explain me 10 common heart diseases with ecg changes and ecg images of those diseases

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common heart diseases ECG changes electrocardiogram findings with images

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ECG images myocardial infarction atrial fibrillation heart block LVH site:litfl.com OR site:ecgwaves.com

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ECG images pericarditis STEMI ventricular tachycardia heart block Brugada WPW ecgwaves litfl

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STEMI inferior ECG image litfl.com OR ecgwaves.com Q wave ST elevation

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10 Common Heart Diseases: ECG Changes & Images

1. ST-Elevation Myocardial Infarction (STEMI)

What it is: Complete occlusion of a coronary artery causing transmural myocardial necrosis.

ECG Changes:

Hyperacute phase: Tall, peaked ("hyperacute") T waves - the earliest sign
Acute phase: ST elevation ≥1 mm in ≥2 contiguous limb leads, or ≥2 mm in precordial leads, with a convex (tombstone) or straight appearance
Evolving: Development of pathological Q waves (>40 ms wide, >25% of R wave height) - indicate irreversible necrosis
Reciprocal ST depression in opposite leads (e.g., inferior STEMI in II, III, aVF causes reciprocal depression in I, aVL)
Late: T-wave inversion, persistent Q waves

Localisation:

Territory	Leads with ST elevation
Inferior	II, III, aVF
Anterior	V1-V4
Lateral	I, aVL, V5-V6
Posterior	R>S in V1-V2, ST depression V1-V3

ECG - Inferior STEMI (note ST elevation in II, III, aVF with pathological Q waves and reciprocal change in aVL):

Inferior STEMI 12-lead ECG showing ST elevation in inferior leads II, III, aVF with Q waves

2. Atrial Fibrillation (AF)

What it is: Chaotic, disorganised atrial electrical activity with multiple simultaneous re-entrant wavelets, causing irregular ventricular response. Associated with hypertension, valvular disease, heart failure, thyrotoxicosis, and alcohol ("holiday heart").

ECG Changes (from Tintinalli's Emergency Medicine):

Absent P waves - replaced by a chaotic, irregular fibrillatory baseline (best seen in V1)
Irregularly irregular ventricular rhythm - the hallmark finding
Atrial rate >600 bpm (not visible as distinct waves)
Ventricular rate typically 120-170 bpm when AV node is unaffected
Narrow QRS complexes (unless aberrant conduction or bundle branch block)

ECG - Three examples of Atrial Fibrillation (A: rapid ventricular response, B: controlled rate, C: slow response):

Three ECG strips of atrial fibrillation showing absent P waves and irregularly irregular rhythm

Source: Tintinalli's Emergency Medicine

3. Complete (Third-Degree) AV Heart Block

What it is: Complete failure of conduction between the atria and ventricles. The atria and ventricles beat independently, with the ventricles under control of a slow junctional or ventricular escape pacemaker.

ECG Changes (from Goldman-Cecil Medicine and Harrison's Principles):

P waves and QRS complexes are completely dissociated - P waves "march through" at their own rate with no relationship to QRS
Atrial rate is faster than ventricular rate (key distinguishing feature)
Ventricular rate typically 20-40 bpm (ventricular escape) or 40-60 bpm (junctional escape)
QRS may be narrow (junctional escape) or wide/bizarre (ventricular escape)
Causes: acute inferior MI, infiltrative disease (sarcoidosis, amyloid), Lyme disease, drugs (digoxin, beta-blockers)

ECG - Idioventricular escape rhythm (slow, wide complex beats at ~30 bpm - seen in complete heart block with ventricular escape):

Idioventricular escape rhythm ECG strip showing slow wide complex beats at approximately 30 beats per minute

Source: Tintinalli's Emergency Medicine

4. Left Ventricular Hypertrophy (LVH)

What it is: Thickening of the left ventricular wall, commonly due to hypertension, aortic stenosis, or hypertrophic cardiomyopathy.

ECG Changes:

Increased QRS voltage (Sokolow-Lyon criterion: S in V1 + R in V5 or V6 ≥35 mm; or R in aVL ≥11 mm)
Left axis deviation
Strain pattern: ST depression and T-wave inversion in I, aVL, V5-V6 (lateral leads)
Left atrial enlargement (P mitrale): Biphasic P wave in V1, prolonged P wave duration >120 ms in II
Widened QRS (but usually <120 ms unless combined with LBBB)

As noted in Braunwald's Heart Disease: LV hypertrophy and left atrial enlargement on ECG may indicate left heart disease rather than pulmonary arterial hypertension as the cause of elevated pressures.

5. Pericarditis

What it is: Inflammation of the pericardial sac, most often viral in origin. Produces characteristic pleuritic chest pain and serial ECG changes that evolve through four stages.

ECG Changes (4 classical stages):

Stage	Timing	ECG Findings
I	Hours-days	Diffuse concave ("saddle-shaped") ST elevation in multiple leads (I, II, aVL, aVF, V2-V6); PR depression (virtually all leads except aVR which shows PR elevation)
II	Days	ST returns to baseline; PR depression persists
III	Weeks	Diffuse T-wave inversion
IV	Weeks-months	ECG returns to normal

Key distinguishing features from STEMI:

ST elevation is diffuse (not territory-based) and concave up (not convex)
PR depression is a hallmark not seen in MI
No reciprocal changes (except aVR)
No pathological Q waves

ECG - Pericarditis (note concave ST elevation in multiple leads with PR depression; compare with benign early repolarisation):

ECG of pericarditis showing diffuse concave ST elevation and PR depression compared to benign early repolarisation

Source: LITFL ECG Library

6. Ventricular Tachycardia (VT)

What it is: A potentially life-threatening arrhythmia originating below the bundle of His, most commonly in the setting of ischaemic heart disease, dilated cardiomyopathy, or electrolyte imbalance.

ECG Changes (from Goldman-Cecil Medicine):

Wide QRS complex tachycardia - QRS duration >120 ms (often >140 ms) at rate >100 bpm
AV dissociation - P waves march independently of QRS complexes (pathognomonic of VT when visible)
Fusion beats - P wave partially captures the ventricle, producing a QRS morphology intermediate between sinus and VT beats (pathognomonic)
Capture beats - occasional narrow QRS when a P wave fully conducts through to the ventricle
Concordance - all precordial leads pointing in the same direction (positive or negative)
Northwest axis (extreme left axis deviation)

The combination of fusion beats or AV dissociation during a wide-QRS complex tachycardia confirms VT and distinguishes it from SVT with aberrancy (Goldman-Cecil Medicine).

7. Wolff-Parkinson-White (WPW) Syndrome

What it is: An accessory pathway (Bundle of Kent) bypasses the AV node, causing ventricular pre-excitation and risk of re-entrant tachycardia. Can be life-threatening if AF develops with rapid conduction down the accessory pathway.

ECG Changes:

Short PR interval (<120 ms) - because conduction bypasses AV nodal delay
Delta wave - slurred upstroke at the beginning of the QRS complex (initial pre-excitation)
Wide QRS (>120 ms) - due to fusion of pre-excited and normally conducted impulses
Secondary ST-T changes opposite to the delta wave direction
In AF with WPW: extremely rapid, irregular wide complex tachycardia (>250 bpm) - a medical emergency

The LITFL Killer ECG infographic below illustrates the delta wave and short PR interval characteristic of WPW:

Killer ECG patterns infographic showing WPW with delta wave and short PR, Brugada syndrome with coved ST elevation, LVH with dagger Q waves, and other patterns

Source: LITFL ECG Library - Killer ECG Patterns

8. Brugada Syndrome

What it is: An inherited sodium channelopathy causing sudden cardiac death from ventricular fibrillation in structurally normal hearts. More common in Asian males.

ECG Changes (Type 1 - diagnostic):

Coved-type ST elevation ≥2 mm in right precordial leads V1-V3
Negative T wave (inverted) in V1-V3 following the coved ST elevation
The pattern resembles a "shark fin" or right bundle branch block morphology
Type 2 and 3 have saddle-shaped ST elevation and are not diagnostic without clinical criteria
The Type 1 pattern can be dynamic - triggered or unmasked by fever, sodium channel blockers, or vagal tone

ECG pattern - see the Brugada entry in the LITFL infographic above (top right): coved ST elevation >2 mm in V1-3 with negative T wave.

9. Hypertrophic Cardiomyopathy (HCM)

What it is: Genetic sarcomere mutation causing asymmetric septal hypertrophy, dynamic LV outflow tract obstruction, and high risk of sudden cardiac death, especially in young athletes.

ECG Changes:

Voltage criteria for LVH (deep S in V1-V2, tall R in V5-V6)
"Dagger" Q waves - deep, narrow Q waves in lateral (I, aVL, V5-V6) and/or inferior leads - due to septal hypertrophy (not ischaemia)
Left axis deviation
T-wave inversion - widespread, often dramatic in lateral leads
Left atrial enlargement - broad, bifid P wave
Giant T-wave inversion (particularly deep in V3-V5) - a hallmark in the apical variant (Yamaguchi syndrome)
Atrial fibrillation in 20-25% of patients

ECG pattern - see the HCM entry in the LITFL infographic above (bottom right): LVH voltage + dagger Q waves.

10. Pulmonary Embolism (PE) / Right Heart Strain

What it is: Acute obstruction of pulmonary circulation causing acute pressure overload on the right ventricle, producing characteristic but variable ECG changes.

ECG Changes:

Sinus tachycardia - the most common and sensitive finding (in >40% of cases)
S1Q3T3 pattern - S wave in Lead I, Q wave in Lead III, T-wave inversion in Lead III (present in ~20%, not specific)
Right bundle branch block (RBBB) or incomplete RBBB
T-wave inversion in V1-V4 - right ventricular strain pattern
Right axis deviation
P pulmonale - tall, peaked P waves in inferior leads (>2.5 mm) indicating right atrial overload
As noted in Braunwald's Heart Disease: RV strain pattern (RV hypertrophy with ST depression in V1-V3) may be evident in advanced disease

ECG - Athlete's heart 12-lead ECG from Goldman-Cecil Medicine (illustrating normal variant voltage changes, early repolarisation, and variable P wave morphology at bradycardia - for context of normal vs pathological voltage):

12-lead ECG from Goldman-Cecil Medicine showing normal cardiac electrical activity with voltage and repolarisation patterns

Source: Goldman-Cecil Medicine - Figure 42-7 Athlete's Heart

Quick Reference Summary Table

Disease	Key ECG Finding	Leads Affected
STEMI	Convex ST elevation, Q waves, hyperacute T	Territory-specific
Atrial Fibrillation	Absent P waves, irregularly irregular RR	All leads
Complete Heart Block	P-QRS dissociation, slow escape rhythm	All leads
LVH	High voltage, strain pattern, left axis	V1/V5-V6, I, aVL
Pericarditis	Diffuse concave ST elevation, PR depression	Diffuse (not V1, aVR)
Ventricular Tachycardia	Wide QRS tachycardia, AV dissociation	All leads
WPW	Short PR, delta wave, wide QRS	All leads
Brugada	Coved ST elevation, negative T wave	V1-V3
HCM	Dagger Q waves, massive LVH voltage	Lateral/inferior
Pulmonary Embolism	Sinus tachycardia, S1Q3T3, RBBB, RV strain	I, III, V1-V4

Sources:

Tintinalli's Emergency Medicine: A Comprehensive Study Guide - ECG sections on arrhythmias
Goldman-Cecil Medicine (International Edition) - ECG interpretation chapters
Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine - Pulmonary hypertension and arrhythmia chapters
Harrison's Principles of Internal Medicine 22E - Atrial fibrillation chapter
LITFL ECG Library - Inferior STEMI, Pericarditis, Killer ECG patterns

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