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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.
ParameterValue
Paper speed25 mm/s (standard)
1 small square (1 mm)0.04 s (40 ms)
1 large square (5 mm)0.20 s (200 ms)
Standard voltage1 mV = 10 mm (2 large squares tall)
Half-standard1 mV = 5 mm (written on trace)

MODULE 4 - ECG Waveforms and Intervals

Basic ECG waveforms: P wave, QRS complex, ST segment, T wave, U wave, with PR, QRS, and QT intervals labeled
(Harrison's Principles of Internal Medicine 22E, Fig. 247-2)

The Waves

WaveRepresentsNormal
P waveAtrial depolarization<120 ms wide, <2.5 mm tall; upright in II, inverted in aVR
QRS complexVentricular depolarization<100-110 ms (2.5 small squares)
Q waveSeptal depolarization (normal) or infarction (pathological)Normal: <0.04 s, <25% of R height
ST segmentPlateau of action potential (phase 2)Isoelectric (flat)
T waveVentricular repolarizationUpright in I, II, V3-V6; inverted in aVR normal
U waveAfter-depolarization / Purkinje repolarizationSame direction as T, low amplitude

The Intervals

IntervalNormal RangeMeaning
PR120-200 ms (3-5 small squares)AV conduction time
QRS<100-110 msVentricular conduction
QT<450 ms men, <460 ms women (rate-corrected)Total ventricular repolarization
RRDepends on rateUsed 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)

LeadLooks atPositive Pole Direction
ILateral0° (left)
IIInferior+60°
IIIInferior+120°
aVRCavity (right shoulder)-150°
aVLLateral (left shoulder)-30°
aVFInferior (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)

LeadPositionLooks at
V14th ICS, right sternal borderSeptal / RV
V24th ICS, left sternal borderSeptal
V3Between V2 and V4Anterior
V45th ICS, midclavicular lineAnterior
V5Anterior axillary lineLateral
V6Midaxillary lineLateral

Grouping Leads by Territory

TerritoryLeadsCoronary Artery
InferiorII, III, aVFRCA (right coronary)
AnteroseptalV1, V2, V3, V4LAD (left anterior descending)
LateralI, aVL, V5, V6LCx (left circumflex)
PosteriorReciprocal changes in V1, V2RCA / LCx
Right ventricleV3R, 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

Hexaxial diagram showing normal, left, right, and extreme axis deviation zones
(Harrison's Principles of Internal Medicine 22E, Fig. 247-4)
AxisDegreesLeads
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)

BlockAxisQRS durationPattern
Left Anterior Fascicular Block (LAFB)LAD > -45°Normal or slightly prolongedSmall Q in I, aVL; small R in II, III, aVF
Left Posterior Fascicular Block (LPFB)RAD > +120°NormalSmall 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

LocationST Elevation InReciprocal ST Depression InCulprit Artery
InferiorII, III, aVFI, aVLRCA (80%), LCx (20%)
AnteriorV1-V4II, III, aVF (sometimes)LAD
AnteroseptalV1-V3-LAD proximal
Apical/ExtensiveV1-V6-LAD proximal (widow maker)
LateralI, aVL, V5-V6V1-V2LCx
PosteriorTall R + ST depression V1-V2ST elevation in V7-V9RCA or LCx
Right VentricularV1 + 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)

  1. Rate: Fast / slow / normal?
  2. Regular or irregular?
  3. QRS wide or narrow?
  4. P waves present? What is the relationship to QRS?

Narrow Complex Tachycardias (QRS < 120 ms)

ArrhythmiaRateRhythmP wavesKey feature
Sinus tachycardia100-160RegularPresent, normalGradual onset/offset
Atrial flutter250-350 atrial; 150 ventricular (2:1)RegularSawtooth in II, III, aVF150 bpm = think flutter
Atrial fibrillation100-160 ventricularIrregularly irregularNo discrete P waves (fibrillatory baseline)Most common sustained arrhythmia
AVNRT140-280RegularP buried in QRS or just afterPseudo-R' in V1, pseudo-S in II
AVRT (WPW)150-250RegularRetrograde P after QRSDelta wave in sinus rhythm
Atrial tachycardia150-250RegularAbnormal P before QRSDifferent P morphology
Multifocal atrial tachycardiaVariable >100Irregular≥3 different P wave morphologiesCOPD patients

Wide Complex Tachycardias (QRS ≥ 120 ms) - THE HIGH-STAKES AREA

Causes:
  1. VT (ventricular tachycardia) - most dangerous, assume this first
  2. SVT with aberrant conduction (LBBB/RBBB)
  3. SVT with pre-excitation (WPW with AF = most dangerous SVT)
  4. 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

ArrhythmiaECG FeatureManagement
Sinus bradycardiaRegular rhythm <60, P before each QRSTreat if symptomatic: atropine, pacing
Sick Sinus SyndromeSA dysfunction: Brady-tachy, sinus pauses, sinus arrestPPM if symptomatic
Junctional escapeNarrow QRS, rate 40-60, P absent/inverted/retrogradeTreat underlying cause
Ventricular escapeWide QRS, rate 20-40Emergency 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/LPeaked ("tented"), narrow T waves
6.5-7.5 mEq/LProlonged PR, flattened P waves
7.5-8.0 mEq/LWide QRS
>8.0 mEq/LSine-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

FeatureAcute PericarditisSTEMI
ST elevationDiffuse (all/most leads)Regional (contiguous leads)
ST morphologyConcave (saddle-shaped)Convex (domed/tombstone)
PR depressionPresent (classic)Absent
Reciprocal ST depressionAbsent (except aVR)Present in opposite leads
Q wavesNoDevelop over hours-days
Chest pain positionPleuritic, worse lying, better leaning forwardCentral, 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.
StepWhat to AssessWhat to Look For
1Calibration & technical1 mV = 10 mm, 25 mm/s, correct lead placement
2RhythmSinus? Regular? P before every QRS?
3Heart rate300 rule for regular; count in 10 s for irregular
4PR interval120-200 ms; short = WPW/junctional; long = AV block
5QRS duration<110 ms; wide = BBB, aberrancy, pacing, hyperK
6QT/QTc interval<450 ms men / <460 ms women
7Mean QRS axisI and aVF method; -30° to +90° normal
8P wavesMorphology, size, axis - atrial hypertrophy?
9QRS voltagesLVH? Low voltage (pericardial effusion, obesity, COPD)?
10R-wave progressionV1 (small r) → V5 (tall R). Poor progression = anterior MI
11Q wavesPathological? Location? Old vs new?
12ST segmentsElevation? Depression? Which leads? Shape?
13T wavesTall? Inverted? Symmetric? Asymmetric?
14U wavesProminent (hypokalemia, bradycardia)?
Always compare with previous ECGs.

MODULE 18 - High-Yield Exam Mnemonics

MnemonicWhat it's for
WILLIAM MARROWBBB: W in V1 = LBBB; M in V1 = RBBB
300-150-100-75-60-50Heart rate from R-R large squares
I See aVF (Both up = Normal axis)Quick axis check
Longer, longer, longer, DROPWenckebach (Mobitz I)
DEADVT clues: Dissociation, Extreme axis, Absence of P-QRS relationship, Duration >160 ms
ABCDE for PEArrhythmia, BBB (RBBB), Cor pulmonale (P pulmonale), Deviation (RAD), S1Q3T3
Tented T = hyperK; Flat T + prominent U = hypoKElectrolytes
Concave ST = pericarditis; Convex ST = MIDistinguishing causes of ST elevation
PR depression + ST elevation = pericarditisClassic 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

  1. Paper calibration + waveform basics (Module 3, 4)
  2. Leads and normal ECG (Module 5, 6)
  3. Ischemia/STEMI localization (Module 10) - highest exam yield
  4. Bundle branch blocks (Module 8)
  5. AV blocks (Module 9)
  6. Arrhythmias systematic approach (Module 11)
  7. Metabolic effects (Module 13)
  8. 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!

Give me all ecgs for stepwise learning with explanation

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I have all images verified and ready. Now composing the full visual ECG atlas:

ECG Visual Atlas: Stepwise Learning with Real ECGs

All ECGs sourced from Harrison's Principles of Internal Medicine (22nd ed.) and Rosen's Emergency Medicine.

LEVEL 1 - The Foundation

ECG 1: Normal Sinus Rhythm - Your Baseline

Normal 12-lead ECG from a healthy male, sinus rhythm 75 bpm
What you're seeing: This is the template every other ECG is compared against.
Step-by-step analysis:
FeatureThis ECGNormal?
Rate75 bpm✅ 60-100
RhythmRegular, P before every QRS✅ Sinus
PR interval160 ms (4 small squares)✅ 120-200 ms
QRS duration80 ms (2 small squares)✅ <110 ms
QT interval360 ms, QTc ~390 ms✅ <450 ms
Axis~+70° (upright in I and aVF)✅ Normal
R-wave progressionSmall r in V1 → tall R in V5✅ Normal
Train your eye here first. Every abnormal ECG will deviate from this pattern in at least one way.

ECG 2: Ventricular Depolarization - How the QRS is Born

Ventricular depolarization phases: septal vector (left→right) and main LV vector (right→left), shown in relation to V1 and V6
This diagram explains why V1 looks different from V6:
  • Phase 1 (septum): Depolarizes left → right. V1 sees it coming → small upward r wave. V6 sees it going away → small downward q wave.
  • Phase 2 (ventricles): LV dominates, vector swings left → right. V1 sees it going away → deep S wave. V6 sees it coming → tall R wave.
Result:
  • V1 = rS (small r, big S)
  • V6 = qR (tiny q, big R)
  • V1 → V5 = R wave progressively gets bigger (R-wave progression)
Poor R-wave progression (R stays small across V1-V4) = anterior MI until proven otherwise.

LEVEL 2 - Atrial and Ventricular Enlargement

ECG 3: P Wave Morphology - Atrial Abnormalities

P wave comparison: Normal vs Right atrial (peaked, tall in II) vs Left atrial (broad, notched in II; deep terminal negative in V1)
How to read this diagram:
Lead IILead V1
NormalSmall, smooth P (RA then LA humps)Small biphasic P
Right atrial enlargementTall (>2.5 mm), peaked P ("P pulmonale")Large initial positive deflection
Left atrial enlargementBroad (>120 ms), notched P ("P mitrale")Large terminal negative component >1 mm²
Clinical causes:
  • RAE (P pulmonale): COPD, pulmonary hypertension, tricuspid stenosis, PE
  • LAE (P mitrale): Mitral stenosis, mitral regurgitation, LVH, dilated cardiomyopathy
Exam pearl: In V1, the terminal (second) negative deflection = left atrial component. If it's >1 mm wide AND >1 mm deep = LAE.

ECG 4: LVH and RVH Patterns

LVH showing tall R waves in lateral leads with ST depression/T-wave inversion (strain pattern); RVH showing dominant R in V1 with RAD and right precordial T inversions
The normal ECG above has normal voltages. For LVH/RVH, study the voltage criteria below:
LVH Criteria (Sokolow-Lyon):
  • S in V1 + R in V5 or V6 ≥ 35 mm
  • R in aVL ≥ 11 mm (women); ≥ 28 mm (men) - Cornell criteria
  • LV strain pattern: ST depression + asymmetric T inversion in I, aVL, V5, V6
RVH Criteria:
  • Dominant R wave in V1 (R ≥ S in V1)
  • Right axis deviation (axis > +90°)
  • RV strain pattern: T inversion in V1-V3
Memory: LVH = tall left; RVH = tall right (V1)

LEVEL 3 - Ischemia and Infarction (Highest Exam Yield)

ECG 5: The Mechanism of ST Deviation

Diagram showing subendocardial ischemia causing ST depression (vector points inward) vs transmural epicardial ischemia causing ST elevation (vector points outward)
This diagram is the conceptual key to all ischemia ECGs:
  • Panel A (Subendocardial ischemia): Injury current vector points inward → leads overlying the LV see ST depression. This is NSTEMI/unstable angina territory.
  • Panel B (Transmural/epicardial ischemia): Injury current vector points outward → leads overlying the zone see ST elevation. This is STEMI territory.
Think of it like a compass: The ST segment points toward the injured zone.

ECG 6: Anterior STEMI (LAD occlusion)

Anterior STEMI with ST elevation in V1-V4, oblique straight morphology. Patient had 90% LAD stenosis
What you're seeing:
  • ST elevation in V1-V4 (anteroseptal leads) - convex/oblique ST morphology
  • Note the tall R waves progressing V1-V4, then cut short by the ST change
  • This patient had a 90% LAD stenosis - went to cath lab immediately
Systematic read:
  1. Rate: ~70 bpm, sinus
  2. ST elevation: V1, V2, V3, V4 - ≥2 mm in V1-V3 = diagnostic STEMI
  3. Reciprocal changes: Look for ST depression in II, III, aVF (inferior leads)
  4. Q waves: May be developing - marker of established necrosis
  5. ACTION: Activate cath lab. Door-to-balloon time target: <90 min

ECG 7: Anterolateral STEMI (LAD + circumflex territory)

Anterolateral STEMI with ST elevation in V2-V6, I, and aVL. In-stent thrombosis of LAD
What you're seeing:
  • ST elevation spreading across V2-V6, I, and aVL = extensive anterolateral territory
  • This is a large territory MI - "widowmaker" territory (proximal LAD)
  • Patient had in-stent thrombosis of previous LAD stent
Comparison with ECG 6:
FeatureAnterior STEMI (ECG 6)Anterolateral STEMI (ECG 7)
ST elevationV1-V4 onlyV2-V6 + I + aVL
TerritoryAnteroseptalExtensive anterior + lateral
CulpritMid-LADProximal LAD or wrapping LAD
SeveritySignificantVery large - high risk

ECG 8: Wellens Syndrome (Critical LAD Stenosis Warning)

Wellens pattern: deep symmetric T-wave inversions in V2-V4 with preserved R waves and no ST elevation - indicates critical proximal LAD stenosis
This ECG can save a life - memorize it.
What you're seeing:
  • Deep, symmetric T-wave inversions in V2-V4 (precordial leads)
  • Note: no current ST elevation, R waves preserved (no Q waves yet)
  • Patient had chest pain that may have resolved
Why this matters: This is the "reperfusion pattern" of a critical proximal LAD stenosis. The artery opened briefly, but will re-occlude causing massive anterior MI.
Wellens Type A: Biphasic T waves in V2-V3 (earlier stage) Wellens Type B: Deep symmetric T inversions in V2-V4 (shown here - more advanced)
⚠️ DO NOT do a stress test on this patient - can precipitate VF and death. Refer urgently for coronary angiography.

ECG 9: Left Main / Proximal LAD Occlusion - aVR Elevation

ST elevation in aVR with widespread ST depression in all other leads - left main coronary artery occlusion
What you're seeing:
  • ST elevation in aVR > 1 mV (the lead pointing at the right shoulder / LV cavity)
  • Widespread ST depression in most other leads (I, II, aVL, V4-V6 at minimum)
  • This pattern = diffuse subendocardial ischemia from left main occlusion
Rule of thumb:
ST elevation in aVR + widespread ST depression elsewhere = Left main stenosis (78% sensitive, 83% specific) or severe proximal LAD disease
This is a cardiology emergency - highest-risk STEMI equivalent.

LEVEL 4 - Bundle Branch Blocks

ECG 10: RBBB vs LBBB - The WiLLiaM MaRRow Rule

The following shows the BBB patterns in V1 and V6:
V1V6
RBBBM-shaped (rSR') = rabbit earsW-shaped (wide S)
LBBBW-shaped (QS or rS)M-shaped (broad notched R)
Mnemonic: WiLLiaM MaRRow
  • WiLLiam = LBBB has W in V1, M in V6
  • MaRRow = RBBB has M in V1, W in V6
RBBB Diagnostic Criteria:
  • QRS ≥ 120 ms
  • rSR' ("rabbit ears") in V1
  • Wide slurred S in I, aVL, V5, V6
  • T wave inverted in V1-V2 (secondary - normal with RBBB, not ischemia)
LBBB Diagnostic Criteria:
  • QRS ≥ 120 ms
  • Broad monophasic R in I, aVL, V5, V6 (no Q wave, no S wave)
  • Deep QS or rS in V1
  • T wave inverted in I, aVL, V5, V6 (secondary - normal with LBBB)
Clinical significance:
  • RBBB: Often benign; new RBBB in acute anterior MI = proximal LAD (septal branch involvement)
  • LBBB: New LBBB + chest pain = treat as STEMI (modified Sgarbossa criteria)
Sgarbossa Criteria for MI in LBBB (score ≥ 3 = MI):
FindingPoints
ST elevation ≥ 1 mm concordant with QRS (same direction)5
ST depression ≥ 1 mm in V1-V33
ST elevation ≥ 5 mm discordant with QRS2

LEVEL 5 - AV Blocks (Visual Patterns)

ECG 11-13: The Three AV Blocks

1st Degree AV Block:
P----P----P----P      (every P conducts)
QRS  QRS  QRS  QRS   (every P has a QRS)
↕PR: >200ms (stretched but constant)
Benign. PR > 5 small squares. All P waves conduct.

2nd Degree - Mobitz I (Wenckebach):
P    P    P    P    P    P    P
QRS  QRS  QRS  ---  QRS  QRS  ---
PR:  ↑    ↑↑   ↑↑↑  drop  ↑    ↑↑   drop
PR gets longer and longer until a QRS is dropped, then resets. "Longer longer longer DROP."
  • Benign, usually AV node level
  • Common in athletes (high vagal tone) and inferior MI

2nd Degree - Mobitz II:
P    P    P    P    P    P
QRS  QRS  ---  QRS  QRS  ---
PR:   =    =         =    =   (CONSTANT then sudden drop)
Fixed PR, then sudden non-conducted P without warning.
  • Dangerous - below the AV node (His-Purkinje)
  • Associated with wide QRS, anterior MI
  • Requires pacemaker - high risk of complete block

3rd Degree (Complete AV Block):
P    P    P    P    P    P    P    P   (fast, ~70-80/min)
   QRS      QRS      QRS      QRS     (slow, 30-50/min)
P waves and QRS complexes march completely independently.
  • Narrow QRS escape = junctional (40-60/min) = AV node still working below block
  • Wide QRS escape = ventricular (20-40/min) = dangerous, more hemodynamically unstable
  • Emergency: atropine (narrow complex), transcutaneous pacing, urgent permanent pacemaker

LEVEL 6 - Metabolic ECGs (Must Know for Exams)

ECG 14: Hyperkalemia - The Deadly Progression

Hyperkalemia ECG progression: mild-moderate showing peaked T waves in V1-V2; moderate-severe showing wide QRS and flattened P waves; very severe showing sine-wave pattern in leads I and II
Read this image panel by panel:
PanelK+ LevelECG Changes
Mild-Moderate (V1, V2 left panel)5.5-6.5 mEq/LTall, narrow, peaked ("tented") T waves - classic first sign
Moderate-Severe (V1, V2 middle panel)6.5-8 mEq/LWide QRS, flat/absent P waves, peaked T waves still visible
Very Severe (Lead I, II right panel)>8 mEq/LSine wave pattern - imminent asystole
Why this matters clinically:
  • Peaked T waves = call for ECG immediately in any CKD/renal patient
  • Sine wave = life-threatening emergency - give calcium gluconate NOW
  • Treatment sequence: C-BIG-K-D (Calcium, Bicarbonate, Insulin+Glucose, Kayexalate, Dialysis)

ECG 15: Hypokalemia - The U Wave

Hypokalemia ECG showing flattened T wave in lead II and prominent U wave in V3 (U wave taller than T wave)
What you're seeing:
  • Lead II (left): Flat T wave, barely visible, slight prolongation of the QT interval
  • V3 (right): Prominent U wave labeled - note it is taller than the T wave in this lead
Key features of hypokalemia:
  • T wave flattening → T wave inversion
  • U wave prominence (U > T = significant hypokalemia)
  • Apparent QT prolongation (actually QU prolongation - U wave merging with T)
  • Risk: Torsades de Pointes especially if on QT-prolonging drugs
Causes to recognize: Diuretics (thiazide, loop), vomiting, diarrhea, Conn's syndrome, hypomagnesemia

ECG 16: Pericarditis with Cardiac Tamponade - Electrical Alternans

Pericardial effusion with tamponade: sinus tachycardia + low QRS voltage + electrical alternans (QRS height alternating beat-to-beat, best seen in V2 and V4)
The classic triad of cardiac tamponade on ECG:
  1. Sinus tachycardia (compensatory, filling impaired)
  2. Low QRS voltage (<5 mm all limb leads and/or <10 mm chest leads) - fluid insulating the heart
  3. Electrical alternans - QRS height alternates every other beat (arrows in V2, V4) - heart swinging inside fluid
Acute pericarditis ECG features (before effusion develops):
  • Diffuse saddle-shaped (concave) ST elevation in most leads (not just regional)
  • PR segment depression (very specific for pericarditis)
  • No reciprocal ST depression (except aVR)
  • No Q waves
Pericarditis vs STEMI - the critical distinction:
FeaturePericarditisSTEMI
ST shapeConcave (saddle)Convex (dome/tombstone)
DistributionDiffuse (all leads)Regional (2+ contiguous)
PR depressionPresentAbsent
Reciprocal ST depressionAbsentPresent
Q wavesNeverDevelop hours-days

LEVEL 7 - Clinical Syndromes (Advanced)

ECG 17: Inferior STEMI - RCA Occlusion

What to look for:
  • ST elevation in II, III, aVF (inferior leads)
  • Reciprocal ST depression in I and aVL (lateral leads)
  • III > II elevation = more likely RCA (proximal)
  • II > III elevation = more likely LCx
Critical associated findings to always check:
  1. Right-sided leads (V3R, V4R): If ST elevation here = RV infarction (25-40% of inferior STEMIs)
    • RV MI = give fluids (not nitrates!), no diuretics, no morphine
  2. Posterior leads (V7-V9) or V1-V2: Tall R + ST depression in V1-V2 = posterior extension
  3. Complete AV block: RCA supplies AV node - inferior MI can cause bradycardia / heart block

ECG 18: WPW (Wolff-Parkinson-White) Pattern

What to look for in sinus rhythm:
  • Short PR (<120 ms) - bypassing the AV node
  • Delta wave - slurred initial upstroke of QRS (most visible in lateral leads)
  • Wide QRS (>120 ms) - fusion beat (normal + accessory pathway conduction)
  • Pseudo-Q waves and ST-T changes - secondary to abnormal depolarization
Location of pathway by delta wave:
Delta waveLeadPathway location
PositiveV1-V3Left-sided (most common, type A)
NegativeV1Right-sided (type B)
NegativeII, III, aVFPosterior/inferior
The WPW arrhythmia danger:
  • Orthodromic AVRT: Narrow complex tachycardia (down AV node, up AP) - treat with adenosine
  • Antidromic AVRT: Wide complex tachycardia (down AP, up AV node)
  • AF with WPW: Irregular wide complex tachycardia - VERY FAST rate (>250 bpm possible) → risk of VF
⚠️ Never give adenosine, digoxin, verapamil, diltiazem in AF+WPW - these block AV node but not accessory pathway, driving all conduction down the fast AP → VF Use: DC cardioversion (if unstable) or IV procainamide/ibutilide

ECG 19: Pulmonary Embolism - S1Q3T3

PE ECG findings (in order of frequency):
  1. Sinus tachycardia - most common, most sensitive
  2. T-wave inversions V1-V4 - right heart strain pattern (right precordial leads)
  3. New RBBB or RBBB morphology - acute RV pressure overload
  4. S1Q3T3 - classic but actually uncommon (<20% of PE cases)
  5. Right axis deviation
  6. P pulmonale - peaked P waves from acute RA overload
  7. Atrial fibrillation or flutter
S1Q3T3 breakdown:
  • S in lead I (deep S = left lateral lead sees delayed RV activation)
  • Q in lead III (inferior lead)
  • T inversion in lead III (RV strain)
Exam tip: Normal ECG or just sinus tachycardia does NOT rule out PE. The most sensitive PE ECG finding is sinus tachycardia, not S1Q3T3. ECG in PE is used to increase/decrease probability, not diagnose.

ECG 20: Brugada Pattern

Type 1 (Diagnostic - the only one that counts):
  • Coved ST elevation ≥ 2 mm in V1 (and sometimes V2)
  • Down-sloping ST segment
  • T wave inversion in V1
Types 2 and 3: Saddleback pattern - not diagnostic without Type 1 either spontaneous or after sodium channel blocker challenge
Clinical importance:
  • Risk of sudden cardiac death from VF (especially at night, during fever)
  • Sodium channel mutation (SCN5A - autosomal dominant)
  • Unmasked by: fever, cocaine, alcohol, flecainide, procainamide (sodium channel blockers)
  • Treatment: ICD (implantable cardioverter defibrillator) for symptomatic patients
  • Quinidine for recurrent VF episodes or fever-triggered events

LEVEL 8 - Arrhythmia Recognition (Rhythm Strips)

How to Systematically Approach Any Rhythm Strip

Use this 4-question framework every time:
1. RATE → Fast? Slow? Normal?
2. REGULAR? → Measure R-R intervals
3. QRS WIDTH → Narrow (<120ms) or Wide (≥120ms)?
4. P WAVES → Present? Before QRS? Normal morphology?

Arrhythmia Quick Recognition Table

ArrhythmiaRateRegular?QRSP wavesDistinguishing Feature
Sinus tach100-160YesNarrowNormal, before QRSGradual onset, normal P morphology
AF100-160 ventricularNo (irregularly irregular)NarrowAbsent (fibrillatory baseline)Irregularly irregular, no P waves
AFL150 ventricularYes (usually 2:1)NarrowSawtooth in II, III, aVFRate 150 = think flutter!
AVNRT150-250YesNarrowBuried in QRS or pseudo-R' in V1Abrupt onset/offset, no visible P
AVRT (WPW)150-250YesNarrow (or wide)Retrograde P after QRSDelta wave in sinus rhythm
VT>100YesWide (≥120ms)Dissociated (march independently)AV dissociation = definitive VT
VFChaoticNoNo organized QRSNoneNo output - cardiac arrest
TorsadesVariableNoWide, twistingNone visibleQRS alternates direction around baseline
1° AVBAnyYesNormalNormalPR >200ms, all P's conduct
WenckebachNormal-slowGrouped beatingNormalSome P's blockedProgressive PR then dropped QRS
Mobitz IINormal-slowMostlyNormal/WideSudden blocked PFixed PR, sudden drop
3° AVBSlow ventricularP regular, QRS regular but different ratesWide or narrowDissociated from QRSP rate > QRS rate, independent

The Wide Complex Tachycardia Decision Tree

Wide Complex Tachycardia (QRS ≥120ms, Rate >100)
                    ↓
     Is patient UNSTABLE? (hypotensive, altered consciousness, pulmonary edema)
         YES ──────────────────→ SYNCHRONIZED DC CARDIOVERSION
          ↓NO
     Look for AV Dissociation?
         YES ──────────────────→ DEFINITELY VT → Amiodarone or Cardioversion
          ↓NO
     Capture beats or Fusion beats?
         YES ──────────────────→ DEFINITELY VT → Amiodarone
          ↓NO
     Brugada morphology criteria? QRS >160ms? Concordance?
         YES ──────────────────→ LIKELY VT → Amiodarone
          ↓NO
     Could this be AF + WPW? (irregular wide complex + very fast)
         YES ──────────────────→ Procainamide or Cardioversion (NOT adenosine/verapamil)
          ↓NO
     LIKELY SVT with aberrancy → Adenosine trial (have crash cart ready)
Rule: When uncertain, treat wide-complex tachycardia as VT. Adenosine is safe for narrow complex. For wide complex, amiodarone is the safest drug.

LEVEL 9 - Special ECG Patterns (Exam Favourites)

Quick Pattern Recognition Summary

PatternKey ECG FindingDiagnosis
Sawtooth waves in II, III, aVF at 300/minFlutter wavesAtrial flutter
Irregularly irregular, no P wavesAFAtrial fibrillation
Short PR + delta wave + wide QRSPre-excitationWPW syndrome
Coved ST elevation V1-V2Type 1 BrugadaBrugada syndrome
Peaked T waves → wide QRS → sine waveHyperkalemiaSevere hyperkalemia
Prominent U waves, flat THypokalemiaHypokalemia
Diffuse concave ST + PR depressionPericarditisAcute pericarditis
Regional convex ST elevationIschemic injurySTEMI
Electrical alternans + low voltage + tachycardiaTamponadeCardiac tamponade
S1Q3T3 + sinus tachycardia + new RBBBPE patternPulmonary embolism
Deep T inversions V2-V4 + no ST elevationWellensCritical LAD stenosis
ST elevation V1-V2 + aVR > ST in other leadsLeft main / proximal LADLeft main disease
J wave (Osborn wave) at J pointHypothermiaHypothermia
Scooping ST depression + short QTDigoxin effectDigoxin
Prolonged QT + polymorphic VTTorsadesLong QT syndrome

Clinical Practice Summary Card

Every ECG you pick up, run through this checklist in 30 seconds:
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━
1. RATE        → Count (300 rule) / Irregular → count × 6
2. RHYTHM      → P before QRS? Regular? Sinus?
3. PR          → 120-200ms? Short (WPW)? Long (AVB)?
4. QRS         → <110ms? Wide (BBB/VT/pace)?
5. AXIS        → I and aVF upright = normal
6. ST SEGMENTS → Elevation (which leads)? Depression?
7. T WAVES     → Inverted (where)? Peaked (hyperK)?
8. QT          → Prolonged (drugs/electrolytes/long QT)?
9. P WAVES     → Peaked (RAE)? Broad (LAE)?
10. U WAVES    → Prominent (hypoK)?
11. COMPARE    → With previous ECG!
━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━━

Sources: Harrison's Principles of Internal Medicine 22nd ed. (2025) Ch. 247 - Electrocardiography; Rosen's Emergency Medicine 9th ed. Ch. 64 - Acute Coronary Syndromes; Tintinalli's Emergency Medicine.

Next steps: Want me to drill you with ECG cases (show ECG → you diagnose → I explain), or go deeper on any specific pattern - arrhythmias, STEMI localization, BBBs, or electrolyte changes?
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