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ECG changes 10 common heart diseases STEMI atrial fibrillation heart block illustrative

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STEMI ECG ST elevation myocardial infarction classic ECG image site:ecgwaves.com OR site:litfl.com

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Brugada syndrome hypertrophic cardiomyopathy long QT syndrome ECG image examples litfl site:litfl.com

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I now have excellent ECG images and comprehensive information to deliver a detailed, well-illustrated answer. Here is the full guide:

10 Common Heart Disease ECG Changes - Illustrated Guide

1. ST-Elevation Myocardial Infarction (STEMI)

Mechanism: Complete occlusion of a coronary artery causes transmural ischemia, producing ST-segment elevation in leads overlying the infarcted territory, with reciprocal ST depression in opposite leads. Q waves develop within hours as tissue necrosis occurs.

ECG Features:

ST elevation ≥1 mm in ≥2 contiguous limb leads, or ≥2 mm in V2-V3
Reciprocal ST depression in mirror-image leads
Hyperacute (peaked, broad) T waves early on
Pathological Q waves (>40 ms wide, >25% of R-wave height) develop later
T-wave inversion in the recovery phase

Localization:

Territory	Leads with ST Elevation	Artery
Anterior	V1-V4	LAD
Inferior	II, III, aVF	RCA
Lateral	I, aVL, V5-V6	LCx
Posterior	ST depression V1-V3 (mirror)	RCA/LCx

Anterior STEMI: Note ST elevation in precordial leads with reciprocal changes

2. Atrial Fibrillation (AF)

Mechanism: Chaotic, rapid electrical impulses from multiple re-entrant circuits in the atria (often originating from pulmonary vein sleeves) replace organized atrial depolarization. The AV node conducts irregularly, producing an irregularly irregular ventricular response.

ECG Features:

Absent P waves - replaced by fibrillatory (f) baseline (fine or coarse)
Irregularly irregular RR intervals - the hallmark finding
Narrow QRS complexes (unless aberrant conduction/LBBB)
Ventricular rate typically 100-160 bpm if uncontrolled
No distinct isoelectric baseline between complexes

Causes: Hypertension, ischemic heart disease, valvular disease (especially mitral), hyperthyroidism, alcohol, cardiomyopathy, sleep apnea

3. Left Bundle Branch Block (LBBB)

Mechanism: Block in the left bundle branch forces ventricular depolarization to travel right-to-left in an abnormally slow, cell-to-cell manner (not via the specialized conduction system), producing a broad, abnormally shaped QRS.

ECG Features (use the WiLLiaM pattern):

QRS duration >120 ms (broad complex)
Lead V1: broad, deep QS or rS complex ("W" shape)
Lead V6/I/aVL: broad, notched or M-shaped R wave ("M" shape) - no septal Q waves
ST depression and T-wave inversion in lateral leads (I, aVL, V5-V6) - these are "appropriate discordant" changes
Left axis deviation may be present

Clinical significance: New LBBB with chest pain was historically treated as STEMI-equivalent. Sgarbossa criteria help identify true occlusion MI in setting of LBBB.

LBBB 12-lead ECG showing broad notched R waves in lateral leads

LBBB: Note broad QRS, notched R waves in lateral leads, deep S in V1, and discordant ST-T changes

4. Complete (3rd Degree) AV Heart Block

Mechanism: Complete failure of conduction between atria and ventricles. The atria fire independently from the SA node; the ventricles are driven by a slow escape rhythm from the AV junction or ventricles. There is total AV dissociation.

ECG Features:

P waves present at normal rate (~60-100 bpm) - but no P wave conducts to ventricles
QRS complexes present at much slower escape rate (40-60 bpm for junctional; 20-40 bpm for ventricular)
P waves and QRS complexes are completely independent of each other ("march through" each other)
QRS may be narrow (junctional escape) or wide/bizarre (ventricular escape)
No consistent PR interval

Causes: Inferior MI (usually reversible), anterior MI, Lyme disease, drugs (digoxin, beta-blockers, calcium channel blockers), infiltrative disease (sarcoid, amyloid)

Complete (3rd degree) AV block ECG showing dissociated P waves and QRS complexes

Complete heart block: P waves (upward arrows) and QRS complexes (downward arrows) beat independently

5. Left Ventricular Hypertrophy (LVH)

Mechanism: Increased myocardial mass from chronic pressure overload (hypertension, aortic stenosis) produces larger electrical vectors, causing increased QRS voltages. The thickened wall also repolarizes abnormally.

ECG Features (multiple criteria exist; Sokolow-Lyon most used):

Sokolow-Lyon: S in V1 + R in V5 or V6 ≥35 mm
Cornell: R in aVL + S in V3 ≥28 mm (men), ≥20 mm (women)
Left axis deviation
ST depression with asymmetric T-wave inversion in lateral leads (I, aVL, V5-V6) - "strain pattern"
Prolonged QRS (~100-120 ms, but <120 ms)
Left atrial enlargement (broad notched P waves, P mitrale)

Causes: Hypertension (most common), aortic stenosis, hypertrophic cardiomyopathy, coarctation of aorta

6. Wolff-Parkinson-White Syndrome (WPW)

Mechanism: A congenital accessory pathway (Bundle of Kent) bypasses the AV node, pre-exciting part of the ventricle before the normal conduction system depolarizes it. This creates the characteristic delta wave and short PR interval.

ECG Features:

Short PR interval (<120 ms)
Delta wave - slurred upstroke at the start of the QRS (ventricular pre-excitation)
Broad QRS (>120 ms) due to fusion of pre-excited and normally conducted depolarization
Secondary ST-T changes (discordant to QRS)
Risk: AF with WPW is life-threatening - rapid conduction via the accessory pathway can cause VF

WPW Type	V1 morphology	Accessory Pathway location
Type A	Dominant R wave V1	Left-sided pathway
Type B	QS or rS in V1	Right-sided pathway

Wolff-Parkinson-White accessory pathway diagram and ECG showing delta wave

WPW: Accessory pathway diagram (top) and classic ECG showing short PR + delta wave + broad QRS (bottom)

7. Ventricular Tachycardia (VT)

Mechanism: Rapid rhythm originating from ventricular myocardium (below the bundle of His), usually via re-entry around a scar from prior MI. Since conduction is cell-to-cell rather than via the His-Purkinje system, QRS complexes are broad and bizarre.

ECG Features:

Rate: 100-250 bpm
Broad QRS ≥120 ms, often ≥160 ms, with bizarre morphology
AV dissociation - P waves independent of QRS (when visible, pathognomonic for VT)
Fusion beats - QRS morphology partway between normal and VT (P wave conducts during VT)
Capture beats - occasional narrow normal QRS during VT (P wave fully captures ventricles)
Concordance in precordial leads (all positive or all negative V1-V6)
Northwest axis (negative in I and aVF)

Brugada criteria help differentiate VT from SVT with aberrancy.

Ventricular tachycardia (B) compared to normal sinus rhythm (A) - note the chaotic, broad complexes

Panels: A = Normal sinus rhythm, B = Ventricular fibrillation/flutter, C & D = Ventricular tachycardia patterns

8. Hypertrophic Cardiomyopathy (HCM)

Mechanism: Asymmetric septal hypertrophy with myofibrillar disarray causes abnormal depolarization vectors, prominent septal forces, and impaired diastolic relaxation. ECG findings reflect massive left ventricular hypertrophy plus septal abnormalities.

ECG Features:

LVH voltage criteria (usually extreme)
"Dagger" Q waves - deep, narrow Q waves in lateral (I, aVL, V5-V6) and/or inferior leads - due to septal hypertrophy, NOT infarction
ST depression and T-wave inversion in lateral leads
Left axis deviation
Giant negative T waves in mid-precordial leads (apical variant HCM - Yamaguchi)
P-wave abnormalities (left atrial enlargement)
5% of HCM patients have a normal ECG

HCM 12-lead ECG showing deep Q waves and LVH changes

HCM ECG: Deep LVH voltages, lateral Q waves, ST-T changes characteristic of hypertrophic cardiomyopathy

9. Brugada Syndrome

Mechanism: Loss-of-function mutation in sodium channels (SCN5A gene, ~30% of cases) causes abnormal repolarization predominantly in the right ventricular outflow tract (RVOT), creating a characteristic ST pattern in V1-V3 and predisposing to polymorphic VT and sudden cardiac death.

ECG Features (3 types, only Type 1 is diagnostic):

Type	V1-V2 pattern	Diagnostic?
Type 1	Coved ST elevation ≥2 mm + negative T wave	YES - Diagnostic
Type 2	Saddleback ST elevation ≥2 mm + positive/biphasic T wave	No (screen positive)
Type 3	ST elevation <1 mm	No

RBBB-like pattern in V1-V2
Pattern may be intermittent ("concealed Brugada")
Sodium channel blockers (ajmaline, flecainide) can unmask concealed Brugada

Clinical: Predominantly young males, Asian descent; causes sudden death especially at night/rest during fever.

Brugada Syndrome Type 1 ECG showing coved ST elevation in V1

Brugada Type 1: Characteristic "coved" ST elevation >2mm with negative T wave in V1-V2

10. Acute Pericarditis

Mechanism: Diffuse inflammation of the pericardium causes widespread myocardial irritation affecting repolarization globally (not in a vascular territory), producing the characteristic pattern of widespread concave ST elevation with PR depression.

ECG Features (4 stages):

Stage	ECG Changes	Timing
Stage I	Diffuse concave ("saddle-back") ST elevation + PR depression in most leads; ST depression + PR elevation in aVR/V1	Days 1-2 (acute)
Stage II	ST and PR return to baseline, T waves flatten	Days 3-7
Stage III	Diffuse T-wave inversion	Weeks 1-3
Stage IV	ECG normalizes	Weeks to months

Key differentiators from STEMI:

ST elevation is concave (saddle-shaped), not convex/tombstone
Widespread in multiple vascular territories (not anatomically contiguous)
PR segment depression - highly specific for pericarditis
No reciprocal ST depression (except aVR)
No Q waves

Causes: Viral (Coxsackievirus), idiopathic, post-MI (Dressler syndrome), autoimmune, uremic, neoplastic

Quick Summary Reference

Killer ECG infographic showing key patterns: Brugada, WPW, HCM, pericardial effusion, ARVD, hyperkalaemia

Key patterns summary: Note how each condition has a distinctive morphological fingerprint on ECG

Summary Table

Condition	Key ECG Finding	Pathological Structure
STEMI	Convex ST elevation + Q waves (regional)	Occluded coronary artery
Atrial Fibrillation	Absent P waves + irregularly irregular QRS	Chaotic atrial foci
LBBB	Broad QRS, WiLLiaM pattern, no septal Q waves	Left conduction system failure
3rd Degree AV Block	Complete P-QRS dissociation	AV node/His bundle block
LVH	Tall voltages + strain pattern	Thickened LV wall
WPW	Short PR + delta wave + broad QRS	Accessory pathway (Bundle of Kent)
Ventricular Tachycardia	Broad complex tachycardia + AV dissociation	Ventricular re-entry circuit
HCM	LVH + dagger Q waves	Asymmetric septal hypertrophy
Brugada Syndrome	Coved ST elevation V1-V2 + RBBB pattern	SCN5A sodium channel mutation
Acute Pericarditis	Concave ST elevation (all leads) + PR depression	Diffuse pericardial inflammation

Sources: Harrison's Principles of Internal Medicine 22E; Tintinalli's Emergency Medicine; Ganong's Review of Medical Physiology; LITFL ECG Library; ECGwaves.com; REBEL EM

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