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ECG (Electrocardiogram): Basic to Advanced - A Complete Guide

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PART 1 - FOUNDATIONS

What is an ECG?

The ECG Paper

• Small box = 1 mm = 0.04 seconds (horizontal) = 0.1 mV (vertical)
• Large box = 5 mm = 0.2 seconds = 0.5 mV
• 5 large boxes = 1.0 second

Calculating Heart Rate (Quick Method)

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PART 2 - THE 12 LEADS

Limb Leads (Frontal Plane)

• Standard (bipolar): I, II, III
• Augmented (unipolar): aVR, aVL, aVF
• Key rule: Lead II is parallel to the heart's electrical axis and gives the clearest P waves

Precordial Leads (Horizontal Plane)

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PART 3 - NORMAL INTERVALS

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PART 4 - SYSTEMATIC APPROACH (Harrison's 14-Step Method)

1. Standardization/calibration and lead placement
2. Rhythm
3. Heart rate
4. PR interval / AV conduction
5. QRS interval
6. QT/QTc interval
7. Mean QRS electrical axis
8. P waves
9. QRS voltages
10. Precordial R-wave progression
11. Abnormal Q waves
12. ST segments
13. T waves
14. U waves

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PART 5 - HEART RATE & RHYTHM DISORDERS

Normal Sinus Rhythm

• Rate 60-100 bpm
• Upright P before every QRS in II
• Regular P-P and R-R intervals
• PR 0.12-0.20 s

Sinus Tachycardia

• Rate > 100, normal morphology
• Clinical causes: fever, pain, anemia, hypovolemia, PE, hyperthyroidism, anxiety
• ECG: regular, normal P waves, rate typically 100-160

Sinus Bradycardia

• Rate < 60, normal morphology
• Clinical causes: athletes, hypothyroidism, inferior MI, vasovagal syncope, beta-blockers
• Usually benign; treat only if symptomatic

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PART 6 - ATRIAL ARRHYTHMIAS

Atrial Fibrillation (AF)

• Mechanism: chaotic, disorganized atrial activity from multiple reentry circuits
• ECG features:
  • No discrete P waves - replaced by irregular fibrillatory baseline
  • Irregularly irregular R-R intervals (this is the key!)
  • Normal QRS unless aberrant conduction
  • Ventricular rate typically 100-180 bpm if uncontrolled
• Clinical: palpitations, dyspnea, fatigue, dizziness, stroke risk
• Causes: hypertension, valvular disease, HF, thyrotoxicosis, alcohol, post-cardiac surgery

Atrial Flutter

• Mechanism: single large reentry circuit in right atrium
• ECG features:
  • Classic "sawtooth" flutter waves at 250-350/min (best seen in II, III, aVF)
  • Usually 2:1 AV block → ventricular rate ~150 bpm (classic tip: any regular tachycardia at ~150 bpm = flutter until proven otherwise)
  • Regular or regularly-irregular rhythm
• Clinical: palpitations, dyspnea; less embolic risk than AF but still warrants anticoagulation

Multifocal Atrial Tachycardia (MAT)

• Rate 100-180 bpm, irregularly irregular
• Key differentiator from AF: 3+ distinct P-wave morphologies, visible P waves before each QRS
• Clinical: almost exclusively associated with severe COPD, hypoxia, theophylline toxicity, hypomagnesemia

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PART 7 - AV CONDUCTION BLOCKS

First-Degree AV Block

• ECG: PR interval > 0.20 s (> 1 large box), every P followed by QRS
• Clinical: usually benign; seen with increased vagal tone, inferior MI, digoxin, beta-blockers
• No treatment needed

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

• ECG: Progressive PR lengthening → dropped QRS → cycle repeats
• Memory: "Longer, longer, longer... DROP. Then you have a Wenckebach"
• Site of block: Usually at AV node
• Clinical: Often benign, may be vagal (athletes), inferior MI; rarely needs pacing

Second-Degree AV Block - Mobitz Type II

• ECG: Constant PR interval, then sudden dropped QRS (no warning)
• Site of block: Below AV node (His-Purkinje system)
• Clinical: DANGEROUS - unpredictable, can progress to complete heart block; wide QRS common; pacemaker often indicated
• Associated with anterior MI, degenerative conduction disease

Third-Degree (Complete) AV Block

• ECG: Complete AV dissociation - P waves and QRS complexes march independently with no relationship
  • P rate > QRS rate
  • QRS may be narrow (junctional escape, ~40-60 bpm) or wide (ventricular escape, ~30-40 bpm)
• Clinical: Severe bradycardia, syncope (Stokes-Adams attacks), hemodynamic compromise
• EMERGENCY - requires temporary then permanent pacemaker
• Causes: inferior MI (often transient), anterior MI (often permanent), Lyme disease, digoxin toxicity, infiltrative disease

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PART 8 - BUNDLE BRANCH BLOCKS

Right Bundle Branch Block (RBBB)

• ECG features:
  • Wide QRS ≥ 0.12 s
  • RSR' pattern ("bunny ears") in V1 - the second R is taller
  • Wide, slurred S wave in I and V6
  • Secondary ST-T changes in right precordial leads
• Mnemonic: MaRRoW - RBBB has M shape in V1, W shape in V6
• Clinical: May be normal variant; also RV strain (PE, pulmonary hypertension), anterior MI, myocarditis

Left Bundle Branch Block (LBBB)

• ECG features:
  • Wide QRS ≥ 0.12 s
  • Broad monophasic R in I, aVL, V5, V6 (no septal q waves)
  • Deep QS or rS in V1
  • Secondary ST-T changes opposite to QRS direction
• Mnemonic: WiLLiaM - LBBB has W in V1, M in V6
• Clinical: ALWAYS pathological - CAD, cardiomyopathy, severe LVH, aortic stenosis
• New LBBB with chest pain = STEMI equivalent, treat as ACS

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PART 9 - ISCHEMIA, INJURY & INFARCTION

ST Elevation - Localizing the Infarct

STEMI vs. Pericarditis vs. Early Repolarization

The ECG strip of subarachnoid hemorrhage vs. normal - QT effects:

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PART 10 - QT INTERVAL & DANGEROUS REPOLARIZATION

Corrected QT (QTc)

• Normal QTc: < 440 ms (men), < 460 ms (women)
• QTc > 500 ms = HIGH risk of torsades de pointes (TdP)

Causes of Long QT

Short QT

• Hypercalcemia shortens ST segment → short QT
• Digoxin toxicity: "scooped" ST with shortened QT (digitalis effect)

The Hypocalcemia vs. Hypercalcemia ECG:

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PART 11 - VENTRICULAR ARRHYTHMIAS

Premature Ventricular Complexes (PVCs)

• Wide QRS (> 0.12 s) with bizarre morphology, no preceding P wave
• Usually followed by compensatory pause
• Isolated PVCs are common and often benign
• Frequent PVCs (> 10% of beats) with symptoms or reduced EF need evaluation

Ventricular Tachycardia (VT)

• Definition: ≥ 3 consecutive wide complex beats at > 100 bpm
• ECG features:
  • Wide, bizarre QRS complexes (> 0.12 s)
  • AV dissociation (independent P waves - look for "marching" P waves)
  • Fusion beats (sinus + VT = intermediate morphology) - pathognomonic
  • Capture beats (sinus captures ventricle briefly - narrow QRS amid wide beats)
  • Concordance (all chest leads positive or all negative)
• Clinical: Palpitations, syncope, hemodynamic collapse
• Rule: Wide complex tachycardia = VT until proven otherwise

Distinguishing VT from SVT with Aberrancy (Brugada Algorithm)

1. No RS complex in any precordial lead? → VT
2. RS interval > 100 ms in any precordial lead? → VT
3. AV dissociation? → VT
4. LBBB morphology with QRS negative in V1 and positive in V6, OR RBBB morphology with positive concordance? → VT

Ventricular Fibrillation (VF)

• ECG: Chaotic, irregular deflections with no identifiable QRS, ST, or T waves
• Clinical: No cardiac output = cardiac arrest
• Treatment: Immediate defibrillation + CPR

Torsades de Pointes (TdP)

• VT with QRS complexes that "twist" around the baseline (polymorphic VT)
• Occurs in setting of prolonged QT
• Treatment: IV magnesium sulfate, correct electrolytes, remove causative drugs; overdrive pacing

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PART 12 - CARDIAC TAMPONADE

1. Sinus tachycardia
2. Low QRS voltages (< 5 mm in limb leads, < 10 mm in precordial leads)
3. Electrical alternans (alternating QRS amplitude due to swinging heart)

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PART 13 - ADVANCED PATTERNS

Wolf-Parkinson-White (WPW)

• ECG features:
  • Short PR (< 0.12 s) - early ventricular activation via accessory pathway
  • Delta wave - slurred upstroke of QRS
  • Wide QRS, ST-T changes (discordant to delta wave)
• Clinical: Palpitations, SVT (usually narrow but can be wide if antidromic), risk of sudden death in AF
• DANGER: Do NOT give AV nodal blocking drugs (adenosine, beta-blockers, digoxin) in WPW with AF - can accelerate conduction via accessory pathway → VF

Brugada Syndrome

• ECG features: Coved-type (Type 1) ST elevation in V1-V2 with RBBB-like pattern, terminal negative T wave
• Clinical: Young males, Asian descent, sudden cardiac death during sleep/rest
• Type 1 (diagnostic): Coved ST elevation ≥ 2 mm descending to inverted T wave

Hyperkalemia (Progressive Changes with Increasing K+)

Hypokalemia

• ST depression, T-wave flattening/inversion
• Prominent U waves (U > T wave = significant hypokalemia)
• QT(U) prolongation → risk of TdP

Digitalis Effect vs. Toxicity

• Effect (therapeutic): Scooped ST ("reverse tick" or "Salvador Dali mustache"), short QT, PR prolongation - expected finding
• Toxicity: PAT with block (rapid atrial tachycardia with AV block), PVCs, bidirectional VT, any arrhythmia + AV block

Pulmonary Embolism (PE)

• Most common: sinus tachycardia (most sensitive finding)
• Classic S1Q3T3 pattern (S wave in I, Q wave + T inversion in III) - specific but insensitive
• RBBB (acute or incomplete) from RV strain
• T-wave inversions V1-V4 (RV strain pattern)
• Right axis deviation

Hypothermia

• Osborn (J) wave: Positive deflection at J point (junction of QRS and ST segment), best seen in V4-V6 and II
• Bradycardia, prolonged intervals (PR, QRS, QT), muscle tremor artifact

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PART 14 - MASTER DIFFERENTIATOR TABLE

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PART 15 - CLINICAL PEARLS

1. Wide complex tachycardia = VT until proven otherwise. Never give verapamil empirically - it can cause hemodynamic collapse in VT.
2. New LBBB + chest pain = treat as STEMI (Sgarbossa criteria can help if previous LBBB exists).
3. Any rate of ~150 bpm = think atrial flutter with 2:1 block first.
4. AV dissociation (P waves independent of QRS) = complete heart block OR VT - both are serious.
5. The first ECG change in STEMI is hyperacute T waves, not ST elevation. Do not miss this.
6. Reciprocal changes confirm STEMI and rule against pericarditis (pericarditis has no reciprocal changes but has PR depression).
7. Osborn waves + bradycardia = hypothermia until proven otherwise.
8. Peaked T waves in a dialysis patient = hyperkalemia emergency.
9. Electrical alternans = pericardial effusion/tamponade until proven otherwise.
10. Short PR + delta wave + wide QRS = WPW - do NOT use digoxin or AV nodal blockers if they develop AF.

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For Further Practice

• Harrison's Principles of Internal Medicine 22E, Chapter 247
• Medical Physiology (Boron & Boulpaep), Chapter 21, Box 21-2
• Braunwald's Heart Disease, 12th Ed - Chapter 12
• Frameworks for Internal Medicine - AV Block and Arrhythmia chapters
• Tintinalli's Emergency Medicine - Chapter 18