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Common Heart ECG Patterns - Complete Guide

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The Cardiac Conduction System

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Basic ECG Waveforms and Intervals

Normal 12-Lead ECG (sinus rhythm, HR 75 bpm, PR 160 ms, QRS 80 ms)

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1. Sinus Rhythms

Normal Sinus Rhythm (NSR)

• Rate: 60-100 bpm
• Upright P wave before every QRS in leads I, II, aVF
• Regular P-P and R-R intervals
• PR interval 120-200 ms

Sinus Tachycardia

• Rate: > 100 bpm; identical to NSR otherwise
• Causes: fever, pain, anxiety, anemia, hypovolemia, PE, heart failure, drugs (atropine, sympathomimetics)

Sinus Bradycardia

• Rate: < 60 bpm; otherwise normal morphology
• Causes: athletes, vagal tone, inferior MI, hypothyroidism, beta-blockers, calcium channel blockers

Sinus Arrhythmia

• P-P interval varies with respiration (> 120 ms variation)
• Normal variant, especially in young people

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2. Atrial Arrhythmias

Premature Atrial Complexes (PACs)

• Early, abnormally shaped P wave followed by narrow QRS
• May be non-conducted (blocked PAC) or conducted with aberrancy

Atrial Fibrillation (AF)

• No distinct P waves - replaced by irregular fibrillatory baseline (best seen in V1)
• Irregularly irregular ventricular rhythm
• Rate: ventricular rate 100-160 bpm (uncontrolled); variable QRS morphology possible if aberrant conduction
• Most common sustained arrhythmia; major risk factor for stroke

Atrial Flutter

• Sawtooth flutter waves at ~300 bpm (best in II, III, aVF)
• Regular ventricular rate, typically at 2:1, 3:1, or 4:1 block (150, 100, or 75 bpm)
• Flutter waves may be buried in QRS; carotid sinus massage unmasks them

Supraventricular Tachycardia (SVT / AVNRT)

• Narrow-complex tachycardia, regular, rate 150-250 bpm
• P waves hidden within or just after QRS (retrograde conduction)
• Abrupt onset and termination

Multifocal Atrial Tachycardia (MAT)

• Rate > 100 bpm
• At least 3 different P-wave morphologies
• Irregular rhythm
• Associated with COPD, severe illness

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3. AV Block

First-Degree AV Block

• PR interval > 200 ms
• Every P wave conducts to ventricles
• Benign; may reflect increased vagal tone or digitalis effect

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

• Progressive PR prolongation until a P wave is not conducted (dropped QRS)
• Grouped beating; RR interval shortens before the drop
• Usually due to AV node disease; often benign

Second-Degree AV Block - Mobitz Type II

• Constant PR interval, then sudden non-conducted P wave (dropped QRS without warning)
• Indicates infranodal (His-Purkinje) disease
• Higher risk of progression to complete heart block; requires pacing consideration

Third-Degree (Complete) AV Block

• Complete dissociation of P waves and QRS complexes
• Atrial rate > ventricular rate
• Escape rhythm: junctional (narrow QRS, rate 40-60) or ventricular (wide QRS, rate 20-40)
• Causes: inferior MI, Lyme disease, digoxin toxicity, fibrosis of conduction system

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4. Bundle Branch Blocks

Right Bundle Branch Block (RBBB)

• QRS ≥ 120 ms
• rSR' ("rabbit ears") in V1
• Wide, slurred S wave in I, aVL, V5-V6
• Secondary T-wave inversion in V1-V3 (normal with RBBB)
• Can be normal variant or seen with RVH, PE, ASD, ischemia

Left Bundle Branch Block (LBBB)

• QRS ≥ 120 ms
• Broad, notched R wave in I, aVL, V5-V6 (no septal q waves)
• QS or rS pattern in V1
• T-wave inversion in leads with broad R wave (discordant)
• Almost always pathological; associated with CAD, cardiomyopathy, hypertensive heart disease
• Makes ST analysis unreliable - new LBBB with symptoms = treat as STEMI equivalent

Left Anterior Fascicular Block (LAFB)

• QRS < 120 ms (fascicular blocks don't widen QRS significantly)
• Left axis deviation (more negative than -45°)
• Small q in I, aVL; small r in II, III, aVF
• Most common cause of marked LAD in adults

Left Posterior Fascicular Block (LPFB)

• Right axis deviation (> +110°)
• Small r in I; small q in III
• Rare; must exclude other causes of RAD (RVH, PE, lateral MI)

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5. Ventricular Arrhythmias

Premature Ventricular Complexes (PVCs)

• Wide QRS (> 120 ms), bizarre morphology, no preceding P wave
• Full compensatory pause
• Isolated PVCs common and often benign; frequent PVCs (> 10,000/day) may cause cardiomyopathy

Ventricular Tachycardia (VT)

• Wide-complex tachycardia, rate 100-250 bpm, ≥ 3 consecutive beats
• AV dissociation (P waves marching through QRS) = diagnostic of VT
• Fusion beats and capture beats also diagnostic
• Sustained VT: lasts > 30 seconds or causes hemodynamic compromise
• Monomorphic vs. polymorphic (includes Torsades de Pointes)

Torsades de Pointes

• Polymorphic VT with twisting QRS axis around the baseline
• Associated with prolonged QT interval
• Triggers: hypokalemia, hypomagnesemia, class IA/III antiarrhythmics, tricyclics, certain antibiotics

Ventricular Fibrillation (VF)

• Chaotic, irregular waveforms, no organized QRS complexes
• Causes cardiac arrest; requires immediate defibrillation

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6. Ventricular Hypertrophy

Left Ventricular Hypertrophy (LVH)

• Tall R waves in left leads (V5, V6, I, aVL) + deep S in V1-V2
• Sokolow-Lyon criterion: S(V1) + R(V5 or V6) > 35 mm
• Cornell criterion: R(aVL) + S(V3) > 28 mm (men) or > 20 mm (women)
• Associated ST depression and T-wave inversion in V5-V6 ("strain pattern")
• Causes: hypertension, aortic stenosis, hypertrophic cardiomyopathy

Right Ventricular Hypertrophy (RVH)

• Tall R wave in V1 (R > S in V1)
• Right axis deviation (QRS axis > +100°)
• ST depression and T-wave inversion in V1-V3 ("RV strain")
• Causes: pulmonary hypertension, severe pulmonic stenosis, congenital heart disease

Atrial Enlargement

• Tall, peaked P waves > 2.5 mm in II, III, aVF

• Broad, notched P waves in limb leads (> 120 ms)
• Biphasic P wave in V1 with prominent negative terminal component
• Seen with mitral valve disease, LV dysfunction

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7. Myocardial Ischemia and Infarction

ST-Elevation MI (STEMI)

• ST elevation (≥ 1 mm in ≥ 2 contiguous limb leads; ≥ 2 mm in ≥ 2 contiguous precordial leads)
• Followed by T-wave inversion, then pathological Q waves (> 40 ms wide, > 25% of R-wave amplitude)
• Reciprocal ST depression in opposite leads

Anterior vs. Inferior STEMI ECG sequence

NSTEMI / Unstable Angina

• ST depression (horizontal or downsloping) ± T-wave inversion, without ST elevation
• No Q waves develop
• Subendocardial ischemia pattern

Wellens' Syndrome

• Characteristic T-wave changes in V2-V3 (deep symmetric inversions or biphasic) in a pain-free period
• Indicates critical LAD stenosis; high risk for massive anterior MI

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8. Specific ECG Syndromes

Wolff-Parkinson-White (WPW)

• Short PR (< 120 ms)
• Delta wave (slurred upstroke of QRS)
• Wide QRS (> 120 ms)
• Pseudoinfarct Q waves possible
• Risk: pre-excited AF can cause VF if AV nodal blockers given

Brugada Syndrome

• Right bundle branch block morphology with ST elevation in V1-V3 (coved or saddle-back pattern)
• Structurally normal heart
• Risk of sudden cardiac death via VF
• Unmasked by sodium channel blockers, fever, cocaine

Long QT Syndrome (LQTS)

• QTc > 450-460 ms
• Congenital (LQTS1, LQTS2, LQTS3) or acquired
• Risk of Torsades de Pointes and sudden death

Short QT Syndrome

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

Hypertrophic Cardiomyopathy (HCM)

• LVH pattern with deeply inverted T waves in lateral leads
• Prominent septal Q waves in I, aVL, V5-V6
• "Dagger-like" Q waves

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9. Metabolic and Drug-Induced Changes

Hyperkalemia ECG Progression

1. Mild-moderate: Narrow, peaked ("tented") T waves
2. Moderate-severe: PR prolongation, P-wave flattening, QRS widening
3. Severe: Sine-wave pattern → asystole

Hypokalemia

• Prominent U waves (often taller than T waves)
• ST depression, T-wave flattening
• Prolonged QU interval (mimics long QT)

Hypocalcemia

• Prolonged QT interval (prolonged ST segment)

Hypercalcemia

• Shortened QT interval

Digitalis Effect

• "Scooped" ST-T complex (reverse tick appearance)
• Shortened QT interval
• Toxicity: PAT with block, junctional rhythms, VT, AV block

Hypothermia

• Osborn (J) wave: positive deflection at J point, best in V4-V6
• Bradycardia; prolonged all intervals

Pericarditis (Acute)

• Diffuse, concave ST elevation in multiple leads (saddle-shaped)
• PR depression (best seen in II, aVF)
• Unlike MI: no reciprocal ST changes (except aVR), no Q waves
• Evolves through 4 stages (ST elevation → normalization → T inversion → resolution)

Pulmonary Embolism (Acute)

• Most common: sinus tachycardia
• Classic (uncommon): S1Q3T3 - S wave in I, Q wave and T inversion in III
• Right axis deviation, new RBBB, T inversion V1-V4

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10. Quick Reference Summary Table

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