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Complete ECG Guide: Normal ECG, How to Read It, and All Major Abnormalities

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Part 1 - The Cardiac Conduction System (Foundation)

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Part 2 - The ECG Paper and Basic Calibration

• Regular rhythm: divide 300 by the number of large boxes between two R waves
• Alternatively: count R waves in 10-second strip and multiply by 6

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Part 3 - Normal ECG Waveforms and What They Mean

The Waves

• Guyton and Hall Textbook of Medical Physiology; Harrison's Principles of Internal Medicine, 22E

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Part 4 - The 12 ECG Leads

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Part 5 - How to Read an ECG Systematically (Step-by-Step)

1. Rate - calculate heart rate (normal: 60-100 bpm)
2. Rhythm - regular vs. irregular; is there a P before every QRS?
3. P wave - present? Upright in II? Each P followed by QRS?
4. PR interval - 120-200 ms?
5. QRS duration - ≤110 ms? Wide or narrow?
6. QRS axis - normal (-30 to +90°)?
7. R wave progression - V1 to V6 transition normal?
8. ST segments - elevation or depression?
9. T waves - concordant with QRS? Inverted?
10. QT interval - prolonged?
11. U waves - present?

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Part 6 - Example of a Normal 12-Lead ECG

• Rate ~78 bpm, slightly irregular (sinus arrhythmia - normal variant)
• Axis approximately +60 degrees (QRS positive in I and II)
• PR ~140 ms, QRS ~90 ms, QTc normal
• Upright P waves in II; negative in aVR
• Transition at V3-V4; septal q waves in V5-V6 (normal)
• Isoelectric ST segments; concordant T waves
• Goldman-Cecil Medicine

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Part 7 - ECG Abnormalities (Comprehensive)

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7A - P Wave Abnormalities

Right Atrial Enlargement (P pulmonale)

• Mechanism: Increased right atrial mass causes larger, taller P waves
• ECG changes: P wave amplitude >2.5 mm (tall, peaked) in leads II, III, aVF; P wave axis >75°
• Seen in: COPD, pulmonary hypertension, tricuspid stenosis

Left Atrial Enlargement (P mitrale)

• Mechanism: Delayed left atrial depolarization
• ECG changes: P wave duration >120 ms; bifid (notched) P wave in lead II ("M-shaped"); in V1, terminal negative component of P >1 mm wide and >1 mm deep
• Seen in: Mitral stenosis/regurgitation, hypertension

Absent P waves

• Causes: Atrial fibrillation (replaced by irregular fibrillatory baseline), sinoatrial block, junctional rhythm (P may be retrograde - negative in II, positive in aVR)

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7B - PR Interval Abnormalities

First-Degree AV Block

• ECG: PR interval >200 ms (>1 large box), constant, every P conducts
• Meaning: Slow AV node conduction; benign in isolation
• Causes: Increased vagal tone, AV nodal disease, digoxin, inferior MI

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

• ECG: Progressive PR lengthening with each beat until a QRS is dropped, then resets
• Pattern: "Longer, longer, longer, drop"
• Location: Usually AV node; often reversible
• Causes: Inferior MI, increased vagal tone

Second-Degree AV Block - Mobitz Type II

• ECG: Constant PR interval (normal or prolonged), then sudden non-conducted P wave (QRS drop without warning PR lengthening)
• Location: Below AV node (His bundle or bundle branches); more serious
• Risk: Can progress to complete heart block
• Causes: Anterior MI, fibrosis

Third-Degree (Complete) Heart Block

• ECG: Complete dissociation - P waves and QRS complexes have no relationship to each other; P-P interval regular, R-R interval regular but different rate
• Escape rhythm: If junctional (narrow QRS, rate 40-60 bpm) or ventricular (wide QRS, rate 20-40 bpm)
• Emergency when due to inferior MI or acquired

Short PR Interval (<120 ms)

• Causes: WPW syndrome (with delta wave), AV nodal bypass tract, accelerated junctional rhythm, Lown-Ganong-Levine syndrome

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7C - QRS Abnormalities

Right Bundle Branch Block (RBBB)

• QRS duration ≥120 ms
• RSR' ("rabbit ears") pattern in V1 (rSR' or rsR' morphology)
• Wide, slurred S wave in leads I, V5, V6
• Secondary T-wave inversions in V1-V2 (discordant to last QRS deflection)

Left Bundle Branch Block (LBBB)

• QRS duration ≥120 ms
• Broad, notched R wave (no q) in leads I, aVL, V5, V6
• rS or QS pattern in V1-V2 (wide, deep, notched S wave)
• Discordant ST-T changes across all precordial leads (ST and T wave opposite to QRS direction)
• NEVER a normal finding - always investigate

Left Anterior Fascicular Block (LAFB)

• ECG: QRS <120 ms; marked left axis deviation (more negative than -45°); qR pattern in aVL; rS in II, III, aVF
• Most common cause of left axis deviation in adults

Left Posterior Fascicular Block (LPFB)

• ECG: QRS <120 ms; right axis deviation >+110°; rS in I, aVL; qR in III, aVF
• Rare as isolated finding; must exclude RVH and pulmonary disease first

Wolff-Parkinson-White (WPW) Pattern

• ECG: Short PR (<120 ms), delta wave (slurred upstroke of QRS), wide QRS, secondary ST-T changes
• Mechanism: Accessory pathway (Bundle of Kent) bypasses AV node, pre-excites ventricle
• Risk: Can conduct rapidly in AF causing ventricular fibrillation

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7D - Axis Deviation

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7E - Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

• ECG voltage criteria (Sokolow-Lyon): S in V1 + R in V5 or V6 ≥35 mm
• Cornell criteria: R in aVL + S in V3 >28 mm (men) or >20 mm (women)
• Repolarization abnormality: ST depression and T-wave inversion ("strain pattern") in V5, V6, I, aVL
• Causes: Hypertension, aortic stenosis, hypertrophic cardiomyopathy

Right Ventricular Hypertrophy (RVH)

• ECG: Right axis deviation; R>S in V1 (tall R wave in V1); deep S waves in V5, V6; ST-T changes V1-V3
• Causes: Pulmonary hypertension, COPD, mitral stenosis, congenital heart disease

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7F - Ischemia and Infarction

Subendocardial Ischemia (NSTEMI/UA pattern)

• ECG: ST-segment depression (horizontal or downsloping ≥1 mm in two contiguous leads); T-wave inversions
• Mechanism: Ischemia confined to subendocardium; ST vector shifts toward cavity

Transmural Ischemia (STEMI pattern)

• ECG: ST-segment elevation (≥1 mm in limb leads, ≥2 mm in precordial leads in two contiguous leads)
• Mechanism: Complete epicardial vessel occlusion; ST vector shifts toward injured epicardium
• Early sign: Hyperacute (tall, peaked, broad) T waves - often first sign before ST elevation

Evolution of Q-wave MI

Localizing the Territory of Infarction

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7G - Conduction Timing Abnormalities

Prolonged QT Interval (QTc)

• Definition: QTc >450 ms (men), >460 ms (women)
• Risk: Torsades de pointes (polymorphic VT) leading to ventricular fibrillation
• Causes:
  • Congenital: Long QT syndrome types 1-3 (KCNQ1, HERG, SCN5A mutations)
  • Drugs: Antiarrhythmics (amiodarone, sotalol, quinidine), antipsychotics (haloperidol, ziprasidone), antibiotics (azithromycin, moxifloxacin), antiemetics (ondansetron), methadone
  • Electrolytes: Hypokalemia, hypomagnesemia, hypocalcemia
  • Others: Hypothyroidism, hypothermia, intracranial hemorrhage

Shortened QT Interval

• Definition: QTc <340 ms
• Causes: Hypercalcemia, digoxin, short QT syndrome
• Risk: Atrial/ventricular fibrillation

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7H - Electrolyte and Metabolic Changes

Hyperkalemia (sequence of changes as K+ rises)

Hypokalemia

• ECG: Flattening/inversion of T waves; prominent U waves (U wave amplitude > T wave amplitude); apparent QT prolongation (actually QU prolongation); ST depression

Hypercalcemia

• ECG: Shortened QT interval; short ST segment; J waves (rarely)

Hypocalcemia

• ECG: Prolonged QT interval (due to long ST segment); T wave normal duration

Digitalis (Digoxin) Effect (not toxicity)

• ECG: Scooped ("Salvador Dali moustache") ST depression, especially in lateral leads; shortened QT; T wave changes

Digitalis Toxicity

• ECG: Any arrhythmia, but classically: frequent PVCs (bigeminy), junctional tachycardia, paroxysmal atrial tachycardia with block

Hypothermia

• ECG: Sinus bradycardia; prolonged all intervals; Osborn wave (J wave) - a positive hump at the J point between QRS and ST segment, best seen in V3-V4 and inferior leads. Pathognomonic of hypothermia.

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7I - Pericarditis

Acute Pericarditis

• ECG (4 stages):
  1. Stage I (hours-days): Diffuse ST elevation (concave up, "saddle-shaped") in multiple leads except aVR and V1; PR depression (PR elevation in aVR - highly specific sign)
  2. Stage II: ST and PR normalize; T waves flatten
  3. Stage III: Diffuse T-wave inversions
  4. Stage IV (weeks-months): Normalization
• How to distinguish from STEMI: Pericarditis ST elevation is diffuse (not territorial), concave (not convex), with PR depression, and lacks reciprocal changes (except aVR)

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7J - ST Elevation: Key Causes to Distinguish

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7K - Specific Syndromes

Brugada Pattern

• ECG: RBBB-like morphology with coved-type (type 1) ST elevation in V1-V2 (and V3 with high leads)
• Risk: Sudden cardiac death due to ventricular fibrillation, typically during sleep or fever
• Mechanism: Loss-of-function SCN5A mutation (sodium channel)

Early Repolarization

• ECG: Concave ST elevation with a notch or slur at the J point, typically in V3-V5; often in young athletic individuals
• Mostly benign, but high-risk pattern associated with idiopathic VF exists

Pulmonary Embolism (PE)

• Classic ECG (S1Q3T3):
  • S wave in lead I
  • Q wave + T-wave inversion in lead III
  • Present in only ~20% of PE cases; most common ECG findings are sinus tachycardia and right heart strain changes
• Other PE ECG changes: New RBBB, right axis deviation, T-wave inversions in V1-V4, P pulmonale, AF

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7L - Arrhythmias (ECG Recognition)

Sinus Tachycardia

• Rate >100 bpm; normal P-QRS relationship; gradual onset/offset; look for cause (fever, pain, PE, thyrotoxicosis, hypovolemia)

Sinus Bradycardia

• Rate <60 bpm; normal P-QRS; causes: athletes, vagal tone, hypothyroidism, inferior MI, drugs (beta-blockers, digoxin)

Atrial Fibrillation (AF)

• ECG: Irregularly irregular rhythm; absence of distinct P waves (replaced by fibrillatory f-waves); narrow QRS (unless aberrant conduction)
• Rate varies; ventricular response typically 100-180 bpm if untreated

Atrial Flutter

• ECG: "Sawtooth" flutter waves (F waves) at ~300/min in leads II, III, aVF; regular ventricular response at 2:1 (150 bpm), 3:1, or 4:1 conduction

Supraventricular Tachycardia (SVT)

• ECG: Regular, narrow QRS tachycardia (rate 150-250 bpm); P waves may be buried in QRS or appear just after
• Types: AVNRT (most common), AVRT (in WPW), atrial tachycardia

Ventricular Tachycardia (VT)

• ECG: Wide QRS tachycardia (QRS >120 ms), rate >100 bpm; AV dissociation (P waves march independently); fusion beats; capture beats
• Distinguishing VT from SVT with aberrancy: Brugada criteria, AV dissociation = VT until proven otherwise

Ventricular Fibrillation (VF)

• ECG: Chaotic, completely irregular, no recognizable QRS complexes; coarse or fine undulations
• Immediately life-threatening; requires defibrillation

Torsades de Pointes (TdP)

• ECG: Polymorphic VT with QRS complexes that "twist around the isoelectric line"; associated with prolonged QT interval
• Trigger: long-short RR sequence
• Treatment: IV magnesium, correct QT-prolonging cause

Premature Atrial Contractions (PACs)

• ECG: Early P wave with different morphology; may conduct with normal or aberrant QRS; incomplete compensatory pause

Premature Ventricular Contractions (PVCs)

• ECG: Wide, bizarre QRS not preceded by P wave; T wave opposite to QRS; full compensatory pause
• Bigeminy: PVC alternating with normal beat
• Trigeminy: PVC every third beat
• Couplet: Two consecutive PVCs

Junctional Rhythms

• ECG: Narrow QRS without preceding P wave (P absent, retrograde/inverted in II, or buried in QRS); rate 40-60 bpm
• Seen in digoxin toxicity, inferior MI, increased vagal tone

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7M - Pacemaker ECG

• Pacing spike followed by wide QRS (LBBB pattern if right ventricular pacing)
• Failure to capture: Pacing spike without subsequent QRS
• Failure to sense: Pacer fires even when native beat is present

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Quick Reference Summary Table

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