Explain me ten common heart diseases with ecg changes and ecg images of those diseases

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common heart diseases ECG changes with ECG images examples

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ECG images atrial fibrillation ventricular tachycardia heart block LBBB wikimedia commons site:litfl.com OR site:ecgwaves.com

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ECG examples STEMI atrial fibrillation ventricular tachycardia complete heart block pericarditis WPW site:ecgwaves.com OR site:litfl.com

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ECG pericarditis PR depression diffuse ST elevation image litfl.com OR ecgwaves.com

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Ten Common Heart Diseases: ECG Changes and Images

1. ST-Elevation Myocardial Infarction (STEMI)

Pathophysiology: Complete occlusion of a coronary artery causes transmural myocardial ischemia and necrosis. Three major electrophysiological events drive the ECG changes: abnormally rapid repolarization, decreased resting membrane potential from K+ loss, and delayed depolarization of infarcted fibers - all generating current flow that elevates the ST segment in overlying leads. (Ganong's Review of Medical Physiology, p.534)

ECG Changes:

Hyperacute T waves - first change, tall peaked T waves in the territory of infarction
ST-segment elevation ≥1 mm in ≥2 contiguous limb leads, or ≥2 mm in ≥2 contiguous precordial leads - the hallmark finding
Reciprocal ST depression in leads on the opposite side of the heart
Q-wave formation - pathological Q waves develop within hours to days as necrotic tissue becomes electrically silent (>40 ms wide, >25% of R-wave height)
T-wave inversion as the infarct evolves
R-wave loss in the territory of infarction

Localisation by leads:

Anterior STEMI: V1-V4 (LAD territory)
Inferior STEMI: II, III, aVF (RCA or LCx territory)
Lateral STEMI: I, aVL, V5-V6
Posterior STEMI: Tall R + ST depression in V1-V2 (reciprocal)

Current of injury - subendocardial vs. transmural (Harrison's, Fig. 247-11):

Ischemia current of injury - ST depression in subendocardial vs ST elevation in transmural infarction

(A = subendocardial ischemia causes ST depression; B = epicardial/transmural ischemia causes ST elevation)

Wellens T-wave sign (anterior ischemia with severe LAD stenosis):

Wellens T-wave sign - deep T-wave inversions V1-V4 in anterior ischemia

2. Non-ST-Elevation Myocardial Infarction (NSTEMI) / Unstable Angina

Pathophysiology: Partial coronary occlusion causing predominantly subendocardial ischemia, without transmural involvement. Biomarkers are elevated in NSTEMI but not in unstable angina.

ECG Changes:

ST depression ≥0.5-1 mm in ≥2 contiguous leads (horizontal or downsloping is most concerning)
T-wave inversions - may be deep and symmetric
No pathological Q waves in most cases
Normal ECG in up to 30-50% of confirmed NSTEMI cases - a normal ECG does not exclude the diagnosis
Transient ST elevation may occur with coronary vasospasm (Prinzmetal's angina), resolving within minutes

(Harrison's Principles, p.1916; Tintinalli's Emergency Medicine)

3. Atrial Fibrillation (AF)

Pathophysiology: Chaotic, disorganized atrial electrical activity from multiple re-entrant wavelets. The AV node is bombarded with thousands of impulses, passing only some irregularly to the ventricles.

ECG Changes:

Absent P waves - replaced by irregular fibrillatory baseline (f-waves), most visible in V1 and II
Irregularly irregular RR intervals - the hallmark finding; no two RR intervals are the same
Normal narrow QRS complex (unless aberrant conduction or bundle branch block)
Ventricular rate typically 100-180 bpm if uncontrolled
Coarse AF: prominent, irregular f-waves >1mm (often in valvular/rheumatic AF)
Fine AF: very low amplitude f-waves, almost isoelectric baseline

(Tintinalli's Emergency Medicine; Rosen's Emergency Medicine)

ECG of Atrial Fibrillation:

Atrial fibrillation ECG showing irregularly irregular rhythm with absent P waves

4. Ventricular Tachycardia (VT)

Pathophysiology: Rapid ventricular rhythm (>100 bpm, usually 120-250 bpm) arising from ventricular myocardium or His-Purkinje system, bypassing normal conduction. Can be monomorphic (uniform QRS) or polymorphic (varying QRS morphology).

ECG Changes:

Wide QRS complexes (≥120-140 ms) - most important feature
Regular or slightly irregular rhythm at 120-250 bpm
AV dissociation - P waves march through at a different rate, independent of QRS
Fusion beats - hybrid QRS from simultaneous sinus and ventricular depolarisation
Capture beats - occasional narrow QRS when sinus impulse captures ventricles
Concordance in precordial leads - all QRS complexes pointing same direction (positive or negative) strongly suggests VT
Negative concordance (all precordial QRS negative) is highly specific for VT
No P wave precedes each QRS

(Tintinalli's Emergency Medicine; Goldman-Cecil Medicine)

12-lead ECG showing monomorphic Ventricular Tachycardia:

Ventricular tachycardia ECG - wide complex regular tachycardia

5. Complete (Third-Degree) AV Heart Block

Pathophysiology: Complete dissociation between atrial and ventricular electrical activity. No atrial impulses pass through the AV node to the ventricles. An escape rhythm takes over from either the AV junction (narrow QRS, 40-60 bpm) or from the ventricles (wide QRS, 20-40 bpm - the more dangerous pattern).

ECG Changes:

P waves and QRS complexes march independently - the defining feature
Atrial rate > ventricular rate always
Regular PP intervals and regular RR intervals but with no fixed relationship to each other
Escape QRS morphology:
- Junctional escape: narrow QRS (~40-60 bpm) - block above the Bundle of His
- Ventricular escape: wide bizarre QRS (~20-40 bpm) - block below the Bundle of His
PR interval varies randomly (no consistent PR relationship)

(Goldman-Cecil Medicine; Washington Manual of Medical Therapeutics)

6. Pericarditis (Acute)

Pathophysiology: Inflammation of the pericardium spreads to the underlying epicardium, producing diffuse superficial myocardial injury. This causes widespread ST-segment and PR-segment changes across multiple leads - distinguishing it from the regional pattern of MI.

ECG Changes (classic 4-stage progression):

Stage 1 (hours to days): Diffuse concave ("saddle-shaped") ST elevation in most leads (I, II, III, aVF, aVL, V2-V6) + PR depression in the same leads + PR elevation in aVR (reciprocal) + ST depression in aVR and V1
Stage 2 (days): ST and PR return toward baseline
Stage 3 (weeks): Diffuse T-wave inversions
Stage 4: ECG normalises

Key distinguishing features from STEMI:

ST elevation is diffuse (not regional/territorial)
ST elevation is concave upward (saddle-shaped), not convex
No reciprocal ST depression (except aVR and V1)
PR depression present
No Q-wave formation

(LITFL ECG Library; Harrison's Principles of Internal Medicine)

ECG of Acute Pericarditis (saddle-shaped ST elevation with PR depression):

Pericarditis ECG showing diffuse concave ST elevation and PR depression

7. Left Bundle Branch Block (LBBB)

Pathophysiology: Conduction block in the left bundle branch causes delayed, abnormal depolarisation of the left ventricle. The right ventricle activates first via the right bundle, and the left ventricle activates late via slow cell-to-cell conduction, producing a wide, abnormal QRS.

ECG Changes:

QRS duration ≥120 ms (complete LBBB)
Broad notched "M-shaped" R wave in lateral leads (I, aVL, V5, V6) - the "William" pattern
Deep "W-shaped" QS or rS in V1-V2 - the "Marrow" pattern
No septal Q waves in leads I, V5, V6 (first part of septal depolarisation is lost)
ST and T-wave changes discordant with QRS direction - ST depression and T-wave inversion in leads with tall R waves; ST elevation in leads with deep S waves (V1-V3)
Left axis deviation common
New LBBB with chest pain is treated as STEMI equivalent (Sgarbossa criteria used to detect MI in the presence of LBBB)

8. Wolff-Parkinson-White (WPW) Syndrome

Pathophysiology: An accessory pathway (Bundle of Kent) bypasses the AV node, pre-exciting part of the ventricle before the normal impulse arrives. This produces characteristic ECG findings at rest, and predisposes to dangerous tachyarrhythmias.

ECG Changes (at rest, in sinus rhythm):

Short PR interval (<120 ms) - bypass of AV nodal delay
Delta wave - slurred upstroke at the beginning of the QRS (initial slow conduction via accessory pathway)
Wide QRS (>120 ms) - combination of delta wave + normal conduction
Secondary ST-T changes discordant with QRS
Pseudo-infarct patterns (Q waves or ST changes that mimic MI)

During tachycardia:

Orthodromic AVRT (most common, ~70%): narrow QRS tachycardia (antegrade via AV node, retrograde via accessory pathway)
Antidromic AVRT (~5-10%): wide QRS tachycardia (antegrade via accessory pathway) - looks identical to VT
AF with WPW: Irregularly irregular, very rapid (>250 bpm), wide bizarre QRS - life-threatening pattern that can degenerate to VF

(Tintinalli's Emergency Medicine)

WPW ECG showing delta waves and pre-excitation triggering AVRT:

WPW syndrome ECG with delta wave and accessory pathway conduction

(Left portion shows sinus rhythm with delta waves and short PR; right shows the AVRT tachycardia)

9. Hypertensive Heart Disease / Left Ventricular Hypertrophy (LVH)

Pathophysiology: Chronic pressure overload from hypertension causes concentric hypertrophy of the left ventricular wall. The increased muscle mass generates larger electrical voltages on the ECG.

ECG Changes:

Increased QRS voltage - the core finding
- Sokolow-Lyon criteria: S in V1 + R in V5 or V6 ≥35 mm
- Cornell criteria: R in aVL + S in V3 >28 mm (men) or >20 mm (women)
Left axis deviation
LV "strain" pattern - ST depression and asymmetric T-wave inversion in lateral leads (I, aVL, V5, V6) - caused by abnormal repolarisation
Widened QRS (not as wide as BBB, but delayed)
Left atrial enlargement pattern: biphasic P wave in V1 with prominent negative component; P-wave duration >120 ms in lead II
Prolonged QRS-T angle

10. Ventricular Fibrillation (VF)

Pathophysiology: Completely chaotic, disorganized ventricular electrical activity with no coordinated contraction. The ventricles quiver without pumping blood - cardiac arrest. VF is the most common initial rhythm in sudden cardiac death.

ECG Changes:

No identifiable P waves, QRS complexes, or T waves - all organized waveforms are absent
Irregular, chaotic undulations of varying amplitude and frequency
Coarse VF: large irregular oscillations (>3 mm amplitude) - more likely to be shocked to sinus rhythm, typically earlier in the arrest
Fine VF: low amplitude oscillations (<3 mm) - more difficult to shock, often represents prolonged arrest or severe myocardial dysfunction; can mimic asystole
Heart rate: effectively unmeasurable; chaotic baseline
Always fatal without immediate defibrillation

Summary Table

Disease	Key ECG Findings
STEMI	ST elevation (convex), Q waves, reciprocal ST depression
NSTEMI/Unstable Angina	ST depression, T-wave inversion, may be normal
Atrial Fibrillation	Absent P waves, irregularly irregular RR, fibrillatory baseline
Ventricular Tachycardia	Wide QRS, AV dissociation, fusion/capture beats
Complete Heart Block	P waves and QRS march independently, escape rhythm
Acute Pericarditis	Diffuse concave ST elevation, PR depression, no Q waves
LBBB	Wide QRS ≥120 ms, M-shape V5/V6, W-shape V1, no septal Q waves
WPW Syndrome	Short PR, delta wave, wide QRS; tachyarrhythmias
LVH	High voltage, strain pattern (ST-T changes in lateral leads)
Ventricular Fibrillation	Chaotic baseline, no organized waveforms

Overview of killer ECG patterns (from LITFL ECG Library):

Killer ECG patterns overview showing ARVD, Brugada, pericardial effusion, WPW, and hypertrophic cardiomyopathy

Clinical note: ECG interpretation must always be correlated with clinical history, examination, and laboratory findings (troponins, BNP, electrolytes). A single normal ECG never excludes acute MI. Serial ECGs and continuous monitoring are often required. (Harrison's Principles of Internal Medicine 22E, 2025)

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