Explain 10 common heart diseases with ECG changes & ECG images
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ECG images 10 common heart diseases STEMI atrial fibrillation heart block hypertrophy pericarditis
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I now have an excellent collection of textbook ECG images and clinical content. Let me compose the comprehensive response covering all 10 heart diseases.
10 Common Heart Diseases: ECG Changes & Images
Below is a systematic guide to the ECG findings in 10 major cardiac conditions, with images sourced from Harrison's Principles of Internal Medicine 22E, Fuster and Hurst's The Heart 15E, and Tintinalli's Emergency Medicine.
1. ST-Elevation Myocardial Infarction (STEMI)
Pathophysiology: Complete occlusion of a coronary artery causes transmural ischemia, producing a "current of injury" directed outward (epicardial surface), which is recorded as ST elevation by overlying leads.
ECG Changes (evolving sequence):
- Hyperacute phase (minutes): Tall, peaked (hyperacute) T waves - earliest change
- Acute phase (hours): ST elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in ≥2 contiguous precordial leads; reciprocal ST depression in opposing leads
- Evolving phase (hours-days): Pathological Q waves develop (necrosis marker), T wave inversion
- Chronic phase (weeks-months): Q waves persist; ST may normalize
Localization by lead:
| Territory | Culprit Artery | ST Elevation | Reciprocal Depression |
|---|---|---|---|
| Anterior | LAD | V1-V4 | II, III, aVF |
| Inferior | RCA/LCx | II, III, aVF | I, aVL, V1-V4 |
| Lateral | LCx | I, aVL, V5-V6 | V1-V2 |
| Posterior | RCA/LCx | Tall R in V1-V2 | ST depression V1-V3 |
ST vector diagram (subendocardial vs. transmural ischemia):
FIGURE - Ischemic ST vector. (A) Subendocardial ischemia: ST vector points inward - ST depression in overlying leads. (B) Transmural/epicardial ischemia: ST vector points outward - ST elevation in overlying leads. Source: Harrison's Principles of Internal Medicine 22E, Fig. 247-11
Anterior and inferior STEMI - evolving sequence:
FIGURE - Top row: Anterior STEMI sequence (acute → evolving). Bottom row: Inferior STEMI sequence. Note Q-wave formation and reciprocal changes. Source: Harrison's Principles of Internal Medicine 22E, Fig. 247-13
Wellens T-wave sign (critical LAD stenosis):
FIGURE - Wellens T-wave sign: deep symmetric T-wave inversions in V1-V6. This pattern (anterior wall ischemia) is associated with critical stenosis of the LAD. Source: Harrison's Principles of Internal Medicine 22E, Fig. 247-12
2. Non-ST-Elevation ACS (NSTEMI/Unstable Angina)
Pathophysiology: Partial coronary occlusion or severe subendocardial ischemia. The ST vector is directed toward the endocardial surface (cavity), producing ST depression in overlying leads rather than elevation.
ECG Changes:
- ST depression (horizontal or downsloping ≥0.5 mm) - most specific for ischemia
- T-wave inversions (symmetric, deep) in involved territory
- Transient ST depression during episodes of chest pain, resolving with relief
- Normal ECG does NOT exclude NSTEMI (diagnosis requires troponin elevation + clinical context)
- No pathological Q waves
- Diffuse deep T-wave inversions across precordium ("Wellens pattern") - indicates high-grade LAD stenosis even at rest
Key distinction from STEMI: No ST elevation, no new LBBB. Troponin rise without ECG meets NSTEMI criteria.
3. Atrial Fibrillation (AF)
Pathophysiology: Chaotic, rapid electrical activity in the atria (400-600/min) from multiple micro-reentrant circuits, eliminating organized atrial contraction. The AV node acts as a gatekeeper, allowing irregular ventricular conduction.
ECG Changes:
- Absent P waves - replaced by irregular, low-amplitude fibrillatory baseline (f-waves)
- Irregularly irregular RR intervals - the hallmark; no two consecutive RR intervals are the same
- Ventricular rate: 110-160/min if uncontrolled; slower with rate control therapy
- Coarse vs. fine fibrillation: Coarse f-waves (≥1mm) common in rheumatic/valvular disease; fine f-waves (<1mm) common in lone AF
- Narrow QRS unless aberrant conduction (bundle branch block) or pre-excitation (WPW)
- In pulmonary hypertension: right axis deviation, R/S ratio >1 in V1, ST depression V1-V3
(Referenced: Tintinalli's Emergency Medicine, block5.md)
4. Atrioventricular (AV) Heart Block
Pathophysiology: Impaired conduction through the AV node or His-Purkinje system from fibrosis, ischemia, infiltrative disease, or medication toxicity. Three degrees of severity exist.
ECG Changes:
| Degree | ECG Findings | Risk |
|---|---|---|
| 1st degree | PR interval >200 ms; all P waves conduct | Benign |
| 2nd degree Mobitz I (Wenckebach) | Progressive PR lengthening → dropped QRS (then cycle restarts) | Usually benign (AV node) |
| 2nd degree Mobitz II | Fixed PR interval + sudden dropped QRS, often with wide QRS | Serious - risk of complete block |
| 3rd degree (Complete block) | Complete AV dissociation; atrial rate > ventricular rate; escape rhythm (narrow = junctional; wide = ventricular) | Life-threatening |
ECG - AV block progression (1st-degree → complete heart block in endocarditis patient):
FIGURE A - First-degree AV block: Note the prolonged PR interval throughout. Source: Fuster and Hurst's The Heart 15E, Fig. 33-6A
FIGURE B - Second-degree AV block: Progressive PR prolongation with dropped beats visible. Source: Fuster and Hurst's The Heart 15E, Fig. 33-6B
FIGURE C - Complete heart block: Full AV dissociation. P waves and QRS complexes march independently at different rates. Source: Fuster and Hurst's The Heart 15E, Fig. 33-6C
Harrison's schematic of AV block types:
FIGURE - Second-degree Mobitz II block (top, V lead) showing fixed PR then dropped beat; complete AV block (bottom, V3) showing full dissociation. Source: Harrison's Principles of Internal Medicine 22E, Fig. 252-1
FIGURE - First-degree AV block (top) with a fixed prolonged PR interval in every beat; Mobitz I (Wenckebach) AV block (bottom) with progressive PR lengthening prior to a dropped beat. Source: Harrison's Principles of Internal Medicine 22E, Fig. 252-1
5. Left Ventricular Hypertrophy (LVH)
Pathophysiology: Increased left ventricular muscle mass from chronic pressure overload (hypertension, aortic stenosis) or volume overload. Increased muscle mass generates larger electrical forces toward the left and posterior.
ECG Changes:
- Voltage criteria: Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm; or R in aVL ≥11 mm
- Strain pattern: ST depression and asymmetric T-wave inversion in I, aVL, V5-V6 (lateral leads) - reflects "LV strain"
- Left axis deviation: QRS axis <-30° is common
- Prolonged QRS duration (not as wide as bundle branch block, typically 100-120 ms)
- Left atrial enlargement: Broad, notched P waves (P mitrale) - biphasic P in V1 with terminal negative component >1mm depth x 1mm width
- Increased R-wave peak time (intrinsicoid deflection >50 ms in V5-V6)
(Referenced: Goldman-Cecil Medicine International Edition)
6. Hypertrophic Cardiomyopathy (HCM)
Pathophysiology: Genetic sarcomere mutation causing asymmetric septal hypertrophy with myofibrillar disarray. The abnormal depolarization forces and LVH produce dramatic ECG changes.
ECG Changes:
- LVH voltage criteria - present in most patients
- Septal Q waves: Deep, narrow (<40 ms) Q waves in I, aVL, V5-V6 from abnormal septal depolarization - may mimic inferior/lateral MI but no ST evolution
- Widespread ST depression and T-wave inversions: Can be diffuse
- Left axis deviation
- Giant negative T waves in apical HCM (Yamaguchi syndrome): Deep (>10 mm) symmetric T-wave inversions across precordial leads V3-V6, resembling Wellens but without active ischemia
- WPW pattern: In some hereditary forms (PRKAG2 mutations)
- Atrial fibrillation in advanced/dilated phase
(Referenced: Tintinalli's Emergency Medicine block10.md, Harrison's block33.md)
7. Acute Pericarditis
Pathophysiology: Diffuse inflammation of the pericardium causes uniform epicardial "injury current" affecting all ventricular surfaces simultaneously. The PR depression reflects atrial injury.
ECG Changes (4 classic stages):
- Stage 1 (days 1-2): Diffuse ST elevation (concave up/"saddle-shaped") in nearly all leads EXCEPT aVR and V1 (which show ST depression); PR depression in II and other leads (pathognomonic); PR elevation in aVR
- Stage 2 (days 3-7): ST returns to baseline; T waves flatten
- Stage 3 (1-3 weeks): T-wave inversions develop diffusely
- Stage 4 (weeks-months): ECG normalizes
Key distinguishing features from STEMI:
- ST elevation is concave (saddle-shaped) not convex
- Diffuse (all leads) not regional
- No reciprocal ST depression (except aVR/V1)
- PR depression is specific for pericarditis
- No pathological Q waves
8. Wolff-Parkinson-White (WPW) Syndrome
Pathophysiology: An accessory pathway (Bundle of Kent) bypasses the AV node, allowing direct atrial-to-ventricular conduction without the physiological AV delay. This "pre-excites" the ventricle - the first part of the QRS is slurred (delta wave) from slow cell-to-cell conduction through ventricular muscle.
ECG Changes (during sinus rhythm):
- Short PR interval (<120 ms) - AV node delay bypassed
- Delta wave - slurred upstroke at the beginning of the QRS (initial part of ventricular pre-excitation)
- Wide QRS (>120 ms) from fusion of accessory pathway + normal conduction
- Secondary ST-T changes - discordant from QRS direction (pseudo-ischemia)
- Pseudo-Q waves - negative delta waves can simulate MI
- During AVRT tachycardia: Narrow complex regular tachycardia (orthodromic) or very rapid wide-complex irregular tachycardia (antidromic/AF - life-threatening)
WPW 12-lead ECG + accessory pathway diagram:
FIGURE - (A) 12-lead ECG of WPW syndrome in sinus rhythm. (B) Negative delta wave simulating Q wave. (C) Positive delta wave with slurred QRS upstroke. (D) Dual conduction: impulse travels simultaneously through AVN and accessory pathway (AP). Source: Tintinalli's Emergency Medicine, Fig. 18-24
9. Dilated Cardiomyopathy (DCM)
Pathophysiology: Global ventricular dilation with systolic dysfunction. The stretched, fibrotic myocardium disrupts normal conduction pathways, producing characteristic ECG changes.
ECG Changes:
- Left bundle branch block (LBBB): Very common - wide QRS (>120 ms), broad notched R in I/V5-V6, QS in V1; occurs from conduction system fibrosis
- Left ventricular hypertrophy pattern (may be present despite systolic dysfunction)
- Sinus tachycardia - compensatory
- Poor R-wave progression in precordial leads - reflects lateral wall scarring
- Non-specific ST-T changes widespread
- Pathological Q waves from areas of fibrosis/scarring (without ischemia)
- Low voltage: If associated with cardiac amyloid, sarcoid, or effusion
- Atrial fibrillation - common with progressive disease
- Frequent PVCs / nonsustained VT: From reentrant circuits around fibrotic areas
- No specific diagnostic ECG pattern - diagnosis is echocardiographic
(Referenced: Braunwald's Heart Disease block12.md - "There are no specific ECG findings. Nonspecific T wave abnormalities, reduced voltage, and left atrial enlargement may be present. Atrial fibrillation is common.")
10. Pulmonary Embolism (PE)
Pathophysiology: Acute pulmonary artery occlusion causes right heart pressure overload. The acutely dilated and strained right ventricle shifts the cardiac axis rightward and affects the conduction system. Most ECG changes reflect acute cor pulmonale.
ECG Changes:
- Sinus tachycardia - most common finding (~40% of cases); most sensitive but non-specific
- S1Q3T3 pattern: Deep S wave in lead I + Q wave in lead III + T-wave inversion in lead III - classic but present in only ~20% of cases
- Right heart strain pattern: T-wave inversions in V1-V4 (right precordial leads) ± III, aVF - more sensitive than S1Q3T3
- Right axis deviation - from acute RV pressure/volume load
- New right bundle branch block (RBBB): Complete or incomplete - from RV strain
- P pulmonale: Tall peaked P waves in II >2.5 mm from right atrial dilation
- Atrial fibrillation or flutter (10-35% of cases)
- Low voltage or electrical alternans if associated massive PE with tamponade physiology
- Normal ECG in up to 20% of cases
- Mimics: anterior STEMI (T inversions V1-V4), inferior MI (S1Q3T3)
(Referenced: Tintinalli's Emergency Medicine block5.md, Fishman's Pulmonary Diseases block16.md)
Summary Table
| Condition | Key ECG Findings | Most Specific Sign |
|---|---|---|
| STEMI | Regional ST elevation, Q waves, reciprocal depression | ST elevation in ≥2 contiguous leads |
| NSTEMI/UA | ST depression, T inversions; no ST elevation | Horizontal/downsloping ST depression |
| Atrial Fibrillation | Absent P waves, irregularly irregular RR | Irregularly irregular narrow complex |
| AV Block | PR prolongation / dropped QRS / AV dissociation | 3rd degree: P and QRS independent |
| LVH | High voltage, lateral strain, LAE | Sokolow-Lyon ≥35 mm + strain |
| HCM | LVH + septal Q waves; giant T inversions (apical) | Deep narrow Q in I, aVL, V5-V6 |
| Acute Pericarditis | Diffuse saddle ST, PR depression | PR depression in II + diffuse ST |
| WPW | Short PR, delta wave, wide QRS | Delta wave + short PR |
| DCM | LBBB, low voltage, AF, PVCs | New LBBB + cardiomegaly |
| Pulmonary Embolism | Sinus tach, S1Q3T3, RV strain V1-V4 | New RBBB + right precordial T inversions |
Sources:
- Harrison's Principles of Internal Medicine 22E (2025), Ch. 247, 252
- Fuster and Hurst's The Heart, 15th Edition, Ch. 33
- Tintinalli's Emergency Medicine: A Comprehensive Study Guide, Ch. 18
- Braunwald's Heart Disease, 2-Vol Set
- Goldman-Cecil Medicine International Edition
Create a visual summary PDF: ECG patterns comparison chart for all 10 diseases
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ECG Patterns Comparison
PDF Document · PDF
What's inside
Page 1 - Cover & Overview
- Color-coded index of all 10 diseases
- ECG component key (P, PR, QRS, ST, T, QT intervals with normal values)
Pages 2-6 - Individual Disease Cards (2 per page)
Each card contains:
- Drawn ECG waveform on pink grid paper with annotated features (ST arrows, delta waves, PR markers, etc.)
- Mechanism of the ECG change
- 6 key ECG findings as bullet points
- Localization / lead territories
- Clinical pearl (treatment traps, mimics, action thresholds)
Page 7 - Master Comparison Table + Emergency Summary
- 12-column comparison table across all 10 conditions (heart rate, P wave, PR, QRS, ST, T wave, key sign)
- Emergency ECG recognition quick-reference with immediate actions (STEMI → cath lab, WPW+AF → cardioversion, complete heart block → pacing, etc.)
- Source citations from Harrison's, Braunwald's, Tintinalli's, Fuster & Hurst
Generate an interactive ECG lead anatomy poster showing all 12-lead placement and vectors
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ECG Lead Anatomy Poster
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What's interactive in the poster
Body diagram (SVG)
- Full body silhouette with torso, limbs, head, and rib cage hints
- Animated heart icon in anatomical position
- 10 clickable pulsing electrode dots (RA, LA, RL, LL in color-coded positions + V1-V6 on chest)
- Hover tooltips on every electrode showing placement and polarity
- ECG machine boxes on both sides with mini trace animations
- Lead wires as color-coded dashed lines (red=RA, yellow=LA, green=LL, black=RL)
Header filter badges
- Limb Leads - highlights I, II, III buttons
- Augmented - highlights aVR, aVL, aVF
- Precordial - highlights V1-V6
- Vectors - toggles animated directional arrows showing Einthoven triangle (I/II/III + aVR/L/F) and precordial horizontal vectors
- Reset - clears all selections
Info panel (right sidebar)
- Updates dynamically on click with: anatomy location, lead vector/angle, clinical significance list, normal waveform description
- Live ECG mini-strip drawn on Canvas with realistic waveforms per lead type (rS pattern for V1/V2, transitional for V3/V4, tall R for V5/V6, inverted for aVR)
Reference diagrams (built into SVG)
- Hexaxial system (bottom-left): color-coded reference wheel with I/II/III/aVR/aVL/aVF axes at their correct angles, normal axis arrow, quadrant labels (Normal/LAD/RAD/Extreme)
- Precordial cross-section (bottom-right): horizontal plane thorax view showing V1-V6 electrode positions relative to RV, LV, and spine
12-lead grid (bottom right) - all 12 leads as clickable color-coded buttons showing axis angle / placement text
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