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ECG: Basic to Advanced - A Complete Learning Guide

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PART 1 - THE FUNDAMENTALS

Why the ECG Works (Electrophysiology)

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The Cardiac Conduction System

1. SA node - right atrium → spreads across both atria (produces P wave)
2. AV node - deliberate delay (120-200 ms) allowing atrial filling - corresponds to PR interval
3. Bundle of His - bifurcates into right bundle branch and left bundle branch (which divides into left anterior and left posterior fascicles)
4. Purkinje fibers - rapid spread through ventricular myocardium endocardium → epicardium (produces QRS)
5. Ventricular repolarization - T wave

The depolarization wavefronts have direction and magnitude and can be represented as vectors - this is the basis of axis calculation. - Harrison's Principles of Internal Medicine 22E, p. 1911

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PART 2 - THE ECG WAVEFORMS AND INTERVALS

The Normal ECG - Labeled Waveforms

The ECG waveforms with intervals

Each Wave Explained

ECG Paper and Speed

• 1 small box = 1 mm = 40 ms (0.04 s)
• 1 large box = 5 mm = 200 ms (0.20 s)
• Vertically: 1 mV = 10 mm (standard calibration)

• Count large boxes between R waves: divide 300 by the number of large boxes
• Or: count small boxes and divide 1500

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PART 3 - THE 12 LEADS

The Lead System

• Standard bipolar: I, II, III
• Augmented unipolar: aVR, aVL, aVF
• These 6 leads form the hexaxial reference system

• V1 (right sternal border, 4th ICS), V2, V3, V4, V5, V6 (left midaxillary line)
• V1-V2 overlie right ventricle
• V3-V4 transition zone / interventricular septum
• V5-V6 overlie lateral left ventricle

The orientation and polarity of the frontal plane leads are represented on a hexaxial diagram. - Harrison's Principles of Internal Medicine 22E, p. 1912

Where to Look for What

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PART 4 - CARDIAC AXIS

What is the Electrical Axis?

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PART 5 - CHAMBER ENLARGEMENT & HYPERTROPHY

Atrial Abnormalities

• Tall, peaked P waves ("P pulmonale") ≥2.5 mm in II, III, aVF
• Associated with COPD, pulmonary hypertension, tricuspid stenosis

• Broad, notched P waves in limb leads ("P mitrale"), duration ≥120 ms
• Biphasic P wave in V1 with prominent negative component
• Associated with mitral stenosis/regurgitation, LVH, heart failure

Ventricular Hypertrophy

• SV1 + RV5 or V6 ≥35 mm
• R in aVL ≥11 mm
• Cornell criteria: RaVL + SV3 ≥28 mm (men), ≥20 mm (women)

LVH increases the amplitude of electrical forces directed to the left and posteriorly. Repolarization abnormalities may cause ST-segment depression and T-wave inversion in leads with a prominent R wave. - Harrison's 22E

• Tall R wave in V1 (R > S in V1), right axis deviation (>+90°)
• Deep S waves in V5-V6
• ST depression and T-wave inversion in right precordial leads ("strain")
• Associated with: pulmonary hypertension, pulmonic stenosis, ASD

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PART 6 - BUNDLE BRANCH BLOCKS

Right Bundle Branch Block (RBBB)

Left Bundle Branch Block (LBBB)

Important: New LBBB in the context of chest pain may represent acute MI (Sgarbossa criteria apply)

1. ST elevation ≥1 mm concordant with QRS (same direction) - 5 points
2. ST depression ≥1 mm in V1-V3 - 3 points
3. ST elevation ≥5 mm discordant with QRS - 2 points Total ≥3 points = STEMI likely

Fascicular Blocks (Hemiblocks)

• Left axis deviation (-45° to -90°)
• Small Q in I/aVL, small R in II/III/aVF
• QRS slightly widened but <120 ms

• Right axis deviation (>+90°)
• Small R in I/aVL, small Q in II/III/aVF
• Must exclude RVH, lateral MI

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PART 7 - ISCHEMIA AND INFARCTION

The ECG Evolution of STEMI

Profound ST elevation or depression in multiple leads usually indicates very severe ischemia. - Harrison's Principles of Internal Medicine 22E

Localizing the Infarct

ST elevation in III > II in inferior STEMI, with ST depression in aVL, suggests RCA. ST elevation in leads II ≈ III suggests LCx territory. - Rosen's Emergency Medicine

NSTEMI / Unstable Angina

• ST depression (horizontal or downsloping = most concerning)
• Symmetric T-wave inversions (deep Wellens waves in V2-V3 = LAD critical stenosis)
• Normal ECG (does NOT rule out ACS - serial ECGs + troponins required)

ST Elevation Mimics

Important differential for ST elevation: acute pericarditis, early repolarization, LVH with strain, LBBB, Brugada syndrome, acute pulmonary embolism, hypothermia (J/Osborn waves), hypercalcemia, Takotsubo syndrome, myocarditis. - Harrison's Principles of Internal Medicine 22E, p. 1917

• Pericarditis: diffuse ST elevation (saddle-shaped, concave up) in multiple territories; PR depression; no reciprocal changes except aVR; no Q waves
• STEMI: focal, convex ST elevation; reciprocal ST depression; Q waves develop

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PART 8 - ARRHYTHMIAS

Systematic Approach to Rhythm

1. What is the rate? (fast / normal / slow)
2. Are P waves present and regular?
3. Is the PR interval normal?
4. Are QRS complexes narrow (<120 ms) or wide (≥120 ms)?
5. What is the relationship between P waves and QRS?

Sinus Rhythms

AV Blocks

• Mobitz type I (Wenckebach): Progressive PR prolongation until a P wave fails to conduct (a "dropped" QRS); group beating; usually at AV node level; often benign; blocks narrow
• Mobitz type II: Fixed PR interval with sudden non-conduction of a P wave; often at bundle of His or below; more dangerous; blocks wide QRS; risk of complete AV block

Mobitz II: sudden unexplained block without prior PR prolongation. Often indicates infranodal (His or bundle branch) disease. - Fuster and Hurst's The Heart 15E

Supraventricular Tachycardias (SVT)

• Irregularly irregular rhythm
• No distinct P waves; chaotic atrial baseline (fibrillation waves)
• Ventricular rate typically 100-160 bpm (if uncontrolled)
• Key risks: stroke (use CHA₂DS₂-VASc), rate vs. rhythm control

• Regular "sawtooth" flutter waves at ~300 bpm (negative in II, III, aVF)
• Usually 2:1 conduction → ventricular rate ~150 bpm
• Clue: Regular tachycardia at exactly 150 bpm = flutter until proven otherwise

• Regular, narrow QRS; rate 150-250 bpm
• Retrograde P waves buried in or just after QRS (pseudo-R' in V1, pseudo-S in inferior leads)
• Vagal maneuvers / adenosine terminate it

• In orthodromic AVRT: narrow QRS with retrograde P in ST segment/early T
• In antidromic AVRT: wide, pre-excited QRS (mimics VT)
• WPW on resting ECG: delta wave (slurred QRS onset), short PR (<120 ms), wide QRS

Ventricular Arrhythmias

• Wide QRS (≥120 ms), bizarre morphology, no preceding P wave
• Usually with full compensatory pause
• Isolated PVCs in structurally normal hearts: benign
• Frequent (>10,000/24 h) or in runs: investigate for cardiomyopathy

• Wide QRS tachycardia ≥3 beats, rate >100 bpm
• AV dissociation is the hallmark (P waves march through at their own slower rate)
• Fusion beats and capture beats confirm VT
• Brugada criteria / Vereckei algorithm to distinguish VT from SVT with aberrancy

• Chaotic, disorganized baseline; no identifiable QRS complexes
• Cardiac arrest - immediate defibrillation

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PART 9 - METABOLIC AND DRUG EFFECTS

Electrolyte Disturbances

1. Peaked, narrow "tented" T waves (first sign)
2. Prolonged PR interval, widened QRS
3. Flattened/absent P waves
4. Sine wave pattern
5. VF/asystole

• Flattened T waves
• Prominent U waves (often merging with T wave)
• Prolonged QU interval (mimics long QT)
• ST depression

Factors that prolong phase 2 or 3 of the action potential (e.g., amiodarone, hypocalcemia) increase the QT interval. Factors that shorten repolarization (e.g., hypercalcemia, digoxin) abbreviate the QT. - Harrison's 22E, p. 1912

Key Drug Effects

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PART 10 - ADVANCED PATTERNS

Brugada Syndrome

• Type 1 (diagnostic): Coved ST elevation ≥2 mm with J point elevation and T-wave inversion in V1-V2
• Associated with SCN5A mutation, sudden cardiac death in young males
• ECG may be dynamic (unmasked by fever, cocaine, Na-channel blockers)

Long QT Syndrome

• Congenital (LQTS1-3) or acquired
• QTc >460 ms women, >450 ms men
• Risk of torsades de pointes (polymorphic VT) → syncope/SCD
• Triggers: exercise (LQTS1), startle/noise (LQTS2), sleep (LQTS3)

Wolff-Parkinson-White (WPW)

• Delta wave + short PR + wide QRS = ventricular pre-excitation
• Risk: AF with rapid conduction over accessory pathway (very short RR intervals, wide irregular QRS) → VF
• Never use adenosine or AV-nodal blockers in pre-excited AF

Acute Pulmonary Embolism - S1Q3T3 Pattern

• Sinus tachycardia (most common)
• S wave in lead I, Q wave in lead III, T-wave inversion in lead III
• New RBBB or incomplete RBBB
• Right axis deviation, sinus tachycardia

Pericarditis

• Stage 1: Diffuse ST elevation (saddle-shaped, concave), PR depression (most leads), PR elevation in aVR
• Stage 2: ST normalizes, T waves flatten
• Stage 3: T-wave inversions
• Stage 4: Return to normal

Takotsubo (Stress Cardiomyopathy)

• Wide, deep T-wave inversions across precordial leads
• Prolonged QT
• Mimics anterior STEMI initially but no fixed coronary occlusion

Hypothermia - Osborn (J) Waves

• Positive deflection at the J point (end of QRS/start of ST)
• Prominent in V3-V5; size proportional to degree of hypothermia
• Bradycardia, prolonged intervals, AF, VF risk

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PART 11 - A SYSTEMATIC APPROACH TO READING ANY ECG

1. Rate - Count RR intervals (fast/normal/slow)
2. Rhythm - Regular or irregular? Sinus P waves present?
3. Axis - Normal / LAD / RAD using leads I and aVF
4. PR interval - Normal (120-200 ms)? Short (WPW, junctional)? Long (AV block)?
5. QRS duration - Narrow (<120 ms) or wide? Bundle branch block pattern?
6. QT interval - Corrected (QTc): normal vs. prolonged
7. P wave morphology - Atrial enlargement? Normal P axis?
8. ST segment - Elevation or depression? Leads involved?
9. T waves - Normal polarity? Tall (hyperkalemia, hyperacute MI)? Inverted?
10. Compare to prior ECG - Is this new or old?

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Quick Reference Summary

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