Complete ECG Interpretation Guide: All Cases & Related Diseases

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Part 1: ECG Basics - The Normal Waveform

Waves, Intervals & Segments

Key principle: Intervals include waves; segments do not. A prolonged PR = AV conduction delay. A wide QRS = abnormal ventricular conduction.

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Part 2: Standard 12-Lead ECG Layout

Limb leads:     I, II, III (frontal plane)
Augmented:      aVR, aVL, aVF (frontal plane)
Precordial:     V1, V2, V3, V4, V5, V6 (horizontal plane)

Territorial Lead Groups (for localizing MI/ischemia)

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Part 3: Systematic ECG Interpretation Steps

1. Rate - Count R-R intervals. Normal: 60-100 bpm. 300 / (number of large boxes between R peaks)
2. Rhythm - Regular or irregular? Is every P followed by a QRS?
3. Axis - Normal: -30° to +90°. Left axis deviation (LAD) vs. Right axis deviation (RAD)
4. P wave - Present? Morphology? Relationship to QRS?
5. PR interval - Short (<120 ms = pre-excitation?) or long (>200 ms = AV block)?
6. QRS duration - Narrow (<120 ms) vs. wide (>120 ms = BBB, aberrancy, ventricular origin)
7. ST segment - Elevation? Depression? Morphology (convex/concave/saddle)?
8. T wave - Upright, inverted, peaked, biphasic?
9. QT interval - Corrected QTc (Bazett formula: QT / √RR)
10. U wave - Present? (hypokalemia, bradycardia)

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Part 4: ECG Patterns by Disease - Complete Reference

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4.1 Sinus Rhythms

Normal Sinus Rhythm

• Rate: 60-100 bpm
• Upright P in I, II; inverted in aVR
• Every P followed by QRS (1:1)
• PR interval 120-200 ms, QRS <120 ms

Sinus Tachycardia

• Rate >100 bpm, identical morphology to NSR
• Causes: fever, pain, anxiety, hypovolemia, PE, anemia, hyperthyroidism, drugs
• NOT a primary arrhythmia - always look for the underlying cause

Sinus Bradycardia

• Rate <60 bpm, normal P-QRS-T morphology
• Causes: athletes (normal), hypothyroidism, hypothermia, vasovagal, beta-blockers, sick sinus syndrome, inferior MI (RCA occlusion affects SA node artery)
• Treat only if symptomatic (atropine, pacemaker)

Sinus Arrhythmia

• Rate varies with respiration (increases on inspiration)
• Normal in young people; phasic variation in R-R with preserved P wave morphology

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4.2 Atrial Arrhythmias

Atrial Fibrillation (AF)

• Absence of discrete P waves (replaced by chaotic fibrillatory baseline, especially in V1)
• Irregularly irregular ventricular rate
• Narrow QRS (unless bundle branch block)
• Ventricular rate typically 100-180 bpm if uncontrolled

Atrial Flutter

• Regular sawtooth flutter waves at ~300 bpm, best seen in II, III, aVF, V1
• Typically 2:1 conduction → ventricular rate ~150 bpm (classic clue: any regular tachycardia at ~150 bpm = flutter until proven otherwise)
• Associated diseases: similar to AF; also after cardiac surgery, structural heart disease

Multifocal Atrial Tachycardia (MAT)

• At least 3 different P wave morphologies
• Irregularly irregular rhythm at 100-180 bpm
• PR intervals vary
• Frequently confused with AF
• Classic cause: COPD, hypoxia, hypomagnesemia

Premature Atrial Contractions (PAC)

• Early, abnormal P wave morphology
• Narrow QRS (unless aberrant conduction)
• Followed by incomplete compensatory pause
• Common triggers: caffeine, stress, alcohol

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4.3 AV Conduction Blocks

First-Degree AV Block

• PR interval >200 ms (>5 small squares) on every beat - no dropped beats
• Conduction delay usually within AV node
• Causes: vagal tone (athletes), inferior MI, digitalis, beta-blockers, calcium channel blockers, myocarditis, aging
• Usually benign; no treatment needed

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

• Progressive PR prolongation until one QRS is dropped
• After the dropped beat, PR resets to shortest interval
• RR intervals progressively shorten before the dropped beat
• Classic "group beating" pattern
• Block is in the AV node - relatively benign
• Causes: inferior MI, increased vagal tone, digitalis toxicity
• Rarely needs pacing (treat underlying cause)

Second-Degree AV Block - Mobitz Type II

• Fixed PR interval before an unexpected dropped QRS
• No warning - PR does not prolong
• QRS often wide (bundle branch block pattern)
• Block is infranodal (His-Purkinje) - more dangerous
• Causes: anterior MI, fibrosis of conduction system, myocarditis
• Always requires permanent pacemaker - high risk of sudden complete block

2:1 AV Block

• Every other P wave is blocked (2 P waves per 1 QRS)
• Cannot distinguish Mobitz I vs II on ECG alone
• If PR <160 ms + wide QRS = likely Mobitz II (infranodal)
• If PR >200 ms + narrow QRS = likely Mobitz I (nodal)

Third-Degree (Complete) AV Block

• Complete AV dissociation - P waves and QRS complexes march out independently
• Atrial rate > ventricular rate (P rate normal; QRS rate 20-40 bpm if ventricular escape, 40-60 bpm if junctional escape)
• Wide QRS = escape from ventricles (His-Purkinje) → unstable, urgent pacing needed
• Narrow QRS = escape from AV junction → more stable
• Causes: inferior MI (usually transient), anterior MI (usually permanent), Lyme disease, degenerative (Lenègre/Lev disease), congenital, digitalis toxicity

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4.4 Myocardial Ischemia & Infarction

Acute STEMI - Anterior (V1-V4)

Acute STEMI - Anterolateral (V2-V6, I, aVL)

STEMI Diagnosis Criteria (Harrison's 22e, ROSEN's)

• New ST elevation at the J point in ≥2 contiguous leads:
  • ≥2 mm in V2-V3 (men ≥40 yr); ≥2.5 mm (men <40 yr); ≥1.5 mm (women)
  • ≥1 mm in all other leads
• New LBBB with symptoms = STEMI equivalent
• Posterior MI: tall R and ST depression in V1-V2 (mirror image)

ECG Evolutionary Changes in STEMI (temporal sequence)

NSTEMI / Unstable Angina

• ST depression ≥0.5-1 mm (horizontal or downsloping) in ≥2 leads
• T wave inversion (deep, symmetric)
• No Q waves, no ST elevation
• Diagnosis confirmed with rising troponin (NSTEMI) vs. no biomarker rise (UA)

Left Main / Proximal LAD Occlusion

• ST elevation in aVR (>1 mm) + diffuse ST depression in ≥6 leads
• ST elevation in aVR > ST elevation in V1 = left main disease
• ST elevation in V1 > aVR = proximal LAD

Right Ventricular Infarction

• Inferior STEMI (II, III, aVF) + ST elevation in V1
• Confirmed with right-sided leads: V4R most sensitive
• Clinical triad: hypotension + JVD + clear lungs in inferior MI
• Avoid nitrates (preload-dependent)

de Winter Pattern (LAD Equivalent)

• Upsloping ST depression at J point in precordial leads
• Tall, symmetric T waves
• ST elevation in aVR
• Equivalent to anterior STEMI - needs urgent PCI

Wellens Syndrome (LAD "warning")

• Type A: biphasic T wave in V2-V3 (small positive then negative)
• Type B: deep symmetric T wave inversion in V2-V3
• Represents reperfused LAD with critical stenosis - patient is pain-free during ECG
• Do NOT perform stress test - high risk of massive anterior MI

ST Elevation Mimics (non-MI causes)

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4.5 Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

• QRS ≥120 ms
• RSR' ("rabbit ears") in V1 - broad terminal R
• Wide S wave in I and V6 (slurred)
• T wave inversion in V1-V3 (secondary change, normal)
• Causes: normal variant, pulmonary embolism (new RBBB = PE until proven otherwise), RV strain, right heart disease, anterior MI, degenerative

Left Bundle Branch Block (LBBB)

• QRS ≥120 ms
• Broad, notched R in I, aVL, V5-V6 (M-shaped)
• No septal Q waves in I, V5-V6
• Deep S in V1 (QS or rS pattern)
• ST/T discordant (ST/T in opposite direction to main QRS deflection)
• Causes: hypertension, coronary artery disease, cardiomyopathy, anterior MI
• New LBBB with chest pain = STEMI equivalent

Left Anterior Fascicular Block (LAFB)

• Left axis deviation (QRS axis -45° to -90°)
• qR in I, aVL; rS in II, III, aVF
• QRS <120 ms (unless combined with RBBB)
• Causes: hypertension, coronary disease, anterior MI

Left Posterior Fascicular Block (LPFB)

• Right axis deviation (+90° to +180°)
• rS in I, aVL; qR in II, III, aVF
• Diagnosis of exclusion (must rule out RVH, lateral MI, PE)

Bifascicular Block

• RBBB + LAFB: most common bifascicular block
• RBBB + LPFB: less common, more serious

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4.6 Ventricular Arrhythmias

Wide-Complex Tachycardia Algorithm

Ventricular Tachycardia (VT)

• Wide QRS >120 ms, rate >100 bpm, regular
• AV dissociation (P waves march through at different rate from QRS) - pathognomonic
• Fusion beats and capture beats (sinus QRS appears mid-tachycardia)
• Concordance in precordial leads (all positive or all negative)
• Brugada criteria, Josephson criteria, Vereckei criteria for VT vs SVT
• Causes: coronary artery disease (scar), cardiomyopathy, channelopathies, electrolyte disturbances
• Treat as VT until proven otherwise - hemodynamic instability → immediate cardioversion

Ventricular Fibrillation (VF)

• Chaotic, completely irregular, no identifiable waves
• Rate >300 bpm (undulations vary in amplitude and morphology)
• No effective cardiac output - cardiac arrest
• Immediate defibrillation + CPR

Torsades de Pointes (TdP)

• Polymorphic VT with QRS complexes that "twist" around the isoelectric axis
• Occurs on background of prolonged QT
• Causes: QT-prolonging drugs (antiarrhythmics, antipsychotics, antibiotics), hypokalemia, hypomagnesemia, congenital Long QT syndrome
• Treatment: IV magnesium, correct electrolytes, remove offending drug; not amiodarone (further prolongs QT)

Premature Ventricular Contractions (PVC)

• Wide, bizarre QRS with no preceding P wave
• Compensatory pause (full compensatory)
• T wave in opposite direction to QRS (discordant)
• Rule of bigeminy (PVC every other beat), trigeminy (every 3rd), couplets (2 in a row)
• Frequent PVCs (>10,000/day or >15%) can cause PVC-induced cardiomyopathy

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4.7 Supraventricular Tachycardias (SVT)

AVNRT (most common SVT)

• Narrow complex tachycardia, rate 150-250 bpm, regular
• P waves buried in or just after QRS (retrograde P in V1 as pseudo-R')
• Abrupt onset and termination
• Mechanism: re-entry circuit in AV node
• Treatment: Valsalva, adenosine, calcium channel blockers

AVRT (Wolff-Parkinson-White - WPW)

• Orthodromic AVRT: narrow QRS (most common WPW tachycardia)
• Antidromic AVRT: wide QRS (uses accessory pathway anterograde)
• Delta wave + short PR + wide QRS in sinus rhythm = WPW pattern
• Pre-excited AF in WPW: irregular wide-complex tachycardia, very fast (>200 bpm), life-threatening - DO NOT give AV nodal blockers (adenosine, verapamil, digoxin) - use procainamide or cardioversion

Junctional Tachycardia

• Narrow QRS, rate 60-130 bpm
• Retrograde P waves (inverted in II, III, aVF) before, during, or after QRS
• Causes: digitalis toxicity, inferior MI, post-cardiac surgery

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4.8 QT Interval Abnormalities

Long QT Syndrome (LQTS)

• QTc >440 ms (men), >460 ms (women)
• Risk of TdP and sudden cardiac death
• Congenital (LQT1, LQT2, LQT3, etc.) or acquired (drugs, electrolytes)

Short QT Syndrome

• QTc <340 ms
• Risk of VF and AF
• Tall, peaked T waves, short ST segment

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4.9 Specific Disease-Related ECG Patterns

Pulmonary Embolism (PE) - "S1Q3T3"

• Sinus tachycardia (most common finding)
• S wave in lead I + Q wave in III + T wave inversion in III
• New RBBB or right axis deviation
• T wave inversion V1-V4 (right heart strain)
• P pulmonale (peaked P >2.5 mm in II)

Pericarditis

• Diffuse saddle-shaped ST elevation (concave upward) in most leads except aVR and V1
• PR depression (key finding - nearly pathognomonic)
• Reciprocal ST depression and PR elevation in aVR
• Evolves through 4 stages over weeks
• No reciprocal ST changes (unlike MI)

Hypertrophic Cardiomyopathy (HCM)

• Left ventricular hypertrophy (LVH) criteria (Sokolow-Lyon: S in V1 + R in V5 or V6 >35 mm)
• Deep, narrow Q waves in lateral leads (I, aVL, V5-V6) - "septal Q waves"
• Left axis deviation
• ST depression and T wave inversion (strain pattern)

Hyperkalemia

Hypokalemia

• Flattened/inverted T waves
• Prominent U waves (>1 mm or taller than T wave)
• ST depression
• Prolonged QU interval (mistaken for QT prolongation)

Hypercalcemia

• Short QT interval (shortened ST segment)
• Wide T waves
• Bradycardia, prolonged PR

Hypocalcemia

• Prolonged QT (long ST segment, T wave normal)

Digitalis Toxicity

• "Scooped" or "hockey-stick" ST depression (Salvador Dali mustache sign)
• Shortened QT
• Bradycardia, AV blocks, junctional rhythms, bidirectional VT (severe toxicity)
• Bidirectional VT (alternating QRS axis) is hallmark of severe digoxin toxicity

Hypothermia

• Osborn (J) wave: positive deflection at J point (junction of QRS and ST), best in V4-V6 and inferior leads
• Bradycardia, prolonged intervals (PR, QRS, QT)
• Atrial and ventricular arrhythmias
• Osborn waves increase in amplitude as temperature falls

Brugada Syndrome

• Type 1 (diagnostic): Coved-type ST elevation ≥2 mm with T wave inversion in V1-V2 (or V1-V3)
• Type 2/3: Saddleback pattern (less specific - may require sodium channel blocker provocation)
• Risk of VF and sudden death - ICD indicated
• Underlying mutation: SCN5A (sodium channel)
• Unmasked by: fever, cocaine, antiarrhythmic drugs, alcohol

Wolff-Parkinson-White (WPW) - Sinus Rhythm

• Short PR <120 ms
• Delta wave (slurred QRS upstroke - initial pre-excitation)
• Wide QRS (>120 ms)
• Pseudo Q waves in inferior leads can mimic inferior MI

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4.10 Cardiomyopathy ECG Patterns

Dilated Cardiomyopathy

• Poor R wave progression in precordial leads
• LBBB pattern common
• Low voltage
• Non-specific ST-T changes
• AF common

Hypertrophic Cardiomyopathy (HCM)

• LVH pattern with strain
• Deep narrow septal Q waves in I, aVL, V5-V6
• Often confused with inferior or lateral MI

Arrhythmogenic RV Cardiomyopathy (ARVC)

• T wave inversion in V1-V3 (right precordial leads)
• Epsilon wave (small terminal notch after QRS in V1) - pathognomonic
• RBBB pattern
• QRS duration in V1 >110 ms (longer than in aVL/limb leads)
• PVCs with LBBB morphology (originate in RV)

Cardiac Amyloidosis

• Low voltage in limb leads despite LVH on echo ("voltage-mass discordance")
• Pseudo-infarct pattern (poor R wave progression, Q waves without infarction history)
• Conduction abnormalities (AV blocks, BBB)

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4.11 Congenital and Channelopathy ECG Patterns

Catecholaminergic Polymorphic VT (CPVT)

• Normal resting ECG
• Exercise-induced bidirectional or polymorphic VT
• Ryanodine receptor mutation (RYR2)

Short QT Syndrome

• QTc <340 ms; tall, symmetric T waves
• Risk of AF, VF

Early Repolarization Syndrome

• J-point elevation ≥1 mm in ≥2 inferior or lateral leads
• Distinct notch or slur at J point
• Associated with idiopathic VF in some patients (inferior/lateral distribution highest risk)

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Part 5: Quick-Reference Summary Table

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Part 6: Key Clinical Pearls

1. Any regular tachycardia at ~150 bpm = suspect 2:1 atrial flutter until proven otherwise
2. Wide-complex tachycardia = treat as VT unless you have absolute proof it is not - wrong treatment for VT (calcium channel blockers) can be fatal
3. New LBBB + chest pain = STEMI equivalent - activate cath lab
4. aVR ST elevation + diffuse depression = left main or proximal LAD occlusion
5. Inferior STEMI + hypotension = get right-sided leads, suspect RV infarction - fluids, not nitrates
6. PR depression = pericarditis (nearly pathognomonic)
7. Osborn J waves = hypothermia (the colder, the bigger)
8. Epsilon wave in V1 = ARVC
9. Delta wave + short PR = WPW - do NOT give AV nodal blockers if AF is present
10. Bidirectional VT = digitalis toxicity until proven otherwise
11. Low voltage + pseudo-infarct + no coronary disease = think cardiac amyloidosis
12. S1Q3T3 + sinus tachycardia = PE (though non-specific)

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