Explain me 10 common heart diseases with ECG changes and ECG images of those diseases

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Here is a comprehensive overview of 10 common heart diseases with their ECG changes and images, drawn from Harrison's Principles of Internal Medicine 22E, Ganong's Review of Medical Physiology, Tintinalli's Emergency Medicine, and Guyton and Hall Textbook of Medical Physiology.

10 Common Heart Diseases: ECG Changes and Images

1. ST-Elevation Myocardial Infarction (STEMI)

Mechanism: Acute transmural ischemia due to complete coronary artery occlusion. Ischemia lowers resting membrane potential and shortens action potential duration, generating a "current of injury."

ECG Changes (sequential evolution):

Hyperacute phase (minutes): Tall, broad, positive "hyperacute" T waves over the ischemic zone
Acute phase (hours): ST-segment elevation in leads overlying the infarct zone; reciprocal ST depression in opposite leads
Evolving phase (hours-days): T-wave inversions develop; pathological Q waves appear (>40 ms wide, >25% R-wave depth)
Chronic phase (weeks-months): Persistent Q waves; ST may normalize

Localization by leads:

Territory	Culprit artery	Leads with ST elevation
Anterior	LAD	V1-V4, I, aVL
Inferior	RCA	II, III, aVF
Lateral	LCx	I, aVL, V5-V6
Posterior	RCA/LCx	Reciprocal ST depression V1-V3
Right ventricle	RCA	V3R, V4R

Current of injury diagram - subendocardial vs transmural ischemia:

Current of injury diagram: subendocardial ischemia causes ST depression (A), transmural injury causes ST elevation (B)

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

Anterior STEMI - Wellens pattern (deep T inversions V1-V4):

Anterior wall ischemia - Wellens T-wave sign: deep symmetric T-wave inversions in V1-V6

Wellens T-wave sign: deep T inversions in V1-V6, indicating high-grade LAD stenosis (Harrison's Principles of Internal Medicine 22E)

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

Mechanism: Subtotal occlusion or subendocardial ischemia. The ST injury vector shifts toward the subendocardium and ventricular cavity.

ECG Changes:

ST-segment depression (horizontal or downsloping) in anterior/lateral leads
T-wave inversions - may be deep and symmetric
No pathological Q waves (by definition, no transmural necrosis)
ST elevation in aVR with widespread ST depression suggests left main or proximal LAD disease
The ECG may be normal in up to 6% of confirmed NSTEMIs

3. Atrial Fibrillation (AF)

Mechanism: Multiple re-entrant wavelets circulating chaotically through atrial myocardium. Atrial rate >600 bpm; AV node filters to produce an irregular ventricular response.

ECG Changes (classic hallmarks):

Absence of distinct P waves - replaced by irregular fibrillatory baseline (most visible in V1)
Irregularly irregular RR intervals (no two RR intervals are the same)
QRS complexes are usually narrow (unless aberrant conduction or bundle branch block is present)
Ventricular rate typically 120-170 bpm if AV node is unaffected
Very rapid rate (>200 bpm) suggests an accessory pathway (WPW + AF)

ECG - Atrial Fibrillation (Guyton and Hall):

Atrial fibrillation ECG - lead II: no P waves, irregularly irregular QRS complexes

Figure 13.20 - Atrial fibrillation (lead II): ventricular QRS and T waves with absent P waves (Guyton and Hall Textbook of Medical Physiology)

Three real-patient AF tracings:

Three examples of atrial fibrillation with irregular ventricular response - leads A, B, C

Three clinical examples of atrial fibrillation (lead II) showing absent P waves and irregular RR intervals (Tintinalli's Emergency Medicine)

4. Heart Block (AV Conduction Disease)

Mechanism: Impaired conduction through the AV node or His-Purkinje system, due to ischemia, fibrosis, infiltration, or drugs.

ECG Changes by degree:

First-degree AV Block:

PR interval prolonged > 200 ms (0.20 s), but every P wave conducts
QRS is normal; rhythm is regular

First-degree heart block ECG: PR interval = 0.38 s

First-degree heart block: PR interval = 0.38 s (Ganong's Review of Medical Physiology)

Second-degree AV Block - Mobitz I (Wenckebach):

Progressive PR lengthening with each beat until one P wave is not conducted (dropped QRS)
The cycle then resets

Second-degree heart block - Wenckebach phenomenon: P waves labeled, progressive PR lengthening then dropped beat

Wenckebach (Mobitz I) second-degree block: progressive PR prolongation until dropped beat (Ganong's Review of Medical Physiology)

Third-degree (Complete) AV Block:

P waves and QRS complexes beat independently - AV dissociation
P-P intervals regular; RR intervals regular; but PR has no fixed relationship
Escape QRS rate: 40-60 bpm (junctional escape) or 20-40 bpm (ventricular escape, wide QRS)

Complete heart block: P waves labeled, independent QRS complexes labeled - atrial rate 107, ventricular rate 43

Complete heart block: atrial rate 107, ventricular rate 43 - fully independent rhythms (Ganong's Review of Medical Physiology)

5. Wolff-Parkinson-White (WPW) Syndrome

Mechanism: Accessory pathway (Bundle of Kent) bypasses the AV node, causing ventricular preexcitation. Dual conduction via the accessory pathway and normal AV node sets up re-entrant arrhythmias.

ECG Changes (in sinus rhythm):

Short PR interval (< 120 ms) - bypass of AV node delay
Delta wave - slurred upstroke at the beginning of QRS (cell-to-cell conduction via accessory pathway)
Widened QRS complex (>120 ms) due to fusion of normal and accessory pathway depolarization
Pseudo-infarct pattern - delta waves can cause negative deflections mimicking Q waves
ST-T changes secondary to abnormal depolarization sequence
During AF with WPW: wide, bizarre QRS at >200 bpm (life-threatening)

Full 12-lead WPW with diagram:

12-lead ECG showing WPW syndrome with short PR, delta wave, wide QRS; plus single beat enlargements and conduction pathway diagram

WPW syndrome: 12-lead ECG (A), enlarged single complex showing delta wave (B), normal-conducted complex (C), and conduction pathway diagram showing accessory pathway (AP) alongside AVN (Tintinalli's Emergency Medicine)

6. Bundle Branch Block

Mechanism: Interruption of right (RBBB) or left (LBBB) bundle branch forces conduction to spread slowly through ventricular myocardium (cell-to-cell), widening the QRS.

ECG Changes - RBBB:

QRS duration ≥ 120 ms
rSR' pattern ("rabbit ears") in V1 - terminal broad R'
Broad, slurred S wave in V5-V6 and lead I
Secondary T-wave inversions in V1-V2 (discordant from the last QRS deflection)

ECG Changes - LBBB:

QRS duration ≥ 120 ms
Broad, notched R wave in V5-V6, I, aVL (no septal q waves)
Deep QS or rS in V1
Secondary T inversions in V5-V6 (discordant from last QRS deflection)
Important: LBBB masks STEMI on ECG - use Sgarbossa criteria

RBBB vs LBBB comparison (V1 and V5):

Comparison of RBBB and LBBB vs normal QRS-T in leads V1 and V5, showing rSR' in V1 for RBBB and broad R in V5/V6 for LBBB

(Harrison's Principles of Internal Medicine 22E - RBBB vs LBBB in V1/V5)

7. Hypertrophic Cardiomyopathy (HCM)

Mechanism: Genetic sarcomere mutations cause massive septal hypertrophy and disorganized myocyte architecture, leading to diastolic dysfunction, LVOTO, and risk of sudden death.

ECG Changes (present in >90% of patients):

Left ventricular hypertrophy (LVH) pattern: Increased voltage - Sokolow-Lyon (SV1 + RV5/6 ≥ 35 mm)
Left axis deviation
Deep, narrow "dagger-like" Q waves in inferior (II, III, aVF) and lateral leads (I, aVL, V4-V6) - caused by septal hypertrophy, not infarction
ST depression and T-wave inversions particularly in lateral leads
WPW-like pseudo-preexcitation pattern in some patients
Giant negative T waves in apical HCM (Yamaguchi syndrome) - deep T inversions in V3-V6

8. Dilated Cardiomyopathy (DCM)

Mechanism: Ventricular dilation with systolic dysfunction (reduced EF), from ischemic, viral, toxic, or idiopathic causes.

ECG Changes:

LBBB is very common (present in up to 25-30% of patients with DCM) and worsens dyssynchrony
Sinus tachycardia at rest due to compensatory sympathetic activation
Ventricular ectopy / ventricular tachycardia - risk of sudden death
First-degree AV block or non-specific intraventricular conduction delay
Low voltage if associated with pericardial effusion
Atrial fibrillation (very common due to atrial dilation)
Poor R-wave progression in precordial leads
Non-specific ST-T changes

9. Atrial Flutter

Mechanism: A single re-entrant circuit rotates around the tricuspid annulus (typical flutter), producing regular atrial depolarization at ~300 bpm. The AV node blocks most impulses, producing a 2:1, 3:1, or 4:1 ventricular rate.

ECG Changes:

Sawtooth flutter waves at ~300 bpm - best seen in inferior leads (II, III, aVF) and V1
Flutter waves are negatively deflected (inverted) in inferior leads in typical flutter
Regular ventricular rhythm at a fraction of 300 bpm: 2:1 block → ~150 bpm; 4:1 block → ~75 bpm
No isoelectric baseline between flutter waves
Regular narrow QRS unless aberrant conduction or BBB is present
A regular narrow-complex tachycardia at exactly ~150 bpm should always raise suspicion for atrial flutter with 2:1 block

AF with atrial flutter context - 12-lead ECG:

12-lead ECG with atrial fibrillation and irregular ventricular response across all leads

12-lead ECG showing atrial fibrillation - note absence of organized P waves and irregularly irregular QRS rhythm (Tintinalli's Emergency Medicine)

10. Long QT Syndrome (LQTS)

Mechanism: Congenital (ion channel mutations in SCN5A, KCNQ1, KCNH2, etc.) or acquired (drugs, hypokalemia, hypomagnesemia) prolongation of ventricular repolarization. Risk of triggered ventricular arrhythmia - torsades de pointes (TdP).

ECG Changes:

Prolonged QTc interval - corrected QT (Bazett formula: QT / √RR)
- Normal QTc: < 440 ms (men), < 460 ms (women)
- Borderline: 440-480 ms
- Abnormal/high risk: ≥ 500 ms
T-wave morphology abnormalities: broad/notched T waves; bifid T waves; T-U wave fusion
Torsades de pointes on ECG: rapid (~200-250 bpm) polymorphic ventricular tachycardia where the QRS axis rotates around the isoelectric line - appears as a "twisting of the points"
Each subtype has a characteristic T-wave morphology:
- LQT1: broad-based T waves
- LQT2: notched/bifid T waves
- LQT3: long, flat ST segment with late-peaking T wave

Summary Table

Disease	Key ECG Finding	Leads Affected
STEMI	ST elevation + Q waves → T inversion	Territory-specific (II/III/aVF, V1-V4, etc.)
NSTEMI/UA	ST depression, T inversion, no Q waves	Anterior/lateral
Atrial Fibrillation	No P waves, irregularly irregular RR	All leads
Heart Block (3°)	P-QRS dissociation, slow escape rhythm	All leads
WPW	Short PR, delta wave, wide QRS	All leads
Bundle Branch Block	QRS ≥ 120 ms, rSR' (RBBB) or broad R (LBBB)	V1 vs V5-V6
HCM	LVH, deep septal Q waves, ST-T changes	Lateral, inferior
Dilated CM	LBBB, AF, low voltage, poor R progression	All leads
Atrial Flutter	Sawtooth waves ~300 bpm, regular ventricular rate	II, III, aVF, V1
Long QT Syndrome	Prolonged QTc ≥ 500 ms, torsades de pointes	All leads

Sources: Harrison's Principles of Internal Medicine 22E (2025), Ganong's Review of Medical Physiology 26E, Guyton and Hall Textbook of Medical Physiology, Tintinalli's Emergency Medicine - A Comprehensive Study Guide.Here is a complete overview of all 10 conditions. Key points to remember:

Images included directly from textbooks:

Current of injury diagram (Harrison's) - shows mechanistically why STEMI causes ST elevation vs depression
Wellens T-wave sign (Harrison's) - deep anterior T inversions indicating LAD disease
Atrial fibrillation (Guyton & Hall + Tintinalli's) - absent P waves with irregular RR intervals
First-degree heart block (Ganong's) - prolonged PR = 0.38 s
Second-degree Wenckebach block (Ganong's) - progressive PR lengthening then dropped beat
Complete heart block (Ganong's) - fully independent P and QRS rhythms
WPW syndrome (Tintinalli's) - full 12-lead with delta wave and pathway diagram
12-lead AF ECG (Tintinalli's)

Clinical pearls:

LBBB can completely mask a STEMI - always apply Sgarbossa criteria
A regular narrow tachycardia at exactly 150 bpm = atrial flutter with 2:1 block until proven otherwise
WPW + AF is life-threatening - never give AV nodal blockers (adenosine, verapamil, diltiazem)
QTc ≥ 500 ms = high risk for torsades de pointes - check and correct all offending drugs and electrolytes

Explain me sandhi vata with specific reference and management with treatment

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Sandhi Vata Ayurveda disease definition symptoms management treatment classical references

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https://pdfs.semanticscholar.org/4aff/97362585d63444416abc10…

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Sandhigata Vata osteoarthritis Ayurvedic treatment

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Sandhigata Vata Charaka Samhita Sushruta classical reference nidana samprapti lakshana chikitsa shloka

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Sandhi Vata Panchakarma treatment Basti Janubasti Abhyanga Swedana formulations Guggulu Rasayana

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Ayurveda osteoarthritis knee treatment Panchakarma randomized

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https://wjpr.s3.ap-south-1.amazonaws.com/article_issue/01b1d…

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PMID: 29426006

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