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ECG: From Basics to Advanced - A Complete Guide

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PART 1 - FUNDAMENTALS

What Is an ECG?

• Medical Physiology, p. 731

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The Cardiac Conduction System

• Miller's Anesthesia 10e, p. 1364

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The Cardiac Cycle and ECG Correlation

• P wave - Atrial depolarization; onset of atrial systole coincides with SA node firing
• PR interval - Conduction delay through AV node; onset of P wave to start of QRS
• QRS complex - Ventricular depolarization; mitral valve closes at end of R wave
• ST segment - Plateau phase of ventricular action potential (isoelectric in normal)
• T wave - Ventricular repolarization
• QT interval - Total ventricular depolarization + repolarization time; shortens as heart rate increases

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PART 2 - ECG PAPER AND LEADS

ECG Paper Calibration

• Horizontal axis (time): 0.04 sec per small box (1 mm); 0.2 sec per large box (5 mm)
• Vertical axis (voltage): 0.1 mV per mm; standard calibration = 1 mV = 10 mm tall
• 5 large boxes = 1.0 second

The 12-Lead System

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PART 3 - SYSTEMATIC ECG INTERPRETATION

Step 1 - Rate

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

Step 2 - Rhythm

• Rate 60-100 bpm
• Regular R-R intervals
• Upright P waves in leads I, II, aVF
• Constant PR interval (0.12-0.20 sec)
• Each P followed by a QRS

Step 3 - Intervals and Durations

Step 4 - Electrical Axis

Step 5 - P Wave Morphology

• P pulmonale: Tall, peaked P waves >2.5 mm in lead II - right atrial enlargement
• P mitrale: Broad, notched P wave >0.12 sec in lead II with biphasic P in V1 - left atrial enlargement

Step 6 - QRS Morphology

• Width >0.04 sec (1 small box) OR
• Depth >1/4 of following R wave
• Indicate prior myocardial infarction

Step 7 - ST Segment and T Wave

• ST elevation (>1 mm limb leads, >2 mm precordial leads): STEMI, pericarditis, Brugada, early repolarization
• ST depression: Subendocardial ischemia, digoxin effect, LVH strain
• T wave inversion: Ischemia, PE (right-sided), RBBB, LVH, normal in aVR and V1

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PART 4 - BUNDLE BRANCH BLOCKS

Right Bundle Branch Block (RBBB)

• QRS ≥ 0.12 sec
• RSR' ("M" or "rabbit ears") pattern in V1 (rSR')
• Wide, slurred S wave in leads I and V6
• T wave inversion in V1-V3 (appropriate discordance)

Left Bundle Branch Block (LBBB)

• QRS ≥ 0.12 sec
• Broad, notched R wave in V5, V6, I, aVL (no S wave)
• Deep, wide QS complex in V1
• No septal Q waves in lateral leads
• Discordant ST changes (opposite to QRS deflection)

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PART 5 - ARRHYTHMIAS

Bradyarrhythmias

• Rate <60 bpm, normal P waves, regular rhythm
• Causes: Athletes, vagal tone, hypothyroidism, beta-blockers, sick sinus syndrome

• Goldman-Cecil Medicine, p. 1764

Supraventricular Tachyarrhythmias

• Irregularly irregular rhythm
• No visible P waves - replaced by chaotic fibrillatory baseline (best seen in V1)
• Narrow QRS (unless aberrant conduction)
• Rate: Usually 100-170 bpm (ventricular response)

• Regular "sawtooth" flutter waves at 300 bpm (F waves)
• Typically 2:1 AV block giving ventricular rate of 150 bpm
• Flutter waves best seen in inferior leads (II, III, aVF) and V1
• Unlike AF, flutter waves are organized and regular

• Rate 150-250 bpm, regular
• Narrow QRS
• P waves buried in or just after QRS (retrograde P waves)
• Responds to vagal maneuvers and adenosine

• May be narrow (orthodromic) or wide (antidromic)
• Short PR (<0.12 sec) + delta wave on baseline ECG = WPW pattern
• During tachycardia, typically narrow QRS (conduction goes normal route down His and back via accessory pathway)

• AV dissociation = VT (P waves march through at own rate, independent of QRS)
• Fusion beats = VT (hybrid complexes where normal conduction fuses with ventricular focus)
• Capture beats = VT
• Concordance in precordial leads (all positive or all negative) = VT

Ventricular Arrhythmias

• Wide (>0.12 sec), bizarre QRS
• No preceding P wave
• Followed by compensatory pause
• Isolated PVCs in structurally normal hearts are generally benign

• ≥3 consecutive PVCs at rate >100 bpm
• Wide QRS (>0.12 sec), regular
• AV dissociation, fusion beats, capture beats confirm VT
• Monomorphic VT: all QRS complexes look alike - often from a fixed scar (post-MI)
• Polymorphic VT: changing QRS morphology

• Chaotic, disorganized electrical activity
• No identifiable QRS complexes
• No cardiac output - immediately fatal without defibrillation

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PART 6 - ISCHEMIA AND INFARCTION

The Progression of ECG Changes in MI

STEMI Localization by Leads

Special STEMI Patterns

• Rosen's Emergency Medicine, p. 1004

• Prominent tall T waves with J-point depression (ST depression) in precordial leads
• ST elevation in aVR
• Indicates proximal LAD occlusion; must be treated as STEMI

• Deep symmetric T-wave inversions or biphasic T waves in V2-V3
• Occurs during pain-free period
• Indicates critical proximal LAD stenosis - do NOT stress test; needs urgent cath

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PART 7 - ADVANCED PATTERNS

LVH (Left Ventricular Hypertrophy)

• Sokolow-Lyon: S in V1 + R in V5 or V6 ≥ 35 mm (sensitivity low ~40-60% in middle-age adults)
• Cornell: R in aVL + S in V3 > 28 mm (men) or >20 mm (women)
• Associated with ST-T changes in lateral leads ("strain pattern")

RVH (Right Ventricular Hypertrophy)

• Right axis deviation
• R > S in V1 (dominant R in V1)
• Deep S waves in V5-V6
• ST depression and T inversion in V1-V3

Pericarditis

• Diffuse ST elevation in multiple leads (not restricted to one territory)
• ST elevation is concave (saddle-shaped) upward
• PR depression (a key distinguishing feature from STEMI)
• No reciprocal ST depression (unlike STEMI)
• T wave inversion occurs after ST returns to baseline

Pulmonary Embolism (PE) - S1Q3T3 pattern

• S wave in lead I
• Q wave in lead III
• T wave inversion in lead III
• Also: sinus tachycardia (most common), new RBBB, right heart strain pattern (T inversion V1-V4), right axis deviation
• S1Q3T3 is specific but not sensitive - present in <20% of PE cases

Hyperkalemia - Progressive ECG Changes

1. Peaked (tall, narrow) T waves - earliest sign
2. Prolonged PR interval
3. Widened QRS (loss of P waves)
4. Sine wave pattern (merged QRS and T)
5. Ventricular fibrillation / asystole

Hypokalemia

• Flattened T waves
• Prominent U waves (after T wave, best in V2-V3)
• Prolonged QU interval
• ST depression

Brugada Syndrome

• Type 1 (diagnostic): Coved-type (downsloping) ST elevation ≥2 mm in ≥1 of V1-V2, followed by negative T wave
• Can cause sudden cardiac death from polymorphic VT/VF
• ECG may be dynamic (appears and disappears)

Long QT Syndrome

• Congenital (mutations in ion channel genes) or acquired (drugs, electrolyte disturbances)
• QTc > 0.44 sec (men) or >0.46 sec (women)
• Risk of Torsades de Pointes - polymorphic VT with "twisting" QRS around the isoelectric line
• Acquired causes: hypokalemia, hypomagnesemia, antiarrhythmics (class Ia, III), antipsychotics, azole antifungals, fluoroquinolones

Wolff-Parkinson-White (WPW) Syndrome

• Accessory pathway (Bundle of Kent) bypasses AV node
• ECG features: short PR interval (<0.12 sec) + delta wave (slurred upstroke of QRS) + wide QRS
• Risk: AF with rapid accessory pathway conduction can lead to VF
• Never give AV nodal blocking agents (adenosine, verapamil, digoxin) in AF with WPW - can accelerate conduction down accessory pathway

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PART 8 - STEP-BY-STEP SYSTEMATIC APPROACH (Summary Checklist)

1. RATE         - Calculate bpm (regular: 300/large boxes; irregular: count x6)
2. RHYTHM       - Regular or irregular? P before every QRS?
3. P WAVES      - Present? Morphology? Axis (upright in II)?
4. PR INTERVAL  - 0.12-0.20 sec? Short (preexcitation)? Long (AV block)?
5. QRS          - Width <0.12 sec? Morphology? Pathologic Q waves?
6. AXIS         - Check leads I and aVF; Normal / LAD / RAD?
7. ST SEGMENT   - Elevation or depression? Which leads?
8. T WAVES      - Upright? Inverted? Hyperacute? Location?
9. QT INTERVAL  - Calculate QTc; prolonged?
10. OVERALL     - Clinical context + synthesize findings

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Quick Reference: Key Normal Values

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