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10 common heart diseases ECG changes electrocardiogram findings clinical cardiology

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10 Common Heart Diseases with ECG Changes

1. ST-Elevation Myocardial Infarction (STEMI)

Overview: Acute transmural myocardial infarction caused by complete occlusion of a coronary artery, producing full-thickness myocardial necrosis.

ECG Changes:

Hyperacute T waves - tall, peaked T waves in the earliest minutes (before ST elevation develops)
ST-segment elevation ≥1 mm in two or more contiguous leads (≥2 mm in V1-V3)
Reciprocal ST depression in opposing leads (e.g., inferior MI with ST elevation in II, III, aVF causes reciprocal ST depression in I, aVL)
Pathological Q waves - develop within hours to days, indicating irreversible necrosis (width >40 ms, depth >25% of R wave)
T-wave inversions follow after the acute phase

Lead Localization:

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

Ischemia mechanism - current of injury diagram:

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

Harrison's Principles of Internal Medicine 22E - Current of injury: subendocardial ischemia (A) causes ST depression; transmural/epicardial ischemia (B) causes ST elevation

Acute and evolving STEMI ECG sequences:

Anterior STEMI (top row: acute; bottom row: evolving):

Anterior STEMI ECG - acute (top) and evolving (bottom) showing ST elevation in V2-V6 and Q wave formation

Harrison's 22E - Anterior ST-elevation/Q-wave infarction sequence. Top: acute phase with ST elevation in precordial leads. Bottom: evolving phase with Q wave formation and T-wave inversion.

Inferior STEMI (top row: acute; bottom row: evolving):

Inferior STEMI ECG - acute and evolving showing ST elevation in leads II, III, aVF

Harrison's 22E - Inferior ST-elevation/Q-wave infarction: ST elevation in II, III, aVF with evolving Q waves.

Wellens T-wave sign (severe LAD stenosis):

Precordial leads V1-V6 showing deep symmetric T-wave inversions in anterior wall ischemia

Harrison's 22E - Wellens T-wave sign: deep T-wave inversions in V1-V4, indicating severe LAD stenosis (high-grade anterior ischemia with or without infarction)

2. Atrial Fibrillation (AF)

Overview: The most common pathological tachyarrhythmia, arising from chaotic depolarization in the atria, often associated with hypertension, valvular disease, heart failure, and thyrotoxicosis.

ECG Changes:

Absent P waves - no discernible P waves; replaced by a fine, chaotic, irregular baseline (fibrillatory waves)
Irregularly irregular ventricular rhythm - the hallmark of AF; no two R-R intervals are equal
Narrow QRS complexes unless bundle branch block or pre-excitation (WPW) is present
Rate depends on AV nodal conduction; uncontrolled AF typically runs at 100-170 bpm

ECG Features of Atrial Fibrillation (from Tintinalli's Emergency Medicine):

Feature	Finding
P waves	Absent; flat or chaotic isoelectric baseline
QRS	Narrow unless pre-existing BBB or preexcitation
Rhythm	Irregularly irregular ventricular response

Atrial Flutter ECG (closely related):

Atrial flutter ECG showing regular narrow-complex tachycardia at 155 bpm, sawtooth flutter waves, and response to carotid sinus massage

Tintinalli's Emergency Medicine - Atrial flutter: (A) Regular narrow-complex tachycardia at 155 bpm. (B) Full 12-lead with sawtooth flutter waves best seen in II, III, aVF. (C) Carotid sinus massage unmasks flutter waves by slowing ventricular rate.

3. Complete (Third-Degree) Heart Block

Overview: Complete failure of AV conduction - no atrial impulses reach the ventricles. The atria and ventricles beat completely independently.

ECG Changes:

AV dissociation - P waves and QRS complexes march independently with no relationship
Atrial rate > ventricular rate - P waves occur at the sinus rate (~60-100 bpm); ventricles beat at their escape rate (~30-40 bpm)
Widened QRS complexes (>120 ms) if escape rhythm is junctional or ventricular origin; narrow QRS if junctional escape
Regular ventricular rate (escape rhythm is regular even though unrelated to P waves)
Bradycardia - ventricular rate typically 30-45 bpm

ECG Features of 3rd Degree AV Block (from Tintinalli's):

Feature	Finding
P-QRS association	None (completely dissociated)
Atrial rate	Greater than ventricular rate
QRS	Usually widened; occasionally narrow
Ventricular rate	Slow and regular

First-degree AV block and electrophysiology tracings:

First-degree AV block ECG and His bundle electrogram showing prolonged PR and AH intervals, and complete heart block with dissociated P waves and QRS

Braunwald's Heart Disease - Left: First-degree AV block with PR = 370 ms and His-bundle electrogram. Right: Complete AV block with dissociated atrial (A) and ventricular (V) electrograms.

4. Ventricular Tachycardia (VT)

Overview: Three or more consecutive ventricular ectopic beats at >100 bpm. May be monomorphic (uniform QRS morphology) or polymorphic (changing QRS). Most commonly seen in ischemic heart disease and structural cardiomyopathy.

ECG Changes:

Wide QRS complexes >120 ms with bizarre morphology
Rapid rate - typically 140-180 bpm (range 120-300 bpm)
AV dissociation - P waves march through independently (when visible, diagnostic for VT)
Fusion beats and capture beats - pathognomonic for VT
Concordance - all precordial leads deflect in same direction
No P waves associated with QRS

ECG comparison - ventricular vs supraventricular wide complex tachycardias:

Grid of ECGs comparing ventricular source (A-B) vs supraventricular source (C-J) wide complex tachycardias

Tintinalli's Emergency Medicine - Wide complex tachycardias: (A-B) Ventricular source. (C-J) Supraventricular sources with aberrant conduction. Note differences in morphology and regularity.

Monomorphic VT (three examples at different rates):

Three examples of monomorphic VT at rates 270, 220, and 180 bpm - wide, regular QRS complexes

Tintinalli's Emergency Medicine - Monomorphic VT: (A) 270 bpm, (B) 220 bpm, (C) 180 bpm. Wide, regular QRS complexes without associated P waves.

5. Ventricular Fibrillation (VF)

Overview: Disorganized, chaotic ventricular depolarization with no effective mechanical contraction. Results in immediate cardiac arrest. Most common cause of sudden cardiac death, usually from severe ischemic heart disease.

ECG Changes:

Completely disorganized waveforms - no discernible P waves, QRS complexes, or T waves
Irregular, undulating pattern - chaotic, rapid, irregular electrical activity
Variable amplitude - may be coarse (large amplitude), intermediate, or fine (low amplitude)
Fine VF can mimic asystole at low gain - always check gain before diagnosing asystole
Coarse VF may superficially resemble very rapid VT

Three examples of VF (fine, coarse, and intermediate):

Three examples of ventricular fibrillation: A-fine amplitude, B-coarse amplitude, C-coarse mimicking VT

Tintinalli's Emergency Medicine - Ventricular fibrillation: (A) Fine amplitude - nearly flat, (B) Coarse amplitude, (C) Coarse amplitude that can mimic VT. Treatment: immediate defibrillation + CPR.

6. Acute Pericarditis

Overview: Inflammation of the pericardium, most commonly viral/idiopathic. ECG changes result from superficial myocardial involvement (the pericardium itself is electrically silent). ECG evolves through 4 classic stages.

ECG Changes (4 stages):

Stage	Timing	ECG Finding
Stage 1	Days 1-2	Diffuse ST elevation (concave up) + diffuse PR depression; PR elevation in aVR
Stage 2	Days 3-7	ST and PR normalize
Stage 3	Weeks	Diffuse T-wave inversions ± ST depression
Stage 4	Weeks-months	Full normalization

Key distinguishing features from STEMI:

ST elevation is diffuse (not territory-specific) and concave (not convex)
PR depression in multiple leads (opposite to STEMI where PR depression is less common)
No reciprocal ST depression (except aVR which shows ST depression and PR elevation)
No Q waves

Acute pericarditis 12-lead ECG:

12-lead ECG showing diffuse concave ST elevation with PR segment depression in all leads except aVR, characteristic of acute pericarditis Stage 1

Fuster & Hurst's The Heart 15th Ed. - Stage 1 acute pericarditis: diffuse ST elevation with PR segment depression in a non-territory-specific distribution. Note ST depression + PR elevation in aVR (reciprocal).

7. Wolff-Parkinson-White (WPW) Syndrome

Overview: A ventricular pre-excitation syndrome caused by an accessory conduction pathway (Bundle of Kent) that bypasses the AV node. Results in early activation of part of the ventricle. Associated with supraventricular tachycardias and, rarely, sudden death via AF with rapid conduction.

ECG Changes (classic triad during sinus rhythm):

Short PR interval (<120 ms) - atrial impulse reaches ventricle faster via accessory pathway, bypassing AV nodal delay
Delta wave - slurred initial upstroke of the QRS, representing pre-excitation of ventricular myocardium
Wide QRS (>120 ms) - fused complex from simultaneous accessory pathway + normal AV node conduction
Secondary ST-T changes - discordant T waves opposite to major QRS deflection
Pseudo-Q waves can mimic myocardial infarction

WPW ECG:

12-lead ECG of Wolff-Parkinson-White syndrome showing short PR interval and delta waves (slurred QRS upstroke)

Tintinalli's Emergency Medicine - WPW syndrome: short PR interval and widened QRS with delta waves (slurred upstroke) visible across multiple leads.

8. Brugada Syndrome

Overview: A heritable arrhythmia syndrome (often SCN5A mutation) characterized by a distinctive ECG pattern and risk of ventricular arrhythmias and sudden cardiac death, particularly during rest, sleep, or febrile illness. Predominantly affects males. The arrhythmogenic substrate involves the right ventricular outflow tract (RVOT) epicardium.

ECG Changes:

Type 1 (diagnostic): Coved ST-segment elevation ≥2 mm followed by a negative T wave in V1 or V2 (right precordial leads) - this is the only diagnostic pattern
Type 2: Saddle-back pattern with ST elevation ≥0.5 mm and positive or biphasic T wave in V1/V2 (cannot diagnose Brugada alone)
Right bundle branch block morphology (rSR' in V1) is often associated
Pattern may be intermittent or unmasked by fever, sodium channel blockers, or vagotonia
The rest of the ECG may be completely normal between episodes

9. Hypertrophic Cardiomyopathy (HCM)

Overview: A genetic heart muscle disease (sarcomere protein mutations) causing asymmetric left ventricular hypertrophy, most commonly involving the interventricular septum. Leading cause of sudden cardiac death in young athletes.

ECG Changes:

Left ventricular hypertrophy (LVH) voltage criteria - tall R waves in I, aVL, V5, V6 and/or deep S waves in V1-V3 (Sokolow-Lyon: S in V1 + R in V5/V6 >35 mm)
LV strain pattern - ST depression + T-wave inversions in lateral leads (I, aVL, V4-V6)
Deep, narrow Q waves in lateral and inferior leads - caused by septal hypertrophy (not infarction)
Poor R-wave progression in precordial leads
Left axis deviation
Nonspecific ST-T wave changes - the most common finding
P-wave abnormalities suggesting left atrial enlargement

10. Long QT Syndrome (LQTS)

Overview: A group of inherited (and acquired) channelopathies that prolong ventricular repolarization, increasing risk of polymorphic VT (torsades de pointes) and sudden cardiac death. Congenital forms involve mutations in potassium (KCNQ1, KCNH2) or sodium (SCN5A) channel genes.

ECG Changes:

Prolonged QTc interval - the corrected QT is typically >440-460 ms (QTc = QT / √RR interval in seconds; Bazett's formula)
Torsades de pointes - the characteristic arrhythmia: polymorphic VT with QRS complexes that rotate around the isoelectric baseline ("twisting of the points"), associated with prolonged QT
T-wave abnormalities - vary by genetic subtype: broad-based T waves (LQT1), notched/bifid T waves (LQT2), small T waves with prominent U waves (LQT3)
Prominent U waves - may be mistaken for part of the T wave, artificially prolonging measured QT

Summary Reference Table

#	Disease	Key ECG Finding	Rate/Rhythm	QRS Width
1	STEMI	ST elevation + Q waves	Variable	Normal
2	Atrial Fibrillation	No P waves, irregularly irregular	100-170 bpm	Normal
3	Complete Heart Block	P-QRS dissociation, slow rate	30-45 bpm	Wide (usually)
4	Ventricular Tachycardia	Wide QRS, AV dissociation	140-300 bpm	Wide (>120 ms)
5	Ventricular Fibrillation	Chaotic, no QRS	No output	No discernible QRS
6	Acute Pericarditis	Diffuse ST elevation, PR depression	Normal sinus	Normal
7	WPW	Short PR, delta wave, wide QRS	Normal (or SVT)	Wide
8	Brugada Syndrome	Coved ST elevation V1-V2	Normal (between events)	Normal/RBBB
9	HCM	LVH voltage + strain, deep Q waves	Normal sinus	Normal
10	Long QT Syndrome	QTc >440-460 ms, torsades de pointes	Normal / polymorphic VT	Normal

Clinical note: ECG findings must always be interpreted alongside the full clinical picture. A single normal ECG never excludes acute ischemia or arrhythmia syndromes. Serial ECGs and clinical context remain essential.Your credits are exhausted. Your daily credits reset tomorrow, or you can purchase a top-up for more.

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