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ECG (Electrocardiogram) - Full Clinical Guide

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PART 1: ECG BASICS - WAVES, INTERVALS & SEGMENTS

The Normal ECG Waveform

Normal 12-Lead ECG

The 12 Leads - What They See

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PART 2: APPROACH TO ECG INTERPRETATION (SYSTEMATIC)

1. Rate - count R-R intervals (300 / large squares between R waves)
2. Rhythm - regular or irregular? P before every QRS?
3. Axis - normal (0° to +90°); LAD (<0°); RAD (>+90°)
4. P waves - present, morphology, relation to QRS
5. PR interval - short/long/variable
6. QRS duration - narrow (<120 ms) or wide (>120 ms)
7. ST segment - elevation or depression
8. T waves - peaked, inverted, flat
9. QT interval - prolonged?

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PART 3: ATRIAL ABNORMALITIES

Right Atrial Overload (RAO) / P Pulmonale

• Cause: COPD, pulmonary hypertension, tricuspid stenosis
• ECG: Tall, peaked P waves >2.5 mm in II, III, aVF ("P pulmonale")
• V1: Large positive component of P wave

Left Atrial Abnormality (LAA) / P Mitrale

• Cause: Mitral stenosis, LV failure
• ECG: Broad notched P wave >120 ms in limb leads; biphasic P in V1 with prominent negative (terminal) component

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PART 4: VENTRICULAR HYPERTROPHY

Left Ventricular Hypertrophy (LVH)

• Cause: Hypertension (most common), aortic stenosis, HCM
• ECG criteria (Sokolow-Lyon): S in V1 + R in V5 or V6 > 35 mm
• Cornell criterion: R in aVL + S in V3 > 28 mm (men), >20 mm (women)
• Associated findings: ST depression + T-wave inversion in lateral leads (V5-V6, I, aVL) = "LV strain pattern"
• Sensitivity: 30-50%; Specificity: 85-95%

Right Ventricular Hypertrophy (RVH)

• Cause: Pulmonary hypertension, pulmonary stenosis, cor pulmonale
• ECG: Tall R wave in V1 (R > S), right axis deviation >+90°
• Associated: T-wave inversions in V1-V3; prominent S waves in V5-V6

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PART 5: CONDUCTION SYSTEM DISEASES

AV Blocks

First-Degree AV Block

• PR interval > 200 ms (>1 large square)
• Every P wave conducts - just slowly
• Causes: Inferior MI, digitalis toxicity, increased vagal tone, myocarditis

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

• Progressive PR prolongation until a P wave is BLOCKED (no QRS follows)
• Then cycle resets
• Site of block: AV node
• Causes: Inferior MI, digitalis, increased vagal tone
• Usually benign; may not need pacemaker

Second-Degree AV Block - Type II (Mobitz II)

• Constant PR interval with SUDDEN non-conducted P waves (no warning)
• Site of block: Below AV node (His-Purkinje)
• Causes: Anterior MI, sclerodegenerative disease
• High risk of progressing to complete block - PACEMAKER usually needed

Third-Degree (Complete) AV Block

• NO relationship between P waves and QRS complexes (AV dissociation)
• P rate > QRS rate
• Escape rhythm: Junctional (narrow QRS, rate 40-60) or ventricular (wide QRS, rate 20-40)
• Causes: Inferior MI, Lyme disease, surgical trauma, idiopathic fibrosis
• PACEMAKER required

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Bundle Branch Blocks

Left Anterior Fascicular Block (LAFB)

• Left axis deviation (axis around -60°); QRS duration normal
• Small Q waves in I, aVL; small R waves in II, III, aVF
• Delayed precordial R-wave progression

Right Bundle Branch Block (RBBB)

• ECG hallmarks:
  • QRS > 120 ms
  • rSR' (M-shape) in V1
  • Wide, slurred S wave in I, V5, V6
  • Discordant T-wave inversion in V1-V2
• Causes: RV overload, PE, anterior MI, normal variant

Left Bundle Branch Block (LBBB)

• ECG hallmarks:
  • QRS > 120 ms
  • Broad notched ("M-shaped") R in I, aVL, V5-V6
  • Small r with deep S in V1-V3 (dominant S)
  • No septal Q waves in I, V5-V6
  • Discordant ST-T changes
• Causes: CAD, hypertension, cardiomyopathy, aortic stenosis
• New LBBB + symptoms = STEMI equivalent until proven otherwise

Left Posterior Fascicular Block (LPFB)

• Right axis deviation (~+120°); QRS normal duration
• Small R waves in I, aVL; small Q in II, III, aVF
• Diagnosis of exclusion (must rule out RVH)

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PART 6: ISCHEMIA AND MYOCARDIAL INFARCTION

Pathophysiology of ECG Changes in Ischemia

ECG Evolution of STEMI (Typical Sequence)

ST Elevation Localization by Lead

Anterior Wall Ischemia - T-wave Inversions

Non-ST Elevation MI (NSTEMI) / Unstable Angina

• ECG: ST depression, T-wave inversions, or nonspecific changes
• Unlike STEMI, does NOT get immediate primary PCI based on ECG alone
• Diagnosis confirmed by troponin rise

Posterior MI (True Posterior)

• Tall R waves in V1-V2 (R > S); ST depression in V1-V3
• These are reciprocal changes of posterior ST elevation
• Confirm with posterior leads V7-V9 (ST elevation >0.5 mm)

Right Ventricular MI

• Always suspect when inferior STEMI present (II, III, aVF elevation)
• Get right-sided leads (V4R) - ST elevation >1 mm is diagnostic
• Management: AVOID nitrates and diuretics (preload-dependent)

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PART 7: ARRHYTHMIAS

Sinus Node Disorders

Supraventricular Tachycardias (SVT)

Atrial Fibrillation (AF)

• ECG hallmarks:
  • Absent P waves (replaced by irregular fibrillatory "f" waves, rate 350-600/min)
  • Irregularly irregular ventricular rhythm (no two R-R intervals the same)
  • Narrow QRS (unless aberrant conduction or WPW)
• Causes: Hypertension, valvular disease, heart failure, hyperthyroidism, alcohol
• Rate: Ventricular response typically 100-160/min if uncontrolled

Atrial Flutter

• ECG hallmarks:
  • Sawtooth "flutter waves" at atrial rate 250-350/min (typically 300/min)
  • Best seen in II, III, aVF and V1
  • Regular ventricular rate (usually 2:1 block = ventricular rate ~150/min)
• Key: Regular rate of exactly 150 bpm = suspect atrial flutter 2:1
• Carotid sinus massage slows AV conduction, unmasking flutter waves

AVNRT (AV Nodal Re-entrant Tachycardia)

• Most common paroxysmal SVT
• ECG: Narrow complex tachycardia, rate 150-250/min
• P waves buried in or just after QRS (retrograde, short RP interval)
• Treatment: Vagal maneuvers, adenosine

Wolff-Parkinson-White (WPW) Syndrome

• Accessory pathway (Bundle of Kent) bypasses AV node
• ECG (sinus rhythm):
  • Short PR interval (<120 ms)
  • Delta wave (slurred QRS upstroke)
  • Wide QRS complex
• Risk: AF with rapid conduction down accessory pathway → VF
• DANGER: Do NOT give AV nodal blockers (verapamil, digoxin) in AF+WPW

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Ventricular Arrhythmias

Premature Ventricular Contractions (PVCs)

• Wide, bizarre QRS without preceding P wave
• Followed by compensatory pause
• Types: Unifocal (same morphology), multifocal (different morphologies)
• Bigminy = every other beat is a PVC; Trigeminy = every third beat

Ventricular Tachycardia (VT)

• ECG: Wide QRS tachycardia (>120 ms), rate >100 bpm, >3 consecutive beats
• AV dissociation (more QRS than P waves) - pathognomonic of VT
• Fusion beats and capture beats are diagnostic
• Causes: Ischemic heart disease (scar), cardiomyopathy, electrolyte disorders
• Sustained VT = VT lasting >30 seconds (or requiring termination)

Ventricular Fibrillation (VF)

• ECG: Chaotic, rapid, irregular undulations - NO recognizable QRS
• No effective cardiac output - immediate defibrillation required
• Most common initial rhythm in sudden cardiac death

Torsades de Pointes

• "Twisting of the points" - polymorphic VT where QRS axis rotates
• Always preceded by prolonged QT interval
• Causes: Long QT syndrome (congenital or acquired), drugs (antiarrhythmics, antibiotics, antipsychotics), hypokalemia, hypomagnesemia
• Treatment: IV magnesium sulfate, correct electrolytes, pacing

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PART 8: METABOLIC & ELECTROLYTE DISORDERS

Hyperkalemia

• Treatment: Calcium gluconate (stabilizes membrane), then glucose + insulin, bicarbonate, kayexalate

Hypokalemia

• ECG: Flattened T waves, prominent U waves (after T wave), prolonged QU interval
• U waves >T waves = significant hypokalemia
• Risk of torsades de pointes

Hypercalcemia

• ECG: Short QT interval (shortened ST segment)
• Bradycardia, AV block at very high levels

Hypocalcemia

• ECG: Prolonged QT interval (due to prolonged ST segment)

Digitalis Effect (therapeutic level)

• ECG: "Reverse tick" or "Salvador Dali mustache" ST depression (scooped ST in V5-V6)
• Slowed AV conduction (longer PR interval)
• Digitalis toxicity: PVCs, bigeminy, accelerated junctional rhythm, various AV blocks

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PART 9: MISCELLANEOUS CONDITIONS

Pulmonary Embolism (PE)

• Most common ECG finding: Sinus tachycardia
• Classic (uncommon) pattern: S1Q3T3
  • Large S wave in lead I
  • Q wave in lead III
  • Inverted T wave in lead III
• Other findings: New RBBB, right axis deviation, T-wave inversions V1-V4, P pulmonale
• These reflect acute right heart strain

Pericarditis

• ECG (acute stage):
  • Diffuse (saddle-shaped/concave upward) ST elevation in almost ALL leads
  • PR segment depression (very specific for pericarditis)
  • No reciprocal changes (unlike STEMI)
• Evolution over days/weeks: ST normalizes, T-wave inversions, then normalization

Hypertrophic Cardiomyopathy (HCM)

• Often markedly abnormal ECG despite young patient
• LVH criteria; deep Q waves in lateral leads (I, aVL, V5-V6) from septal hypertrophy
• Widespread T-wave inversions

Long QT Syndrome

• QTc > 440-460 ms
• Congenital (Romano-Ward, Jervell-Lange-Nielsen) or acquired (drug-induced)
• Risk of torsades de pointes and sudden death

Brugada Syndrome

• ECG: Right bundle branch block pattern + ST elevation in V1-V3 (coved/saddleback type)
• Normal-appearing heart; risk of sudden VF
• Type 1 (coved): Down-sloping ST elevation ≥2 mm then negative T wave in V1-V2
• Sodium channel mutation (SCN5A)

Hypothermia

• ECG: Osborn wave (J wave) - positive deflection at J point, best in V4-V6
• Bradycardia, prolonged intervals (PR, QRS, QT), muscle tremor artifact
• At severe temperatures: VF risk

Dextrocardia

• ECG: Negative P, QRS, T in lead I; right-sided precordial progression
• R-wave decreases from V1 to V6 (reversed)
• Corrected by reversing arm leads and placing precordial leads on right side

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PART 10: ECG IN SPECIFIC PATIENT SCENARIOS

Cardiac Monitoring in the ICU / OR

• Sinus rhythm with short bursts of atrial tachycardia
• Pseudo-arrhythmia from electrode artifact (mimicking flutter or VT)
• Nonsustained VT: wide, rapid QRS not preceded by P wave
• Pseudo-pacemaker failure artifact (flat ECG with preserved pulse on arterial line)

Post-Cardiac Arrest ECG

• After ROSC, obtain 12-lead ECG immediately
• ST elevation → cardiac catheterization
• Note: ~1/3 of post-arrest patients without ST elevation still have acute coronary occlusion
• New LBBB post-arrest should raise suspicion for anterior MI

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QUICK SUMMARY TABLE - Disease vs ECG Pattern

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• Harrison's Principles of Internal Medicine, 22nd Ed. (2025) - Chapter 247 (ECG)
• Goldman-Cecil Medicine, International Edition - Chapters 42 & 52 (Arrhythmias, Conduction)
• Tintinalli's Emergency Medicine - Chapter 49 (AMI/ECG)
• Costanzo Physiology, 7th Ed. - Chapter 4 (Cardiac Physiology/ECG)
• Braunwald's Heart Disease, 10e - Chapter 61 (Ambulatory/monitoring ECG)