10 ECG of heart disease
Reading File
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ECG electrocardiogram heart disease patterns
Finding Sources
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myocardial infarction ST elevation ECG
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atrial fibrillation ECG irregular rhythm
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complete heart block third degree AV block ECG
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Wolff-Parkinson-White WPW delta wave ECG pre-excitation
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ventricular tachycardia VT wide complex tachycardia ECG
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long QT syndrome QTc prolongation ECG torsades de pointes
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left bundle branch block LBBB ECG
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pericarditis saddle shaped ST elevation diffuse ECG
I now have excellent ECG images for 10 distinct heart disease patterns. Here is a comprehensive ECG atlas covering 10 important cardiac conditions:
10 ECGs of Heart Disease
1. Anterior STEMI — ST-Elevation Myocardial Infarction
Key findings: Convex ("tombstone") ST-segment elevation in V2–V5 and lateral leads I/aVL, with reciprocal ST depression in inferior leads (II, III, aVF). Sinus bradycardia present.
Cause: Proximal left anterior descending (LAD) artery occlusion causing transmural ischemia of the anterior and lateral walls. Requires emergent reperfusion (PCI or thrombolysis).
2. Inferior + Anterior Multi-territory STEMI
Key findings: ST elevation in inferior leads (II, III, aVF) with reciprocal depression in aVL, plus ST elevation in anteroseptal leads V1–V3 with "tombstone" morphology.
Cause: Multi-vessel coronary occlusion or a wrap-around LAD occluding both territories. Indicates extensive infarction with high mortality risk.
3. Wellens' Syndrome — Pre-Infarction LAD Stenosis
Key findings: Biphasic T-waves in V2–V3 (Type A) and deep symmetric T-wave inversions in V4–V5 during chest pain-free period. Normal ST segments in limb leads.
Cause: Critical proximal LAD stenosis. This pattern warns of impending massive anterior MI — stress testing is contraindicated; urgent angiography required.
4. Left Ventricular Hypertrophy (LVH) with Strain
Key findings: Tall R-waves in V5–V6 and deep S-waves in V1–V2 meeting Sokolow-Lyon criteria. ST depression and T-wave inversions in inferolateral leads (II, III, aVF, V5–V6) — the "strain pattern."
Cause: Chronic pressure overload from hypertension, aortic stenosis, or hypertrophic cardiomyopathy. Strain pattern signals increased cardiovascular risk.
5. Atrial Fibrillation (AF)
Key findings: Irregularly irregular R-R intervals, absent P waves replaced by fine fibrillatory (f) waves (best seen in V1 and lead II), rapid ventricular response >100 bpm, narrow QRS complexes.
Cause: Disorganized atrial electrical activity; associated with hypertension, heart failure, valvular disease, hyperthyroidism, and post-surgery. Risk of thromboembolic stroke.
6. Third-Degree (Complete) AV Block
Key findings: Complete AV dissociation — P waves (fast atrial rate) bear no relationship to QRS complexes (slow ventricular escape rhythm). Wide QRS indicates infra-Hisian escape pacemaker.
Cause: AV nodal failure from ischemia, surgery, fibrosis, or endocarditis. Life-threatening bradycardia — requires urgent permanent pacemaker.
7. Wolff-Parkinson-White (WPW) Syndrome
Key findings: Short PR interval (<120 ms), widened QRS with delta wave (slurred upstroke), secondary ST-T changes discordant with QRS. Negative delta waves in inferior leads indicate posteroseptal accessory pathway.
Cause: Bundle of Kent — anomalous AV bypass tract causing ventricular pre-excitation. Risk of sudden death via AF with rapid accessory pathway conduction; treat with catheter ablation.
8. Monomorphic Ventricular Tachycardia (VT)
Key findings: Wide complex tachycardia (~150–200 bpm), uniform QRS morphology, superior axis (negative in II, III, aVF), positive concordance across precordial leads V1–V6, no preceding P waves.
Cause: Structural heart disease (dilated cardiomyopathy, post-MI scar reentry). Hemodynamically unstable — cardiovert immediately; stable VT may be treated with amiodarone or lidocaine.
9. Long QT Syndrome (LQTS) with Torsades de Pointes
Key findings: Markedly prolonged QTc (≥470 ms in panel), broad flat T-waves in baseline. Transition to Torsades de Pointes (TdP) — polymorphic VT with "twisting" QRS complexes around the isoelectric line.
Cause: Congenital channelopathy (KCNQ1, KCNH2, SCN5A mutations) or acquired (drugs, hypokalemia, hypomagnesemia). Magnesium IV is first-line for TdP; avoid QT-prolonging drugs.
10. Acute Pericarditis
Key findings: Diffuse concave ("saddle-shaped") ST elevation across I, II, III, aVF, V2–V6. PR-segment depression in II/inferior leads, PR elevation in aVR (Spodick's sign). No reciprocal changes (unlike STEMI). Sinus tachycardia.
Cause: Pericardial inflammation (viral, post-MI/Dressler's, autoimmune, uremic). Treated with NSAIDs + colchicine. Key distinction from STEMI: diffuse distribution not following one coronary territory.
Quick Reference Summary
| # | Condition | Key ECG Feature |
|---|---|---|
| 1 | Anterior STEMI | Convex ST↑ V2–V5, reciprocal inferior ST↓ |
| 2 | Multi-territory STEMI | ST↑ inferior + anteroseptal simultaneously |
| 3 | Wellens' Syndrome | Biphasic/deep T inversions V2–V4 (pain-free) |
| 4 | LVH + Strain | High voltage + lateral ST↓, T-wave inversions |
| 5 | Atrial Fibrillation | Irregularly irregular, no P waves, fibrillatory baseline |
| 6 | 3° AV Block | Complete AV dissociation, slow escape rhythm |
| 7 | WPW Syndrome | Short PR, delta wave, widened QRS |
| 8 | Ventricular Tachycardia | Wide complex tachycardia, no P waves, AV dissociation |
| 9 | Long QT / TdP | QTc >470 ms → twisting polymorphic VT |
| 10 | Acute Pericarditis | Diffuse saddle ST↑, PR depression, no reciprocal changes |
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