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ECG from the Basics: A Complete Beginner's Guide

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1. What Is an ECG?

• Guyton & Hall Medical Physiology

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2. The Cardiac Conduction System (The Foundation)

Key clinical point: If the SA node fails, the AV node takes over at ~40-60 bpm. If the AV node fails, the ventricles pace themselves at ~20-40 bpm (very slow and dangerous).

• Gray's Anatomy for Students; Harrison's 22E

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3. The ECG Waveform: P-QRS-T

P Wave

• Represents: Atrial depolarization (both atria contract)
• Duration: 0.06-0.12 seconds (1.5-3 small boxes)
• Amplitude: 2-3 mm high normally
• Normal appearance: Small, rounded, upright in lead II; negative in aVR
• In lead V1, it may be biphasic (positive component = right atrium, negative = left atrium)

PR Interval

• Represents: Time from start of atrial depolarization to start of ventricular depolarization - includes the AV node delay
• Normal: 120-200 ms (3-5 small boxes)
• A prolonged PR (>200 ms) = first-degree AV block

QRS Complex

• Represents: Ventricular depolarization (both ventricles contract)
• Duration: Normally ≤100-110 ms (≤2.5 small boxes)
• The QRS is larger than the P wave because ventricular muscle mass is much greater than atrial mass
• Q wave: Small initial downward deflection (septal depolarization, left→right)
• R wave: Tall upward spike
• S wave: Downward deflection after R
• Not every QRS will have all three components

ST Segment

• Represents: Ventricular plateau phase (phase 2 of action potential) - isoelectric period between depolarization and repolarization
• Normally flat (isoelectric)
• ST elevation = acute myocardial infarction (STEMI) or pericarditis
• ST depression = ischemia or NSTEMI

T Wave

• Represents: Ventricular repolarization (ventricles "recharging")
• Occurs 0.25-0.35 seconds after depolarization
• Normally upright in most leads
• This is a repolarization wave (opposite mechanism to the depolarization waves)

QT Interval

• Represents: Total ventricular activity (depolarization + repolarization)
• Normally: ≤460 ms in women, ≤450 ms in men (corrected for rate = QTc)
• Prolonged QT = risk of dangerous arrhythmia (torsades de pointes)

U Wave

• Small wave after T wave; seen in some leads
• May represent late repolarization of Purkinje fibers

Mnemonic: "P-QRS-T" = Please Queen, Rest Some Time

• Harrison's Principles of Internal Medicine 22E; Guyton & Hall Medical Physiology

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4. The ECG Paper

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5. Calculating Heart Rate

1. 300 ÷ number of large boxes between two R waves
   • 1 large box = 300 bpm, 2 = 150, 3 = 100, 4 = 75, 5 = 60, 6 = 50
   • Easy memory trick: "300, 150, 100, 75, 60, 50"
2. For irregular rhythms: Count the number of QRS complexes in 10 seconds (one rhythm strip) and multiply by 6.

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6. The 12 ECG Leads

Limb Leads (6) - view the heart in the frontal plane:

Precordial Leads (6) - view the heart in the horizontal plane:

• Harrison's Principles of Internal Medicine 22E

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7. A Systematic Approach to Reading Any ECG

1. Rate - Is it normal (60-100), slow (<60 = bradycardia), or fast (>100 = tachycardia)?
2. Rhythm - Regular or irregular? Is every P wave followed by a QRS?
3. P wave - Present? Normal shape? Upright in II? Every P followed by QRS?
4. PR interval - Normal (120-200 ms)?
5. QRS duration - Narrow (<120 ms) or wide (≥120 ms)? Wide = bundle branch block or ventricular origin
6. ST segment - Flat, elevated, or depressed?
7. T wave - Upright, inverted, peaked?
8. QT interval - Normal for the rate?
9. Axis - Normal (-30° to +90°)? Left or right axis deviation?

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8. Common Beginner Patterns to Recognize

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9. What to Study Next (Learning Roadmap)

1. Start with: Normal sinus rhythm recognition - master the normal before the abnormal
2. Then: Arrhythmias - sinus tachycardia/bradycardia, atrial fibrillation, SVT
3. Then: Conduction blocks - AV blocks (1st, 2nd, 3rd degree) and bundle branch blocks
4. Then: Ischemia/infarction patterns - STEMI, NSTEMI, old MI (Q waves)
5. Then: Axis determination and chamber hypertrophy
6. Advanced: Electrolyte abnormalities on ECG, drug effects (digoxin, QT-prolonging drugs)

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• Goldberger's Clinical Electrocardiography (10th ed.) - the classic beginner textbook
• Life in the Fast Lane ECG Library - free, comprehensive online reference
• ECG Wave-Maven (Harvard) - free ECG practice cases
• Ninja Nerd ECG Lecture - popular video lecture

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Electrical Axis: How to Calculate It and Identify Axis Deviation

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1. What Is the Electrical Axis?

• Guyton & Hall Textbook of Medical Physiology

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2. The Hexaxial Reference System

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3. Methods of Calculating the Axis

Method 1 - The Precise Vector Method (Guyton)

1. Measure the net QRS deflection in Lead I - add up positive mm, subtract negative mm (R - S - Q = net)
2. Measure the net QRS deflection in Lead III - same method
3. Draw the hexaxial diagram on paper
4. Plot the Lead I net value along the Lead I axis (0° line), measured from the center
5. Plot the Lead III net value along the Lead III axis (120° line), measured from the center
6. Drop perpendicular lines from the tip of each plotted point
7. The point where the two perpendiculars intersect = the tip of the mean QRS vector
8. Draw a line from the center of the diagram to that intersection point - this is your axis
9. Read the angle from the hexaxial reference

Example from Guyton: Lead I net = positive, Lead III net = positive → perpendiculars intersect at approximately +59° = normal axis.

• Guyton & Hall Textbook of Medical Physiology

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Method 2 - The Quick Two-Lead Quadrant Method (Clinical Bedside)

• Lead I positive + aVF negative + Lead II positive → axis between 0° and −30° → normal variant (or physiologic LAD)
• Lead I positive + aVF negative + Lead II negative → axis more negative than −30° → true pathological LAD

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Method 3 - The Isoelectric (Perpendicular) Method

1. Find the lead with the most biphasic/isoelectric QRS (positive and negative deflections roughly equal, net ≈ 0)
2. The true axis is perpendicular to that lead (90° away)
3. Look at the perpendicular lead to determine which of the two possible perpendicular directions is positive

Example: If lead aVL (at −30°) is isoelectric, the axis must be perpendicular = either +60° or −120°. Look at lead II (+60°): if lead II is positive, the axis is +60°.

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4. Normal vs. Abnormal Axis - Reference Table

Note: Some sources define normal as 0° to +90°, treating −30° to 0° as "physiologic LAD." The clinical threshold for pathological LAD is more negative than −30°.

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5. Causes of Axis Deviation

Left Axis Deviation (LAD) - axis more negative than −30°

From Guyton: In LBBB, the left ventricle remains electropositive while the right has already depolarized - creating a strong vector toward the left, producing axis around −50°.

Right Axis Deviation (RAD) - axis more positive than +90°

From Guyton: In right ventricular hypertrophy from pulmonary valve stenosis, the axis can reach +170° - 111° to the right of the normal axis of +59°.

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6. Worked Example - How to Determine Axis Step by Step

• Lead I: tall R wave (positive, net +8 mm)
• aVF: small net negative (−2 mm)
• Lead II: net negative

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7. Quick Summary Card

NORMAL:    Lead I ↑  aVF ↑   → 0° to +90°
LAD:       Lead I ↑  aVF ↓   → more negative than −30°
RAD:       Lead I ↓  aVF ↑   → more positive than +90°
EXTREME:   Lead I ↓  aVF ↓   → "northwest" axis

Refine LAD with Lead II:
  Lead II ↑ = mild/physiologic (0° to −30°)
  Lead II ↓ = pathological (< −30°)

Most common causes:
  LAD → LAFB, LVH, inferior MI
  RAD → RVH, RBBB, LPFB

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Abnormal ECG Patterns: A Complete Advanced Guide

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SECTION 1: ARRHYTHMIAS

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1.1 Atrial Fibrillation (AF)

• No P waves - replaced by a chaotic, irregular baseline (fibrillatory waves), most prominent in V1
• Irregularly irregular RR intervals (the hallmark - no two consecutive RR intervals are equal)
• QRS is narrow (unless aberrant conduction or bundle branch block present)
• Ventricular rate typically 120-170 bpm when AV node is unaffected

• Multifocal atrial tachycardia (MAT) - also irregular, but P waves are present in at least 3 different morphologies
• Atrial flutter with variable block - flutter waves (sawtooth) visible, not truly chaotic

• Tintinalli's Emergency Medicine

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1.2 Atrial Flutter

• Sawtooth flutter waves at ~300 bpm, best seen in inferior leads (II, III, aVF) and V1
• P waves have a single, uniform morphology (downward deflection in inferior leads)
• Ventricular rate is a function of AV block ratio:
  • 2:1 block = 150 bpm (most common - tip: any regular narrow tachycardia at ~150 bpm, always look for flutter)
  • 3:1 block = 100 bpm
  • 4:1 block = 75 bpm
• Regular ventricular rhythm (unless variable block)

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1.3 Supraventricular Tachycardia (SVT) / AVNRT

• Regular narrow-complex tachycardia, rate 150-250 bpm
• P waves absent, buried in QRS, or immediately after QRS (pseudo-r' in V1, pseudo-s in inferior leads)
• Abrupt onset and termination ("paroxysmal")
• QRS typically narrow unless bundle branch block present

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1.4 Ventricular Tachycardia (VT)

• Wide complex tachycardia (QRS ≥120 ms), rate >100 bpm (usually 140-220 bpm)
• Regular rhythm (slight irregularity possible)
• AV dissociation - P waves and QRS complexes are completely independent (P waves "march through" the wide QRS) - pathognomonic but only seen in ~10% of cases
• Fusion beats - hybrid beat where sinus impulse partially captures ventricle during VT (narrow-ish QRS between wide complexes) - confirms VT
• Capture beats - normal narrow QRS in middle of VT run when sinus impulse fully captures ventricle
• QRS morphology: concordance (all precordial leads positive OR all negative) strongly suggests VT
• QRS duration >160 ms in RBBB morphology or >140 ms in LBBB morphology favors VT

1. Absence of RS complex in ALL precordial leads → VT
2. R-to-S interval >100 ms in any precordial lead → VT
3. AV dissociation present → VT
4. Classic LBBB or RBBB morphology absent → VT

• If none of the above → SVT with aberrancy

• Tintinalli's Emergency Medicine; Braunwald's Heart Disease

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1.5 Ventricular Fibrillation (VF)

• Completely chaotic, irregular waveforms of varying morphology and amplitude
• No recognizable P waves, QRS complexes, or T waves
• Coarse VF = larger amplitude waves (early); Fine VF = small amplitude waves (late, near asystole)

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1.6 Torsades de Pointes (TdP)

• Polymorphic VT with characteristic twisting of QRS axis around the isoelectric line
• QRS complexes appear to "twist" above and below the baseline in a spindle shape
• Usually preceded by prolonged QT interval on baseline ECG
• Rate 200-250 bpm, often self-terminating but can degenerate to VF

• Drugs: class IA agents (quinidine, procainamide), class III agents (amiodarone, sotalol, dofetilide), tricyclic antidepressants, antipsychotics, macrolide antibiotics
• Electrolytes: hypokalemia, hypomagnesemia, hypocalcemia
• Congenital: long QT syndrome (Romano-Ward, Jervell-Lange-Nielsen)
• Intracranial hemorrhage / subarachnoid hemorrhage

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SECTION 2: CONDUCTION BLOCKS

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2.1 AV Blocks

First-Degree AV Block

• ECG: PR interval >200 ms (>5 small boxes) on every beat
• All P waves conducted; no dropped beats
• Usually benign; may be caused by vagal tone, AV nodal disease, digoxin, beta-blockers, inferior MI
• No treatment usually needed

Second-Degree AV Block - Mobitz Type I (Wenckebach)

• Mechanism: Progressive fatigue of AV node conduction until a beat is dropped, then cycle resets
• ECG:
  • Progressive PR prolongation with each beat before a dropped beat
  • Shortening RR intervals before the dropped beat
  • Group beating pattern (clusters of QRS followed by a pause)
  • The RR interval containing the dropped beat is less than twice the preceding RR
• Site of block: within the AV node (proximal)
• Prognosis: usually benign; rarely progresses to complete heart block
• Common in: inferior MI, athletes (vagal), post-cardiac surgery

Second-Degree AV Block - Mobitz Type II

• Mechanism: Abrupt, unexpected failure of conduction - no progressive fatigue
• ECG:
  • Fixed PR interval on all conducted beats
  • Sudden dropped beat with no preceding PR change
  • Often associated with wide QRS (bundle branch block coexists)
• Site of block: below the AV node, in the bundle of His or bundle branches (distal)
• Prognosis: dangerous - unpredictably progresses to complete heart block
• Requires pacemaker implantation

• Narrow QRS = more likely Mobitz I (proximal block)
• Wide QRS/bundle branch block = more likely Mobitz II (distal block)

Third-Degree (Complete) AV Block

• Mechanism: No atrial impulses conduct to ventricles; atria and ventricles are driven by completely independent pacemakers
• ECG:
  • P waves and QRS complexes are completely independent (AV dissociation)
  • P rate > QRS rate (SA node fires faster than escape rhythm)
  • Regular PP interval, regular RR interval, but no fixed relationship between P and QRS
  • Escape QRS: narrow (junctional escape ~40-60 bpm) or wide (ventricular escape ~20-40 bpm)
• Causes: inferior MI (usually transient, junctional escape), anterior MI (often permanent, ventricular escape), Lyme disease, infiltrative disease, degenerative (Lev's/Lenègre's disease), congenital
• Requires urgent pacemaker
• Washington Manual of Medical Therapeutics

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2.2 Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

• rSR' ("rabbit ears") in V1 - small r, deep S, tall R' (the terminal R' is the delayed RV depolarization)
• Wide S wave in leads I and V6 (qRS pattern in V6)
• T-wave inversion in V1-V2 (secondary repolarization change, opposite to last QRS deflection - normal for BBB)
• Right axis deviation may be present

Left Bundle Branch Block (LBBB)

• Broad, entirely negative (QS) complex or broad rS in V1 - no normal septal r wave
• Tall, broad, notched (M-shaped) R wave in V6 and lead I - no Q wave in lateral leads
• T-wave inversion in V6, I, aVL (secondary change - opposite to last QRS deflection)
• Left axis deviation often present
• QRS morphology is identical to right ventricular pacing

1. ST elevation ≥1 mm concordant with QRS (same direction) in any lead = 5 points
2. ST depression ≥1 mm in V1, V2, or V3 = 3 points
3. ST elevation ≥5 mm discordant (opposite) to QRS = 2 points

• Score ≥3 = high specificity for MI

• Harrison's Principles of Internal Medicine 22E

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2.3 Fascicular Blocks (Hemiblocks)

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SECTION 3: ISCHEMIA AND MYOCARDIAL INFARCTION

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3.1 Mechanisms of ECG Changes in Ischemia

• Transmural (epicardial) ischemia → ST vector directed outward → ST elevation in overlying leads
• Subendocardial ischemia → ST vector directed inward toward cavity → ST depression in overlying leads + ST elevation in aVR
• Harrison's Principles of Internal Medicine 22E

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3.2 STEMI - ST Elevation Myocardial Infarction

• New ST elevation at the J point in ≥2 contiguous leads:
  • ≥2 mm in V2-V3 (men), ≥1.5 mm in V2-V3 (women)
  • ≥1 mm in all other leads
• New LBBB with ischemic symptoms = STEMI equivalent

1. Hyperacute T waves - tall, broad, pointed T waves (very early, often missed)
2. ST elevation - concave-up ("tombstone" if severe) - confirms ongoing occlusion
3. T-wave inversion - developing in hours as ST starts to resolve
4. Pathological Q waves - usually 8-12 hours; represent necrosis (electrically silent tissue)
5. R-wave loss - diminished R amplitude in infarcted territory

• Inferior STEMI → reciprocal ST depression in I and aVL
• Anterior STEMI → reciprocal ST depression in II, III, aVF

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3.3 Wellens Syndrome

• Type A (biphasic T wave in V2-V3) - positive then negative
• Type B (deep symmetric T-wave inversion in V2-V3) - more common

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3.4 NSTEMI / Unstable Angina

• ST depression (≥0.5 mm, horizontal or downsloping) in ≥2 contiguous leads
• T-wave inversion
• May have normal ECG (NSTEMI is a clinical + troponin diagnosis, not ECG diagnosis)
• No ST elevation, no pathological Q waves (unless old)

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3.5 Posterior STEMI (Easily Missed)

• ST depression in V1-V3 (the ST elevation is on the back of the heart)
• Tall, broad R wave in V1-V2 (reciprocal Q wave)
• Upright T waves in V1-V2 (reciprocal T-wave inversion)

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3.6 Pericarditis

• Diffuse concave-up ("saddle-shaped") ST elevation in nearly all leads (except aVR and V1, which have ST depression)
• PR depression in most leads (PR elevation in aVR) - classic and early finding
• No reciprocal ST depression (unlike STEMI, which has localized elevation + reciprocal depression)
• No Q waves
• Evolves through 4 stages over days-weeks

• Pericarditis: diffuse ST elevation, concave-up, PR depression, no reciprocal changes
• STEMI: localized ST elevation, often convex-up, reciprocal depression, Q waves may develop

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SECTION 4: HYPERTROPHY PATTERNS

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4.1 Left Ventricular Hypertrophy (LVH)

• Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm (in adults >35 years)
• Cornell: R in aVL + S in V3 ≥28 mm (men) or ≥20 mm (women)
• R in aVL ≥11 mm (simple and useful)

• ST depression and T-wave inversion in left lateral leads (I, aVL, V5, V6) - "strain" pattern = pressure overload
• Left axis deviation
• Prolonged QRS (but usually <120 ms)
• Left atrial enlargement pattern (broad notched P wave in II, biphasic P in V1 with large negative component)

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4.2 Right Ventricular Hypertrophy (RVH)

• Dominant R wave in V1 (R > S in V1, or R >7 mm)
• Deep S waves in V5, V6 and leads I (persistent S waves in left lateral leads)
• Right axis deviation (>+90°)
• T-wave inversion in V1-V3 (right ventricular "strain" pattern)
• Often associated with right bundle branch block pattern (especially in ASD with volume overload)

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4.3 Atrial Enlargement

• Tall, peaked P waves ≥2.5 mm in II, III, aVF (P wave is narrow and pointed)
• P wave duration normal
• Causes: COPD, pulmonary hypertension, tricuspid stenosis

• Broad, notched ("M-shaped") P wave ≥120 ms (3 small boxes) in lead II
• Biphasic P wave in V1 with a prominent negative terminal component (≥1 mm deep AND ≥1 mm wide = 1 small box × 1 small box)
• Causes: Mitral stenosis, mitral regurgitation, LVH from any cause, heart failure
• Harrison's Principles of Internal Medicine 22E

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SECTION 5: ELECTROLYTE AND METABOLIC ECG CHANGES

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5.1 Hyperkalemia

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5.2 Hypokalemia

• Prominent U waves (U > T wave amplitude, especially in V2-V3)
• T-wave flattening or inversion
• ST depression
• Apparent QT prolongation (actually QU prolongation as T and U merge)
• Risk of torsades de pointes

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5.3 Hypercalcemia vs Hypocalcemia

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5.4 Hypothermia

• Bradycardia
• Osborn wave (J wave): Distinctive convex "hump" at the J point (junction of QRS and ST), best seen in V4-V6. Pathognomonic of hypothermia.
• Prolonged PR, QRS, QT intervals
• Shivering artifact on baseline
• Risk of VF at core temperatures <28°C

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5.5 Digoxin Effect

• Characteristic "scooping" or "sagging" ST-T wave depression (like a reversed check mark) in lateral leads - the "Salvador Dalí moustache" appearance
• Shortened QT interval
• Flattened or inverted T waves
• PR prolongation (digoxin slows AV conduction)

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5.6 Drug Effects on QT

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SECTION 6: SPECIAL PATTERNS

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6.1 Wolff-Parkinson-White (WPW)

• Short PR interval (<120 ms) - because AV nodal delay is bypassed
• Delta wave - slurred initial upstroke of QRS (the pre-excited ventricle depolarizing slowly via muscle-to-muscle conduction before the normal His-Purkinje wave arrives)
• Widened QRS (>120 ms total, due to delta wave)

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6.2 Brugada Syndrome

• Type 1 (diagnostic): Coved-type ST elevation ≥2 mm, negative T wave in V1-V2
• Type 2: Saddleback ST elevation (not diagnostic alone)

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6.3 Early Repolarization

• Notching or slurring of the terminal QRS (J-point elevation) with ST elevation, most prominent in V4-V6 and inferior leads
• Historically considered benign normal variant in young athletes
• Current understanding: some patterns (especially inferior leads, horizontal/descending ST morphology, high amplitude) carry a small but real risk of VF - still an area of active research

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6.4 Long QT Syndrome (Congenital)

• Corrected QT (QTc) >460 ms in women, >450 ms in men
• Multiple subtypes (LQT1 = KCNQ1, LQT2 = HERG/KCNH2, LQT3 = SCN5A)
• Risk of TdP and sudden cardiac death, often triggered by:
  • LQT1: exercise/swimming
  • LQT2: auditory stimuli (alarm, telephone)
  • LQT3: sleep/rest

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Quick Reference Summary Table

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1. Arrhythmias - AF, atrial flutter, SVT/AVNRT, VT (with Brugada algorithm for VT vs SVT-aberrancy), VF, Torsades de Pointes
2. Conduction Blocks - 1st/2nd/3rd degree AV blocks (Mobitz I vs II differentiation in detail), RBBB, LBBB, Sgarbossa criteria for ischemia in LBBB, fascicular blocks
3. Ischemia/MI - Mechanisms of ST deviation, STEMI by territory with culprit arteries, evolutionary changes, Wellens syndrome, NSTEMI, posterior STEMI (most commonly missed), pericarditis vs STEMI
4. Hypertrophy - LVH voltage criteria (Sokolow-Lyon, Cornell), RVH, right/left atrial enlargement
5. Electrolytes/Drugs - Hyperkalemia progression to sine-wave, hypokalemia U waves, hypo/hypercalcemia, hypothermia Osborn wave, digoxin scooping, QT-prolonging drugs
6. Special Patterns - WPW (with danger of AF+WPW), Brugada syndrome, early repolarization, congenital long QT