Professional Medical Education

Electrocardiography
Comprehensive Guide

A complete, detailed reference for understanding the 12-lead ECG — from fundamental electrophysiology to advanced pathological pattern recognition.

12
Standard Leads
5
Major Waves
0.04s
Per Small Square
25
mm/s Paper Speed

ECG Fundamentals

Electrophysiology & Recording Principles

What is an ECG?

An Electrocardiogram (ECG/EKG) is a non-invasive diagnostic tool that records the electrical activity of the heart over time using electrodes placed on the skin surface. It captures the summation of all cardiac action potentials as they propagate through the myocardium.

Depolarization — the wave of electrical activation spreading across the myocardium, causing contraction
Repolarization — the recovery phase where the myocardium returns to its resting electrical state

Cardiac Conduction System

1
SA Node (Sinoatrial)
Primary pacemaker • 60-100 bpm • Right atrium
2
AV Node (Atrioventricular)
Delays impulse ~0.12s • 40-60 bpm backup • Interatrial septum
3
Bundle of His
Penetrates fibrous skeleton • Divides into left & right bundle branches
4
Bundle Branches & Purkinje Fibers
Rapid conduction (2-4 m/s) • 20-40 bpm backup • Endocardial network

ECG Paper & Calibration

0.20s (1 large box) 0.04s (1 small box) 1 large box = 0.5mV 1 small box = 0.1mV 1mV cal Standard: 25 mm/s • 10 mm/mV
Time (X-axis): 25 mm/s
Voltage (Y-axis): 10 mm/mV

Einthoven's Triangle

🫀 LL + RA - LA +/- Lead II Lead III Lead I

Einthoven's Law: Lead II = Lead I + Lead III. The bipolar limb leads form an equilateral triangle around the heart, providing frontal plane vectors.

Waves, Intervals & Segments

Interactive ECG Complex Analysis

Interactive Normal ECG Complex

Click on any wave component below to see its details

P Q R S T U PR Interval QRS Duration QT Interval ST

P Wave

Represents: Atrial depolarization

Duration: <0.12s (3 small squares)

Amplitude: <2.5mm in Lead II

Morphology: Upright in I, II, aVF; inverted in aVR

Best seen: Lead II and V1

Clinical Pearl: P-mitrale (bifid P in II) = LA enlargement. P-pulmonale (peaked P in II) = RA enlargement.

QRS Complex

Represents: Ventricular depolarization

Duration: 0.06–0.10s (normal)

Q wave: First negative deflection before R

R wave: First positive deflection

S wave: Negative deflection after R

Clinical Pearl: QRS >0.12s = Bundle Branch Block. Pathological Q waves (>1 small sq wide, >1/3 R height) suggest prior MI.

T Wave

Represents: Ventricular repolarization

Direction: Usually concordant with QRS

Amplitude: <5mm limb leads, <10mm precordial

Morphology: Asymmetric (slow rise, rapid descent)

Inverted normally in: aVR, V1 (sometimes V2-V3)

Clinical Pearl: Hyperacute tall T waves = earliest sign of STEMI. Deep symmetric T inversions = Wellens' syndrome (critical LAD stenosis).

Intervals & Segments Reference

Parameter Normal Value Represents Abnormality Significance
PR Interval 0.12–0.20s Atrial depolarization + AV delay >0.20s = 1° AV block; <0.12s = pre-excitation (WPW)
QRS Duration 0.06–0.10s Ventricular depolarization >0.12s = BBB, ventricular rhythm, hyperkalemia
ST Segment Isoelectric Early ventricular repolarization Elevation = STEMI/pericarditis; Depression = ischemia/digitalis
QT Interval 0.36–0.44s Total ventricular electrical activity Prolonged QTc >0.46s = risk of Torsades de Pointes
RR Interval 0.6–1.0s Ventricular rate (300/# large boxes) Irregular = AFib; Regular short = SVT/VT

The 12-Lead ECG System

Electrode Placement & Lead Views

Bipolar Limb Leads (I, II, III)

Lead I

RA (−) → LA (+). Views the lateral wall. Measures horizontal electrical axis.

Lead II +60°

RA (−) → LL (+). Views the inferior wall. Best lead for rhythm analysis — P waves most prominent here.

Lead III +120°

LA (−) → LL (+). Views the inferior wall. Complements Lead II for inferior MI diagnosis.

I II +60° III +120° 🫀

Augmented Unipolar Leads (aVR, aVL, aVF)

aVR −150°

Right arm perspective. Normally all negative (inverted P, negative QRS, inverted T). Upright QRS in aVR = critical finding (sodium channel blockade, dextrocardia, lead misplacement).

aVL −30°

Left arm perspective. Views the high lateral wall. ST elevation here with Lead I = high lateral MI (diagonal branch / LCx).

aVF +90°

Left foot perspective. Views the inferior wall directly. Key lead for inferior MI (RCA territory).

Goldberger's Augmented Leads Principle

Augmented leads are unipolar — they measure voltage at a single electrode relative to a modified Wilson's Central Terminal. They are "augmented" by 50% to produce adequate deflections. Together with bipolar leads, they complete the hexaxial reference system in the frontal plane.

Axis Determination Quick Method:

Look at Lead I and aVF:
• Both positive = Normal axis (0° to +90°)
• Lead I negative, aVF positive = Right axis deviation
• Lead I positive, aVF negative = Left axis deviation
• Both negative = Extreme axis deviation

Precordial (Chest) Leads V1–V6

V1
4th ICS, right sternal border
Septal view • rS pattern normal
V2
4th ICS, left sternal border
Septal view • rS pattern normal
V3
Between V2 and V4
Anterior view • Transition zone
V4
5th ICS, midclavicular line
Anterior view • R/S ratio ≈ 1
V5
5th ICS, anterior axillary line
Lateral view • qR pattern
V6
5th ICS, midaxillary line
Lateral view • qR pattern

R-Wave Progression

Normal R-wave progression shows increasing R-wave amplitude from V1 to V5, with the transition zone (R=S) normally at V3-V4.

V1 V2 V3 V4 V5 V6 R-wave progression → ↑ Transition zone

Poor R-wave Progression (PRWP):

Anterior MI, LBBB, LVH, COPD, cardiomyopathy, or lead misplacement.

Lead Groups & Coronary Artery Territories

Inferior Wall

Leads: II, III, aVF

Artery: Right Coronary Artery (RCA) — 80% of cases; Left Circumflex (LCx) — 20%

Reciprocal changes in: I, aVL

Anterior Wall

Leads: V1, V2, V3, V4

Artery: Left Anterior Descending (LAD)

Reciprocal changes in: II, III, aVF

Lateral Wall

Leads: I, aVL, V5, V6

Artery: Left Circumflex (LCx) or diagonal branches of LAD

Reciprocal changes in: V1, III

Septal

Leads: V1, V2

Artery: LAD (septal perforators)

Posterior Wall

No direct leads (use V7–V9)

Artery: RCA or LCx (posterior descending)

Mirror changes: tall R and ST depression in V1–V3

Right Ventricle

Right-sided leads: V3R, V4R

Artery: Proximal RCA

Always check V4R in inferior STEMI!

Systematic ECG Interpretation

Step-by-Step Approach

Methods to calculate heart rate:

300 Method (Regular)

HR = 300 ÷ (# large boxes between R-R)

Example: 4 large boxes = 75 bpm

1500 Method (Precise)

HR = 1500 ÷ (# small boxes between R-R)

6-Second Method (Irregular)

Count QRS in 30 large boxes × 10

Normal: 60–100 bpm • Bradycardia: <60 bpm • Tachycardia: >100 bpm

Criteria for Normal Sinus Rhythm:

Upright P waves in leads I, II, aVF (inverted in aVR)
Every P wave followed by a QRS complex
Constant PR interval (0.12–0.20s)
Regular R-R intervals (variation <10%)
Rate 60–100 bpm

Irregularly irregular = AFib • Regularly irregular = 2° AV block, PACs/PVCs in pattern

Quick Axis Determination (Lead I + aVF):

Normal (−30° to +90°): Lead I ↑, aVF ↑
LAD (−30° to −90°): Lead I ↑, aVF ↓
RAD (+90° to +180°): Lead I ↓, aVF ↑
Extreme (−90° to ±180°): Lead I ↓, aVF ↓

Causes of LAD: LAFB, inferior MI, LVH. Causes of RAD: LPFB, RVH, PE, lateral MI.

P Wave Assessment

Shape, size, and consistency. Look for P-mitrale (LA enlargement) or P-pulmonale (RA enlargement). Absent P waves suggest AFib or junctional rhythm.

QRS Morphology

Duration (<0.12s normal), height, pathological Q waves, bundle branch block patterns (rsR' in V1 = RBBB; broad monophasic R in V5-V6 = LBBB).

ST Elevation Causes

STEMI (convex up), Pericarditis (concave up, diffuse, PR depression), Benign early repolarization, LV aneurysm, Brugada syndrome, Prinzmetal angina.

ST Depression Causes

Subendocardial ischemia, Digitalis effect (reverse tick), LVH strain pattern, Reciprocal changes in STEMI, Hypokalemia.

T Wave Abnormalities

Hyperacute T waves: Tall, broad, symmetric = earliest STEMI sign. Deep T inversions: Wellens' (V2-V3) = critical LAD. Peaked T waves: Hyperkalemia. Flattened T waves: Hypokalemia, ischemia.

Bazett's Formula

QTc = QT ÷ √RR

Normal QTc: <440ms (♂) / <460ms (♀). Prolonged QTc increases risk of Torsades de Pointes — check medications (antiarrhythmics, antibiotics, antipsychotics) and electrolytes (↓K⁺, ↓Mg²⁺, ↓Ca²⁺).

Pathological ECG Patterns

Critical Diagnoses & Recognition

🫀 Myocardial Infarction Evolution

Minutes Hyperacute T waves (tall, peaked, broad)
Hours ST elevation (convex), reciprocal depression
Hours-Days Q wave development, T wave inversion begins
Days-Wks ST normalizes, deep T inversions
Months+ Pathological Q waves may persist permanently

Key Arrhythmias

Atrial Fibrillation: Irregularly irregular, no P waves, fibrillatory baseline. CHA₂DS₂-VASc for stroke risk.
Atrial Flutter: Sawtooth F-waves (best in II, III, V1), typically 2:1 or 4:1 block. Ventricular rate usually ~150 bpm.
SVT (AVNRT): Narrow complex, regular, 150-250 bpm. Pseudo-R' in V1 or pseudo-S in inferior leads.
Ventricular Tachycardia: Wide complex (>0.12s), regular, AV dissociation, capture/fusion beats. ALWAYS assume VT until proven otherwise!
Ventricular Fibrillation: Chaotic, no identifiable waves. IMMEDIATE defibrillation required.

🔌 AV Conduction Blocks

1° AV Block: PR >0.20s, all P waves conducted. Usually benign.
2° Type I (Wenckebach): Progressive PR prolongation → dropped QRS. Usually Mobitz I pattern, often benign.
2° Type II (Mobitz II): Constant PR → sudden dropped QRS. Below His bundle. HIGH RISK for complete block — may need pacing.
3° (Complete) AV Block: Complete AV dissociation. P waves and QRS march independently. Requires pacing.

🌿 Bundle Branch Blocks

RBBB — Right Bundle Branch Block:

QRS >0.12s. rsR' pattern ("M-shaped") in V1-V2. Wide S wave in I, V5-V6. Remember: "MaRRoW" — M in V1 (R'), W in V6 (S).

LBBB — Left Bundle Branch Block:

QRS >0.12s. Broad monophasic R in I, V5-V6. Deep rS in V1. Remember: "WiLLiaM" — W in V1, M in V6. New LBBB + chest pain = cath lab!

🧪 Electrolyte Effects

Hyperkalemia (↑K⁺): Peaked T waves → P wave flattening → QRS widening → sine wave → VF/asystole. EMERGENCY!
Hypokalemia (↓K⁺): T wave flattening → U waves → ST depression → QT prolongation → TdP risk.
Hypercalcemia (↑Ca²⁺): Short QT interval. Osborn (J) waves possible.
Hypocalcemia (↓Ca²⁺): Prolonged QT (ST segment elongation specifically).

💪 Chamber Hypertrophy

LVH (Sokolow-Lyon): S(V1) + R(V5 or V6) >35mm. Also: R(aVL) >11mm. Strain pattern: asymmetric ST depression & T inversion in lateral leads.
RVH: Right axis deviation, dominant R in V1 (>7mm or R/S >1), deep S in V5-V6, right atrial enlargement (P-pulmonale).

Test Your Knowledge

Interactive ECG Quiz

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