs, AV blocks
Hypothermia
- Bradycardia
- Osborn (J) wave: positive deflection at J point (most visible in V5, V6)
- Prolonged PR, QRS, QT
- Shivering artifact
MODULE 14 - Pericarditis vs. STEMI
| Feature | Acute Pericarditis | STEMI |
|---|
| ST elevation | Diffuse (all/most leads) | Regional (contiguous leads) |
| ST morphology | Concave (saddle-shaped) | Convex (domed/tombstone) |
| PR depression | Present (classic) | Absent |
| Reciprocal ST depression | Absent (except aVR) | Present in opposite leads |
| Q waves | No | Develop over hours-days |
| Chest pain position | Pleuritic, worse lying, better leaning forward | Central, radiation to arm/jaw |
MODULE 15 - Pulmonary Embolism ECG
ECG is rarely diagnostic but supports clinical suspicion. Classic (but uncommon) finding:
S1Q3T3 pattern:
- Deep S wave in Lead I
- Q wave in Lead III
- T wave inversion in Lead III
Other PE ECG findings:
- Sinus tachycardia (most common sign)
- New RBBB (acute right heart strain)
- RAD
- T wave inversions V1-V4 (RV strain pattern)
- Atrial arrhythmias (AF, flutter)
- P pulmonale
MODULE 16 - The Brugada Pattern
Type 1 (Diagnostic):
- Coved (convex) ST elevation ≥2 mm in V1-V2
- Down-sloping ST segment followed by T wave inversion
- Spontaneous or drug-induced
Types 2 and 3: Saddleback or less elevation - not diagnostic alone
Clinical importance: Risk of sudden cardiac death from VF. Autosomal dominant SCN5A mutation (sodium channel). Fever, alcohol, certain drugs can unmask it.
MODULE 17 - The 14-Step Systematic ECG Approach (Exam and Clinical)
Use this for EVERY ECG. Never skip steps.
| Step | What to Assess | What to Look For |
|---|
| 1 | Calibration & technical | 1 mV = 10 mm, 25 mm/s, correct lead placement |
| 2 | Rhythm | Sinus? Regular? P before every QRS? |
| 3 | Heart rate | 300 rule for regular; count in 10 s for irregular |
| 4 | PR interval | 120-200 ms; short = WPW/junctional; long = AV block |
| 5 | QRS duration | <110 ms; wide = BBB, aberrancy, pacing, hyperK |
| 6 | QT/QTc interval | <450 ms men / <460 ms women |
| 7 | Mean QRS axis | I and aVF method; -30° to +90° normal |
| 8 | P waves | Morphology, size, axis - atrial hypertrophy? |
| 9 | QRS voltages | LVH? Low voltage (pericardial effusion, obesity, COPD)? |
| 10 | R-wave progression | V1 (small r) → V5 (tall R). Poor progression = anterior MI |
| 11 | Q waves | Pathological? Location? Old vs new? |
| 12 | ST segments | Elevation? Depression? Which leads? Shape? |
| 13 | T waves | Tall? Inverted? Symmetric? Asymmetric? |
| 14 | U waves | Prominent (hypokalemia, bradycardia)? |
Always compare with previous ECGs.
MODULE 18 - High-Yield Exam Mnemonics
| Mnemonic | What it's for |
|---|
| WILLIAM MARROW | BBB: W in V1 = LBBB; M in V1 = RBBB |
| 300-150-100-75-60-50 | Heart rate from R-R large squares |
| I See aVF (Both up = Normal axis) | Quick axis check |
| Longer, longer, longer, DROP | Wenckebach (Mobitz I) |
| DEAD | VT clues: Dissociation, Extreme axis, Absence of P-QRS relationship, Duration >160 ms |
| ABCDE for PE | Arrhythmia, BBB (RBBB), Cor pulmonale (P pulmonale), Deviation (RAD), S1Q3T3 |
| Tented T = hyperK; Flat T + prominent U = hypoK | Electrolytes |
| Concave ST = pericarditis; Convex ST = MI | Distinguishing causes of ST elevation |
| PR depression + ST elevation = pericarditis | Classic pericarditis ECG clue |
MODULE 19 - Quick Clinical Decision Rules
Chest pain + ECG → Action:
- ST elevation ≥1 mm in ≥2 contiguous leads → Activate cath lab (STEMI protocol) - door to balloon <90 min
- New LBBB + chest pain → Same as STEMI (Sgarbossa criteria)
- ST depression V1-V4 + inferior STEMI → Posterior MI; do V7-V9
- Inferior STEMI + hypotension + clear lungs → Rule out RV MI with V4R
Hemodynamically unstable tachycardia: Synchronized DC cardioversion regardless of type (except AF narrow complex without hemodynamic compromise)
VT vs SVT with aberrancy: When uncertain in unstable patient → cardiovert. When uncertain in stable patient → adenosine (if narrow) or amiodarone (safest for wide complex)
Prolonged QTc + syncope: Torsades de Pointes until proven otherwise. Give IV MgSO4. Stop QT-prolonging drugs. Correct K+ and Mg2+.
Suggested Study Order for Exams
- Paper calibration + waveform basics (Module 3, 4)
- Leads and normal ECG (Module 5, 6)
- Ischemia/STEMI localization (Module 10) - highest exam yield
- Bundle branch blocks (Module 8)
- AV blocks (Module 9)
- Arrhythmias systematic approach (Module 11)
- Metabolic effects (Module 13)
- Practice 14-step approach on real ECGs (Module 17)
Sources: Harrison's Principles of Internal Medicine, 22nd ed. (2025), Chapter 247 - Electrocardiography; Fuster and Hurst's The Heart, 15th ed., Chapter on Cardiac Conduction System; Gray's Anatomy for Students.
Ask me about any module in more depth - arrhythmia identification, STEMI localization, specific drugs, or work through ECG cases together!