10 ecg common disease with changes and explnation and graph

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10 common ECG patterns diseases changes explained STEMI atrial fibrillation SVT VT hyperkalemia

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10 Common Diseases with ECG Changes - Explained with Graphs

Below is a complete guide to the 10 most important ECG patterns you need to recognize, sourced from Harrison's, Braunwald's Heart Disease, Goldman-Cecil Medicine, Rosen's Emergency Medicine, and Guyton & Hall Physiology.

1. ST-Elevation Myocardial Infarction (STEMI)

ECG Changes:

ST elevation ≥1 mm in two or more contiguous leads (the hallmark finding)
Reciprocal ST depression in opposite leads
Hyperacute T waves (tall, broad, symmetric) - earliest change
Q waves develop within hours (pathological Q = >1 mm wide or >25% of R height)
T wave inversion follows in the evolving phase

Lead Localization:

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

Explanation: Complete occlusion of a coronary artery causes transmural ischemia. The injured epicardial myocardium generates a current of injury that shifts the ST segment upward. As cells die, the Q wave appears because dead tissue produces no electrical signal - the vector "falls through" to the opposite wall.

Goldman-Cecil Medicine: "If the involved coronary artery is completely occluded by fresh thrombus, the patient's ECG shows ST segment elevation. If it is partially occluded, the ECG does not show ST elevation." - Goldman-Cecil Medicine

2. Atrial Fibrillation (AF)

Atrial Fibrillation ECG - Lead II showing irregularly irregular rhythm with absent P waves

Atrial Fibrillation (Lead II) - Note the chaotic baseline and irregularly irregular QRS complexes with absent P waves. From Guyton & Hall Physiology.

ECG Changes:

No identifiable P waves - replaced by chaotic fibrillatory (f) waves at 350-600/min
Irregularly irregular RR intervals (this is pathognomonic - no two RR intervals are the same)
Narrow QRS complex (unless aberrant conduction or bundle branch block)
Ventricular rate typically 100-180/min if uncontrolled

Explanation: Multiple re-entrant circuits fire chaotically throughout both atria. The AV node acts as a gatekeeper, conducting impulses irregularly to the ventricles. Because no organized atrial depolarization occurs, no P wave forms. The result is an irregularly irregular rhythm - the most reliable feature.

3. Acute Pericarditis

Acute Pericarditis ECG - 12-lead showing diffuse ST elevation and PR depression

Acute Pericarditis - 12-lead ECG showing diffuse ST elevation across multiple leads (note especially V2-V3) and PR-segment depression. From Fuster & Hurst's The Heart.

ECG Changes (4 Stages):

Stage 1: Diffuse concave ("saddle-shaped") ST elevation in ALL leads EXCEPT aVR and V1 + PR depression (highly specific for pericarditis)
Stage 2: ST and PR segments normalize
Stage 3: Diffuse T wave inversion
Stage 4: ECG returns to normal

Key Distinguishing Features from STEMI:

ST elevation is diffuse (not localized to a coronary territory)
ST morphology is concave upward (saddle-shaped), not convex
PR segment depression present in most leads
No reciprocal changes (except aVR which shows ST depression)
No pathological Q waves develop

Explanation: Inflammation of the pericardium extends to the superficial myocardium (myopericarditis), injuring the epicardial layer diffusely. This causes widespread current of injury (ST elevation) without the coronary territory pattern of MI. PR depression reflects atrial epicardial involvement.

Braunwald's Heart Disease: "Typical ECG evolution follows four stages: (1) PR depression and/or diffuse ST segment elevation, (2) normalization of ST segment, (3) T wave inversion with or without ST segment depression, and (4) normalization."

4. Hyperkalemia

ECG Changes (progressive with rising K+):

Serum K+	ECG Finding
5.5-6.5 mEq/L	Tall, peaked, symmetric T waves + shortened QT
6.5-7.5 mEq/L	PR prolongation, P wave flattening/disappearance
7.0-8.0 mEq/L	Wide QRS (>0.12 sec), sine wave pattern
>8.0 mEq/L	Ventricular fibrillation or asystole

Explanation: High extracellular K+ depolarizes the resting membrane potential, slowing phase 0 depolarization (fast Na+ channels). This slows conduction through all cardiac tissue: first the atria lose P waves, then the His-Purkinje system widens the QRS, and the T wave becomes peaked because repolarization is accelerated. The sine wave pattern just before cardiac arrest represents merged P-QRS-T complexes.

Harrison's Principles (2025): "Classically, the ECG manifestations in hyperkalemia progress from tall peaked T waves (5.5-6.5 mM), to a loss of P waves (6.5-7.5 mM), to a widened QRS complex (7.0-8.0 mM), and ultimately..." to fatal arrhythmia.

5. Wolff-Parkinson-White (WPW) Syndrome

WPW Syndrome 12-lead ECG showing short PR interval and delta waves

WPW Syndrome - 12-lead ECG. Note the short PR interval (<0.12 s) and the slurred upstroke of the QRS (delta waves), visible across multiple leads. From Tintinalli's Emergency Medicine.

ECG Triad During Sinus Rhythm:

Short PR interval (<0.12 sec) - because the accessory pathway bypasses the AV node delay
Delta wave - slurred, slow upstroke at the beginning of the QRS (pre-excitation of ventricle via accessory pathway)
Wide QRS (>0.12 sec) - due to abnormal ventricular activation combining delta wave + normal AV conduction

During Atrial Fibrillation in WPW - DANGER:

No P waves, wide bizarre QRS complexes with varying morphology
Ventricular rate usually >200/min (life-threatening)
Do NOT give AV nodal blockers (digoxin, verapamil, adenosine) - they block normal conduction and force all impulses down the accessory pathway

Explanation: An accessory bypass tract (Bundle of Kent) connects atria directly to ventricles, bypassing the AV node. Impulses arrive at the ventricles early (pre-excitation), creating the delta wave. This pathway can also conduct retrogradely, creating a re-entry circuit for SVT.

6. Left Bundle Branch Block (LBBB)

ECG Changes:

Wide QRS (≥0.12 sec / 3 small squares)
Broad, notched, monophasic R wave in lateral leads (I, aVL, V5-V6) - the classic "M" or "W" shape
Deep S wave or rS pattern in V1 (broad R then deep S, or just deep QS)
ST and T changes discordant (opposite to QRS direction) - this is normal in LBBB
Leads I, V5-V6: No Q waves (septal q waves are lost)

Explanation: Block of the left bundle branch forces the left ventricle to depolarize late, via cell-to-cell conduction from the right side. This slow, abnormal spread widens the QRS and changes its morphology. ST-T changes are secondary (discordant to QRS) and do NOT necessarily indicate ischemia.

Clinical Pearl: New LBBB in the context of chest pain may be a STEMI equivalent and requires urgent management.

7. Ventricular Tachycardia (VT)

ECG Changes:

Wide QRS tachycardia (QRS ≥0.12 sec, rate 100-250/min)
AV dissociation (P waves and QRS complexes marching independently) - diagnostic of VT when present
Fusion beats and capture beats (hallmarks of AV dissociation)
Concordance in precordial leads (all positive or all negative - no transition)
Northwest axis (extreme axis deviation, "no man's land")
QRS morphology does not match typical LBBB or RBBB pattern

Key Rule (Brugada Criteria): If any doubt, treat wide complex tachycardia as VT until proven otherwise. VT is far more common than SVT with aberrancy in adults with structural heart disease.

Explanation: A ventricular focus fires rapidly, driving the heart. Because impulses travel via slow myocardium rather than the His-Purkinje system, the QRS is wide and bizarre. AV dissociation occurs because the SA node fires independently from the VT focus, and P waves are buried or visible between wide QRS complexes.

8. Pulmonary Embolism (PE)

ECG Changes:

Sinus tachycardia - most common finding (seen in ~44% of PE)
S1Q3T3 pattern - S wave in lead I, Q wave AND T-wave inversion in lead III (classic but present in only ~20%)
Right bundle branch block (new RBBB) - due to acute right heart strain
T wave inversions in V1-V4 (right heart strain pattern)
Right axis deviation
P pulmonale (tall P wave in II) from right atrial enlargement
Atrial fibrillation (in ~10%)

Explanation: Massive PE causes acute obstruction of the pulmonary vasculature, leading to acute right ventricular pressure overload. The dilated, strained RV shifts the heart's electrical axis rightward. The S1Q3T3 pattern reflects this acute cor pulmonale - the QRS axis rotates clockwise when the RV enlarges acutely.

9. Complete Heart Block (Third-Degree AV Block)

ECG Changes:

P waves and QRS complexes march independently (AV dissociation)
PP intervals regular, RR intervals regular, but no fixed relationship between them
PR interval varies with each beat (key finding)
Escape rhythm QRS: narrow if junctional escape (rate 40-60/min), wide if ventricular escape (rate 20-40/min)
Bradycardia (ventricular rate 20-60/min)

Explanation: No impulse from the atria can reach the ventricles. The AV node or bundle of His is completely blocked. A subsidiary pacemaker below the block takes over - if junctional, the QRS is narrow; if below the bifurcation of the bundle of His, the QRS is wide and the rate is very slow (30-40/min). This is a medical emergency requiring pacing.

10. Hypokalemia

ECG Changes (progressive with falling K+):

Serum K+	ECG Finding
3.0-3.5 mEq/L	Flattened T waves, U waves become prominent
2.5-3.0 mEq/L	T-U fusion, apparent QT prolongation (actually QU)
<2.5 mEq/L	ST depression, very prominent U waves (>T wave height)
Severe	Torsades de pointes, ventricular fibrillation

The U Wave: Positive deflection after the T wave, best seen in V2-V3. Normally small; in hypokalemia it becomes >1 mm or taller than the T wave. It represents delayed repolarization of the Purkinje fibers or papillary muscles.

Explanation: Low K+ hyperpolarizes the resting membrane potential, prolonging action potential duration and the refractory period. This delays repolarization, causing the characteristic T wave flattening and U wave prominence. The prolonged QTU interval predisposes to early afterdepolarizations and torsades de pointes, especially dangerous with digoxin use.

Quick Reference Summary Table

#	Disease	Key ECG Feature	Rate	Rhythm
1	STEMI	ST elevation + Q waves in territory	Normal/fast	Regular
2	Atrial Fibrillation	No P waves, irregularly irregular	Variable	Irregular
3	Acute Pericarditis	Diffuse ST elevation + PR depression	Normal	Regular
4	Hyperkalemia	Peaked T → wide QRS → sine wave	Slow/normal	Can vary
5	WPW	Short PR + delta wave + wide QRS	Normal	Regular (sinus)
6	LBBB	Wide QRS, M-shape V5-V6, no Q in lateral	Normal	Regular
7	Ventricular Tachycardia	Wide QRS tachycardia + AV dissociation	Fast >100	Regular
8	Pulmonary Embolism	S1Q3T3, sinus tachycardia, RBBB	Fast	Regular
9	Complete Heart Block	AV dissociation, fixed slow escape rate	Slow	P/QRS independent
10	Hypokalemia	Flat T, prominent U waves, ST depression	Normal	Regular (risk of VF)

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