Explain me 10 common heart diseases with ECG changes and ECG images of those diseases
Reading File
Finding Sources
Searching the Web
ECG changes 10 common heart diseases with ECG images examples
Finding Sources
Finding Sources
Searching the Web
site:litfl.com ECG library heart disease patterns
Reading File
Reading Web Page
ECG changes heart diseases patterns images
Searching the Web
litfl.com ECG myocardial infarction atrial fibrillation heart block LVH WPW Brugada images
Loading Image
Loading Image
Loading Image
Loading Image
Searching the Web
litfl ECG anterior STEMI LVH atrial fibrillation complete heart block pulmonary embolism pericarditis images
Loading Image
Loading Image
Loading Image
Searching the Web
litfl ECG atrial fibrillation pericarditis pulmonary embolism LVH images site:litfl.com
Loading Image
Loading Image
Loading Image
I now have all the ECG images and information needed to write a comprehensive answer. Let me put together the full, detailed guide.
10 Common Heart Diseases: ECG Changes with Images
Here is a detailed guide to the 10 most common heart diseases, their characteristic ECG changes, and real ECG examples from the LITFL ECG Library (sourced from Braunwald's Heart Disease and peer-reviewed ECG resources).
1. ST-Elevation Myocardial Infarction (STEMI)
The disease: STEMI results from complete occlusion of a coronary artery, causing transmural myocardial ischemia and infarction. It is a time-critical emergency requiring immediate reperfusion.
ECG Changes:
- Hyperacute T waves - the earliest sign; tall, broad, asymmetric T waves in the affected territory
- ST elevation - >1 mm in 2 or more contiguous limb leads, or >2 mm in 2 or more contiguous precordial leads
- Reciprocal ST depression in electrically opposite leads (e.g., inferior STEMI shows reciprocal depression in aVL)
- Q waves - pathological Q waves develop as infarction progresses (>40 ms wide, >25% of R wave height)
- T wave inversion - occurs in the subacute and chronic phases
- Loss of R wave - "R wave regression" in precordial leads
Territory localization:
- Anterior STEMI (LAD occlusion): STE in V1-V4
- Inferior STEMI (RCA/LCx): STE in II, III, aVF
- Lateral STEMI: STE in I, aVL, V5-V6
ECG Example - Anterior STEMI (Evolving):
Marked ST elevation in V1-V4 with reciprocal ST depression in the inferior and lateral leads. Note the tall, peaked T waves consistent with early anterior STEMI.
2. Atrial Fibrillation (AF)
The disease: AF is the most common sustained cardiac arrhythmia. It is caused by chaotic, disorganised atrial electrical activity from multiple re-entrant wavelets and focal triggers (often from the pulmonary veins). Common causes include hypertension, valvular disease, heart failure, thyrotoxicosis, and ischemic heart disease.
ECG Changes:
- No visible P waves - replaced by irregular fibrillatory baseline (f-waves), best seen in V1 and lead II
- Irregularly irregular R-R intervals - the hallmark of AF; no two R-R intervals are the same
- Variable ventricular rate - typically 100-180 bpm in untreated AF (controlled or uncontrolled)
- Narrow QRS complexes (unless there is aberrant conduction, LBBB, or pre-excitation as in WPW-AF)
- Fibrillatory baseline - fine or coarse irregular undulations between QRS complexes
ECG Example - Atrial Fibrillation (WPW with AF):
This ECG shows AF conducted via an accessory pathway in WPW syndrome - note the extremely fast (~300 bpm), irregularly irregular, broad QRS complexes. This is a life-threatening pattern that can degenerate to ventricular fibrillation. Source: LITFL ECG Library.
3. Complete Heart Block (3rd Degree AV Block)
The disease: Complete (3rd degree) heart block means there is complete failure of conduction between the atria and ventricles. The atria and ventricles beat completely independently. It can be caused by inferior STEMI (RCA territory affecting the AV node), Lyme disease, drug toxicity (digoxin, beta-blockers), or fibrosis/calcification of the conduction system.
ECG Changes:
- AV dissociation - P waves and QRS complexes are completely independent; more P waves than QRS complexes
- Regular P-P interval (atrial rate ~60-100 bpm)
- Regular R-R interval but slower (junctional escape: 40-60 bpm; ventricular escape: 20-40 bpm)
- Broad, wide QRS if escape is ventricular in origin (>120 ms); narrow if junctional
- No consistent PR interval - the PR interval varies with each beat, confirming complete dissociation
ECG Example - Complete Heart Block (with Inferior STEMI):
Complete AV dissociation: P waves (atrial rate ~80 bpm) march independently through the ECG. The ventricular escape rate is ~40 bpm with broad, slow QRS complexes. Note also the ST elevation in the inferior leads (II, III, aVF) from the causative inferior STEMI. Source: LITFL ECG Library.
ECG Example - Isolated Complete Heart Block:
Classic complete heart block: regular, slow ventricular escape rhythm (~35 bpm) with broad QRS complexes, completely dissociated from the faster atrial rate. The PR interval changes constantly. Source: LITFL ECG Library.
4. Brugada Syndrome
The disease: Brugada syndrome is an inherited channelopathy (SCN5A sodium channel mutation in ~25% of cases) causing abnormal sodium channel function, leading to potentially fatal ventricular arrhythmias (VF/polymorphic VT), typically during rest or sleep. It is a major cause of sudden cardiac death in young, otherwise healthy individuals, particularly in Southeast Asian men.
ECG Changes:
- Type 1 (diagnostic - "coved" pattern): ST elevation ≥2 mm with a coved (downsloping) morphology in V1-V2, followed by a negative T wave. This is the only pattern that is diagnostic of Brugada syndrome.
- Type 2 ("saddleback" pattern): ST elevation with a saddleback morphology in V1-V2 - this is not by itself diagnostic but raises suspicion
- Partial or complete RBBB pattern may accompany the ST changes
- The pattern may be dynamic - it can appear or worsen with fever, sodium channel blocking drugs, vagal tone, or bradycardia
ECG Example - Brugada Syndrome Type 1:
Classic Type 1 Brugada pattern: coved ST elevation >2 mm in V1 and V2 with a downsloping ST segment and terminal T wave inversion. There is also a partial RBBB pattern. This pattern in a symptomatic patient is an indication for ICD implantation. Source: LITFL ECG Library.
5. Left Ventricular Hypertrophy (LVH)
The disease: LVH results from pressure or volume overload on the left ventricle, most commonly from hypertension, aortic stenosis, or hypertrophic cardiomyopathy. The thickened ventricular wall produces larger electrical forces and altered repolarization.
ECG Changes (Voltage criteria):
- Sokolow-Lyon: S in V1 + R in V5 or V6 > 35 mm
- Cornell: R in aVL + S in V3 > 28 mm (men) or >20 mm (women)
- Tall R waves in lateral leads (I, aVL, V5, V6)
- Deep S waves in V1-V3
- LV strain pattern - asymmetric ST depression and T wave inversion in lateral leads (I, aVL, V5, V6) - a "strain" pattern indicating pressure overload
- Left axis deviation (often)
- Prolonged QRS duration (though usually <120 ms)
- Left atrial enlargement - broad notched P wave in lead II ("P mitrale"), terminal negative deflection in V1
ECG Example - LVH:
Marked LVH: very tall R waves in V4-V6, deep S waves in V1-V3 (total voltage greatly exceeding 35 mm by Sokolow-Lyon). There is an LV strain pattern (ST depression and T wave inversion) in the lateral leads. This degree of LVH may be nearly indistinguishable from LBBB - the key clue is the extremely high voltage. Source: LITFL ECG Library.
6. Hypertrophic Cardiomyopathy (HCM)
The disease: HCM is the most common genetic heart disease (prevalence ~1 in 500), caused by mutations in sarcomere protein genes (most commonly MYH7 and MYBPC3). It causes asymmetric hypertrophy of the ventricular septum, with or without outflow tract obstruction. It is the most common cause of sudden cardiac death in young athletes.
ECG Changes:
- LVH voltage criteria - as above, with very large QRS voltages
- Abnormal Q waves - deep, narrow Q waves in the lateral leads (I, aVL, V5-V6) and inferior leads, representing septal hypertrophy (not infarction)
- Giant T wave inversion - most prominent in apical HCM (Yamaguchi type), with deep symmetric T wave inversions in V4-V6 (can reach -10 to -30 mm)
- ST depression - widespread, often in lateral leads
- Left axis deviation
- Left atrial enlargement
- In young patients: an ECG that looks like a "prior lateral infarction" should raise HCM as the differential
ECG Example - HCM:
HCM pattern: massive T wave inversions predominantly in the lateral and inferior leads, with high LVH voltages. The deep T wave inversions in V4-V6 in a young patient should trigger immediate consideration of HCM and apical variant. The absence of ST elevation helps distinguish this from acute infarction. Source: LITFL ECG Library.
7. Dilated Cardiomyopathy (DCM)
The disease: DCM is characterized by dilation and impaired systolic function of the left (and often right) ventricle. It is the most common cardiomyopathy leading to heart failure and cardiac transplantation. Causes include viral myocarditis, alcohol, genetic mutations, peripartum state, and ischemia.
ECG Changes:
- Non-specific ST-T wave abnormalities - widespread ST depression, T wave flattening or inversion
- Left bundle branch block (LBBB) - a key finding in many DCM patients (broad QRS >120 ms, absent septal Q in lateral leads, dominant S in V1, monophasic R in V6)
- Poor R wave progression in precordial leads
- Sinus tachycardia - a common compensatory response in decompensated DCM
- Left atrial enlargement
- Low voltage in some cases (particularly with pericardial effusion complicating DCM)
- Ventricular ectopy (PVCs) and non-sustained VT
- Q waves may mimic prior MI ("ischemic cardiomyopathy" pattern)
ECG Example - Ischemic/Dilated Cardiomyopathy:
DCM pattern: left bundle branch block morphology with broad QRS complexes. There are non-specific ST-T changes across the precordial leads and poor R wave progression. The combination of LBBB and dilated cardiomyopathy is an indication for cardiac resynchronization therapy (CRT). Source: LITFL ECG Library.
8. Pericarditis
The disease: Acute pericarditis is inflammation of the pericardial sac, most commonly caused by viral infection (Coxsackievirus, echovirus), autoimmune disease, post-MI (Dressler syndrome), or uremia. The hallmark symptom is sharp, pleuritic chest pain that worsens lying flat and improves leaning forward.
ECG Changes (4 classic stages):
- Stage 1 (acute - days 1-2): Diffuse concave ("saddle-shaped") ST elevation in multiple leads (I, II, aVF, V2-V6 - NOT V1 or aVR), plus PR segment depression (best seen in lead II) - highly specific for pericarditis. Reciprocal ST depression and PR elevation in aVR.
- Stage 2 (days 3-7): ST returns to baseline, T waves flatten
- Stage 3 (1-3 weeks): T wave inversion (may persist for weeks)
- Stage 4: ECG normalizes
- Spodick's sign - downward sloping TP segment, a sensitive sign of pericarditis
- Key differentiator from STEMI: diffuse (not territorial) ST elevation, concave morphology, PR depression, and absence of reciprocal ST depression in other leads
ECG Example - Pericarditis:
Acute pericarditis: diffuse saddle-shaped (concave) ST elevation in multiple leads without a territorial distribution. Note PR segment depression best seen in lead II, and reciprocal PR elevation in aVR. The ST changes involve both inferior (II, III, aVF) and lateral (I, V4-V6) territories simultaneously, which would be an impossibility for a single coronary occlusion. Source: LITFL ECG Library.
9. Pulmonary Embolism (PE)
The disease: PE occurs when a thrombus (usually from deep vein thrombosis) lodges in the pulmonary arterial circulation, causing acute right heart strain from increased pulmonary vascular resistance. Massive PE can cause sudden circulatory collapse and death. ECG changes reflect acute right heart strain rather than a primary cardiac pathology.
ECG Changes:
- Sinus tachycardia - the most common ECG finding in PE (~44% of cases)
- S1Q3T3 pattern - deep S wave in lead I, Q wave and T wave inversion in lead III (present in only ~20% but specific to PE)
- Right heart strain pattern:
- Right axis deviation
- New RBBB (complete or incomplete) - from right ventricular overload
- ST depression and T wave inversion in V1-V4 (right ventricular strain)
- P pulmonale (tall peaked P waves in inferior leads)
- Clockwise rotation of the QRS (poor R wave progression)
- Atrial fibrillation - may be precipitated by massive PE
- Electrical alternans - in cases with associated pericardial effusion
The ECG is abnormal in ~70% of PE cases but changes are non-specific. Normal ECG does NOT exclude PE.
Key ECG Image - PE:
(The ECG of acute PE with S1Q3T3 is available at LITFL PE ECG Library)
The S1Q3T3 pattern is shown schematically as:
- Lead I: deep S wave
- Lead III: Q wave + inverted T wave
- V1-V4: T wave inversions (right ventricular strain)
10. Wolff-Parkinson-White Syndrome (WPW)
The disease: WPW is a pre-excitation syndrome caused by an accessory conduction pathway (Bundle of Kent) that bypasses the AV node, allowing impulses to reach the ventricle early. It can cause supraventricular tachycardias (AVRT) and, most dangerously, rapid conduction of atrial fibrillation directly to the ventricles, potentially causing VF and sudden death.
ECG Changes in sinus rhythm:
- Short PR interval (<120 ms) - impulse bypasses the slow AV node
- Delta wave - slurred upstroke of the QRS complex, from slow "pre-excitation" spread of the impulse through the accessory pathway and ventricular muscle (not the fast His-Purkinje system)
- Wide QRS complex (>120 ms) - due to the fusion of pre-excited and normally conducted impulses
- Secondary ST-T changes - discordant ST depression and T wave inversion in the direction opposite to the delta wave
- Pseudo-infarction Q waves - delta waves can mimic Q waves in inferior or lateral leads, mimicking old MI
During AF (most dangerous pattern):
- Extremely fast, broad, irregular QRS complexes (can reach 300 bpm)
- Can degenerate to VF - this is life-threatening and requires immediate cardioversion
ECG Example - WPW with AF:
WPW with rapid AF conduction over the accessory pathway: extremely fast (>300 bpm), irregularly irregular, broad, polymorphic QRS complexes. This is pre-excited AF and is a cardiac emergency - standard AV nodal blocking drugs (adenosine, verapamil, digoxin) are contraindicated as they can accelerate conduction down the accessory pathway and precipitate VF. DC cardioversion is the treatment of choice. Source: LITFL ECG Library.
Quick Reference Summary Table
| Disease | Key ECG Finding | Rate | Rhythm | Key Pattern |
|---|---|---|---|---|
| STEMI | ST elevation + Q waves | Normal/Tachy | Regular | Territorial STE + reciprocal STD |
| Atrial Fibrillation | No P waves | Variable | Irregularly irregular | Fine fibrillatory baseline |
| Complete Heart Block | AV dissociation | Slow (20-60) | Regular (escape) | P waves independent of QRS |
| Brugada Syndrome | Coved ST elevation V1-V2 | Normal | Regular (or VF) | Coved STE + partial RBBB in V1-V2 |
| LVH | High voltage + strain | Normal | Regular | S(V1)+R(V5) >35 mm + lateral STD/TWI |
| HCM | Giant T wave inversions | Normal | Regular | Deep TWI V4-V6, abnormal Q waves |
| DCM | LBBB + poor R wave progression | Tachy/Normal | Regular | Broad QRS, low voltage, non-specific ST-T |
| Pericarditis | Diffuse concave STE + PR depression | Tachy | Regular | Saddle-shaped STE + PR depression in II |
| Pulmonary Embolism | S1Q3T3 + sinus tachycardia | Tachy | Regular | S1Q3T3 + TWI V1-V4 (RV strain) |
| WPW | Short PR + delta wave | Normal/Tachy | Regular (or irregular with AF) | Delta wave + broad QRS + short PR |
Sources:
- Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine (10th/11th Ed.)
- LITFL ECG Library - Burns E, Buttner R, Larkin JJ (CC BY-NC-SA 4.0)
- Goldman-Cecil Medicine, International Edition
- Rosen's Emergency Medicine: Concepts and Clinical Practice
This is a shared conversation. Sign in to Orris to start your own chat.