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20 Common Heart Diseases: ECG Findings and Treatment

Below is a complete reference covering 20 major cardiac conditions, each with its characteristic ECG pattern and evidence-based treatment. Sources: Braunwald's Heart Disease (12th ed.), Guyton & Hall Medical Physiology, Goldman-Cecil Medicine, Harrison's Principles (22nd ed., 2025), and The Washington Manual of Medical Therapeutics.

1. ST-Elevation Myocardial Infarction (STEMI)

Pathophysiology: Complete occlusion of a coronary artery causing transmural ischemia and necrosis.

ECG Findings:

ST-segment elevation ≥1 mm in ≥2 contiguous limb leads or ≥2 mm in precordial leads
Hyperacute (tall, peaked) T waves in early phase
Pathological Q waves (>40 ms wide, >25% of R wave) develop within hours to days
Reciprocal ST depression in opposing leads
Location: anterior (V1-V4 = LAD), inferior (II, III, aVF = RCA), lateral (I, aVL, V5-V6 = LCx)

Treatment:

Primary PCI within 90 min of first medical contact (first-line)
Fibrinolysis (alteplase, tenecteplase) if PCI not available within 120 min
Antiplatelet: aspirin 325 mg loading + P2Y12 inhibitor (ticagrelor or clopidogrel)
Anticoagulation: UFH or bivalirudin during PCI
Beta-blockers, ACE inhibitors, high-intensity statins post-MI
Morphine, oxygen (if SpO2 <90%), nitroglycerin for symptom relief

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

Pathophysiology: Partial coronary occlusion or plaque rupture without transmural infarction.

ECG Findings:

ST depression (≥0.5 mm, horizontal or downsloping) in ischemic leads
T-wave inversion - often deep, symmetric ("Wellens' pattern" warns of proximal LAD disease)
No pathological Q waves (differentiates from STEMI)
ECG may be normal in ~30% of cases

Treatment:

TIMI/GRACE risk scoring to guide urgency of catheterization
Dual antiplatelet therapy (aspirin + ticagrelor or clopidogrel)
Anticoagulation: enoxaparin or UFH
Early invasive strategy (PCI within 24-48 h) for high-risk patients
Beta-blockers, nitrates, ACE inhibitors, statins
GPIIb/IIIa inhibitors (eptifibatide, tirofiban) in selected high-risk PCI patients

3. Atrial Fibrillation (AF)

Pathophysiology: Chaotic, rapid atrial depolarizations (350-600/min) from multiple re-entry circuits; irregular ventricular response.

ECG Findings:

Absent P waves replaced by irregular fibrillatory (f) waves, best seen in V1 and II
Irregularly irregular RR intervals (hallmark)
Ventricular rate 100-180/min if uncontrolled
No distinct isoelectric baseline
Narrow QRS (unless aberrant conduction or pre-existing BBB)

Treatment:

Rate control: Beta-blockers (metoprolol), diltiazem, or digoxin (heart failure)
Rhythm control: Flecainide, propafenone (no structural disease); amiodarone, dofetilide, sotalol (structural disease); electrical cardioversion
Anticoagulation (stroke prevention): DOACs (apixaban, rivaroxaban, dabigatran, edoxaban) preferred over warfarin; guided by CHA₂DS₂-VASc score (score ≥2 in men, ≥3 in women = anticoagulate)
Catheter ablation: Pulmonary vein isolation for symptomatic paroxysmal AF refractory to drugs
Left atrial appendage closure (Watchman device) for those intolerant to anticoagulation
Braunwald's: AF occurs in ~12% of patients ≥75 years; all patients ≥75 have CHA₂DS₂-VASc ≥2 and warrant anticoagulation

4. Atrial Flutter

Pathophysiology: Macro-reentrant circuit in the right atrium (cavotricuspid isthmus), rate ~300/min.

ECG Findings:

Classic "sawtooth" flutter (F) waves at 300/min, best seen in inferior leads (II, III, aVF) and V1
Regular atrial rate ~300/min with 2:1 or 4:1 AV block (ventricular rate 150 or 75/min)
2:1 block producing rate of ~150 bpm should always raise suspicion for flutter
No isoelectric baseline between flutter waves

Treatment:

Rate control: Beta-blockers, diltiazem, or digoxin
Rhythm control: Ibutilide (IV, acute conversion), electrical cardioversion (highly effective)
Catheter ablation: Cavotricuspid isthmus ablation - curative in >95% of typical flutter
Anticoagulation: Same as AF (CHA₂DS₂-VASc guided); cardioversion after 48 h requires anticoagulation or TEE to exclude LAA thrombus

5. Ventricular Tachycardia (VT)

Pathophysiology: ≥3 consecutive ventricular beats at rate >100/min; usually from re-entry around scar tissue.

ECG Findings:

Wide QRS complexes (>120 ms), bizarre morphology
Rate 100-250/min, regular or slightly irregular
AV dissociation (P waves marching independently of QRS) - pathognomonic when visible
Capture beats (narrow QRS) and fusion beats
Concordance of QRS in all precordial leads (all positive or all negative)
LBBB or RBBB morphology depending on exit site

Ventricular paroxysmal tachycardia (lead III) - Guyton & Hall Medical Physiology

Treatment:

Unstable VT: Immediate synchronized cardioversion (200 J biphasic)
Stable VT: IV amiodarone (150 mg bolus, then 1 mg/min) or IV lidocaine
Chronic/recurrent VT: ICD (implantable cardioverter-defibrillator) - primary prevention for EF ≤35%
Catheter ablation for recurrent monomorphic VT or VT storm
Treat underlying cause (ischemia, electrolyte disturbances, digitalis toxicity)
Guyton: Amiodarone prolongs action potential and refractory period; lidocaine depresses sodium permeability

6. Ventricular Fibrillation (VF)

Pathophysiology: Completely chaotic ventricular activation with no effective cardiac output; invariably fatal without immediate treatment.

ECG Findings:

Rapid, completely irregular, chaotic deflections of varying amplitude and morphology
No identifiable QRS complexes, P waves, or T waves
Rate unidentifiable (400-600 random activations/min)
Coarse VF (larger amplitude) vs. fine VF (smaller amplitude, worse prognosis)

Treatment:

Immediate unsynchronized defibrillation (200 J biphasic) - do not delay CPR
High-quality CPR (30:2) until defibrillation available
Epinephrine 1 mg IV every 3-5 min
IV amiodarone (300 mg bolus) after 3rd shock
Correct reversible causes (4 Hs and 4 Ts)
ICD implantation in survivors (secondary prevention)
Guyton: Death begins within 4-5 seconds of VF onset; irreversible tissue injury within minutes

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

Pathophysiology: Complete dissociation between atrial and ventricular conduction; no impulse passes through the AV node.

ECG Findings:

P waves and QRS complexes march independently (AV dissociation)
Atrial rate normal (60-100/min); ventricular escape rate 20-40/min (junctional escape 40-60/min)
QRS wide (>120 ms) if ventricular escape; narrow if junctional escape
PP intervals regular; RR intervals regular but at different (slower) rate
PP rate faster than RR rate

Treatment:

Emergency: Atropine (may be ineffective in infranodal block); transcutaneous pacing
Definitive: Permanent pacemaker implantation (Class I indication)
Dual-chamber pacemaker (DDD) preferred to maintain AV synchrony
Treat reversible causes (Lyme disease, drug toxicity, hyperkalemia, inferior MI)

8. Second-Degree AV Block, Type I (Wenckebach)

Pathophysiology: Progressive conduction delay in the AV node until a beat is dropped.

ECG Findings:

Progressively lengthening PR interval with each beat
RR interval progressively shortens
A non-conducted P wave (dropped QRS) occurs cyclically
Group beating pattern on the rhythm strip
Usually narrow QRS (block is at AV node level)

Treatment:

Often benign, especially in athletes or during inferior MI (vagal)
Treat underlying cause (drug toxicity - digoxin, beta-blocker; inferior MI)
Atropine if symptomatic
Pacemaker rarely needed unless symptomatic or associated with wide complex

9. Second-Degree AV Block, Type II (Mobitz II)

Pathophysiology: Intermittent failure of conduction below the AV node (His bundle or bundle branches); more dangerous than Type I.

ECG Findings:

Fixed PR interval (normal or prolonged) with sudden unexpected dropped QRS
No progressive PR lengthening before the dropped beat
Wide QRS complexes (infranodal block)
May progress abruptly to complete heart block

Treatment:

Permanent pacemaker (Class I indication regardless of symptoms)
Higher risk than Wenckebach; may precipitate syncope or sudden death
Transcutaneous/transvenous pacing as bridge

10. Left Bundle Branch Block (LBBB)

Pathophysiology: Block in the left bundle branch causing delayed left ventricular activation.

ECG Findings:

QRS duration ≥120 ms
Broad, notched ("M-shaped") R waves in lateral leads (I, aVL, V5-V6)
rS pattern in V1 (deep S wave)
No septal Q waves in lateral leads
ST depression and T-wave inversion in lateral leads (secondary repolarization changes)
New LBBB + chest pain = STEMI equivalent (Sgarbossa criteria)

Treatment:

Treat underlying cause (CAD, hypertension, cardiomyopathy)
LBBB with EF ≤35% and NYHA Class II-III HF: Cardiac Resynchronization Therapy (CRT/biventricular pacing) - significant mortality and symptom benefit
New LBBB in context of ACS: treat as STEMI

11. Right Bundle Branch Block (RBBB)

Pathophysiology: Block in the right bundle branch; left ventricle activates first, then right ventricle.

ECG Findings:

QRS ≥120 ms
RSR' ("bunny ear") pattern in V1-V2
Wide, slurred S wave in lateral leads (I, aVL, V5-V6)
T-wave inversion in V1-V3 (secondary changes)
Incomplete RBBB: QRS 100-119 ms with same pattern

Treatment:

Isolated RBBB in asymptomatic patients: no treatment needed (often benign)
New RBBB in pulmonary embolism context: suggests RV strain (treat PE)
New RBBB with anterior MI: high risk, may need temporary pacing
Bifascicular block (RBBB + left fascicular block) with syncope: permanent pacemaker

12. Supraventricular Tachycardia (SVT) / AVNRT

Pathophysiology: Re-entry circuit within or near the AV node (AVNRT most common, ~60% of SVTs); sudden onset and termination.

ECG Findings:

Narrow QRS tachycardia, rate 150-250/min, regular
P waves often hidden within or immediately after QRS (pseudo-R' in V1, pseudo-S in inferior leads)
Retrograde P waves (inverted in II, III, aVF) if visible
Abrupt onset and termination
"Long RP" (AVRT) vs. "Short RP" (AVNRT) distinction

Treatment:

Acute: Vagal maneuvers (Valsalva, carotid sinus massage) first
IV adenosine 6 mg (then 12 mg) - drug of choice for acute termination
IV diltiazem or beta-blocker if adenosine fails
Synchronized cardioversion if hemodynamically unstable
Long-term: Catheter ablation (curative >95%); drug prophylaxis (verapamil, beta-blockers) if ablation declined

13. Wolff-Parkinson-White (WPW) Syndrome

Pathophysiology: Accessory pathway (Bundle of Kent) bypasses the AV node causing pre-excitation; risk of rapid conduction in AF.

ECG Findings:

Short PR interval (<120 ms)
Delta wave (slurred upstroke of QRS)
Wide QRS (>120 ms) due to pre-excitation
Secondary ST-T changes
AF with WPW: irregular, very rapid (>250/min), wide complex ("antidromic" - life-threatening)

Treatment:

Symptomatic or AF with WPW: Catheter ablation of accessory pathway (curative, first-line)
Avoid AV nodal blocking agents (digoxin, diltiazem, beta-blockers, adenosine) in AF+WPW - may accelerate conduction via accessory pathway causing VF
Acute AF+WPW with hemodynamic instability: immediate DC cardioversion
Acute AF+WPW stable: IV procainamide or IV ibutilide

14. Heart Failure with Reduced Ejection Fraction (HFrEF)

Pathophysiology: Reduced LV systolic function (EF <40%) causing inadequate cardiac output; neurohormonal activation accelerates progression.

ECG Findings:

Often non-specific; may show:
LVH (Sokolow-Lyon criteria: S in V1 + R in V5-V6 >35 mm)
LBBB (as above)
Signs of underlying ischemia (Q waves, ST changes)
Low voltage in pericardial effusion
Atrial fibrillation (common comorbidity)
Sinus tachycardia (compensatory)

Treatment (4 pillars of HFrEF):

ACE inhibitor or ARB/sacubitril (ARNi - sacubitril/valsartan) - RAAS blockade
Beta-blocker (carvedilol, metoprolol succinate, bisoprolol)
Mineralocorticoid receptor antagonist (spironolactone, eplerenone)
SGLT2 inhibitor (dapagliflozin, empagliflozin) - added as 4th pillar per 2022 guidelines

Loop diuretics (furosemide) for fluid overload
CRT if LBBB + EF ≤35%
ICD for EF ≤35% and NYHA Class II-III
LVAD or heart transplant for refractory Stage D HF

15. Hypertrophic Cardiomyopathy (HCM)

Pathophysiology: Autosomal dominant mutation in sarcomere proteins (usually beta-myosin heavy chain) causing asymmetric LV hypertrophy, diastolic dysfunction, and dynamic LVOT obstruction.

ECG Findings:

LVH criteria (high voltage: deep S in V1 + tall R in V5-V6)
Deep, narrow "dagger-like" Q waves in lateral and inferior leads (septal depolarization)
T-wave inversion in lateral leads (especially in apical variant)
ST depression, left axis deviation
AF (late complication)
Giant T-wave inversions (Yamaguchi/apical HCM variant)

Treatment:

Symptomatic obstruction: Beta-blockers (first-line); verapamil, disopyramide
Mavacamten (cardiac myosin inhibitor) - FDA-approved 2022 for symptomatic obstructive HCM
Alcohol septal ablation or surgical myectomy for drug-refractory LVOT obstruction
ICD for high-risk patients (prior VF, VT, unexplained syncope, family history of SCD, massive LVH ≥30 mm)
Anticoagulation if AF develops
Avoid strenuous competitive athletics

16. Dilated Cardiomyopathy (DCM)

Pathophysiology: LV or biventricular dilation with reduced systolic function; causes include viral myocarditis, alcohol, genetic, idiopathic.

ECG Findings:

Sinus tachycardia
LVH or low voltage
LBBB (common)
Left axis deviation
Non-specific ST-T changes
Atrial fibrillation (common)
Frequent PVCs or NSVT

Treatment:

Same 4-pillar HFrEF treatment (ACEi/ARNi, beta-blocker, MRA, SGLT2i)
ICD for EF ≤35% (primary prevention of SCD)
CRT for LBBB + EF ≤35%
Abstain from alcohol (alcoholic DCM may reverse with abstinence)
Anticoagulation if AF or LV thrombus
Treat underlying cause (immunosuppression for giant cell myocarditis, etc.)

17. Pericarditis (Acute)

Pathophysiology: Inflammation of the pericardium; causes include viral, idiopathic, post-MI (Dressler's), autoimmune, uremic.

ECG Findings - Classic 4 Stages:

Stage 1 (early): Diffuse saddle-shaped (concave up) ST elevation in almost all leads except aVR and V1 (where there is ST depression); PR depression (pathognomonic)
Stage 2: ST returns to baseline; PR depression persists
Stage 3: T-wave inversions (diffuse)
Stage 4: ECG normalizes
Key distinction from STEMI: ST elevation is diffuse (not regional), concave up, PR depression present, no reciprocal ST depression (except aVR/V1)

Treatment:

Aspirin 750-1000 mg every 8h for 1-2 weeks (first-line for idiopathic/viral)
Colchicine 0.5 mg twice daily for 3 months - reduces recurrence by ~50%
NSAIDs (ibuprofen) as alternative to aspirin
Restrict physical activity until resolution
Corticosteroids only if aspirin/NSAID contraindicated (higher recurrence rate)
Treat pericardial effusion/tamponade with pericardiocentesis if hemodynamically significant

18. Pulmonary Embolism (PE)

Pathophysiology: Thromboembolism obstructing pulmonary vasculature causing acute RV pressure overload and strain.

ECG Findings:

Sinus tachycardia (most common finding, ~44%)
S1Q3T3 pattern: S wave in lead I, Q wave and T-wave inversion in lead III (classic but only in ~20%)
Right axis deviation
New incomplete or complete RBBB (RV strain)
T-wave inversions in right precordial leads (V1-V4)
P pulmonale (peaked P waves in II)
AF or atrial flutter
ECG may be normal in small PE

Treatment:

Anticoagulation: DOACs (rivaroxaban, apixaban preferred) or UFH/LMWH bridge to warfarin
Massive PE (hemodynamic instability): Systemic thrombolysis (alteplase 100 mg over 2h) or catheter-directed therapy
Submassive PE (RV dysfunction): Anticoagulation + consider thrombolysis in deteriorating patients
Oxygen, hemodynamic support
IVC filter only if anticoagulation absolutely contraindicated
Extended anticoagulation for unprovoked PE (3-6 months minimum, often indefinite)

19. Sick Sinus Syndrome (SSS)

Pathophysiology: Dysfunction of the SA node causing bradyarrhythmias, often alternating with tachyarrhythmias (tachycardia-bradycardia syndrome).

ECG Findings:

Sinus bradycardia (<50/min)
Sinus pauses/arrest (prolonged PP intervals, no P wave)
Sinoatrial exit block (PP interval doubles)
Alternating with episodes of AF, atrial flutter, or SVT (tachycardia-bradycardia pattern)
Chronotropic incompetence (failure to increase HR with exertion)

Treatment:

Symptomatic SSS: Permanent pacemaker (Class I; AAI or DDD pacing)
Pacemaker implantation allows safe use of antiarrhythmic drugs for the tachycardia component
Anticoagulation if AF episodes occur (CHA₂DS₂-VASc guided)
Avoid drugs that worsen bradycardia (beta-blockers, calcium channel blockers) without pacemaker protection

20. Long QT Syndrome (LQTS)

Pathophysiology: Genetic (congenital) or acquired prolongation of ventricular repolarization; predisposes to torsades de pointes (TdP) - polymorphic VT - and sudden cardiac death.

ECG Findings:

Prolonged QTc interval: >450 ms in men, >460 ms in women (corrected using Bazett formula: QTc = QT/√RR)
QTc >500 ms: high risk for TdP
Abnormal T-wave morphology: notched, bifid, or broad T waves depending on LQTS subtype
U waves (prominent in hypokalemia-associated QT prolongation)
Torsades de pointes: polymorphic VT with QRS complexes rotating around the isoelectric axis ("twisting of points")

Treatment:

Beta-blockers (nadolol, propranolol) - mainstay for congenital LQTS (LQT1 and LQT2)
ICD for prior cardiac arrest, recurrent syncope on beta-blockers, or QTc >550 ms with symptoms
Avoid QT-prolonging drugs (check CredibleMeds/azlist.org)
Correct electrolytes (hypokalemia, hypomagnesemia worsen QT)
Acute TdP: IV magnesium sulfate 2g bolus; correct K+ to 4.5-5 mEq/L; overdrive pacing (isoproterenol or temporary pacing at 100/min)
Left cardiac sympathetic denervation (LCSD) as adjunct therapy

Quick Reference Summary Table

#	Condition	Key ECG Finding	1st-Line Treatment
1	STEMI	ST elevation + Q waves	Primary PCI within 90 min
2	NSTEMI/UA	ST depression, T inversion	Antiplatelet + anticoagulation, early PCI
3	Atrial Fibrillation	Absent P waves, irregularly irregular	Rate/rhythm control + anticoagulation (DOAC)
4	Atrial Flutter	Sawtooth F waves at 300/min	Catheter ablation (cavotricuspid isthmus)
5	Ventricular Tachycardia	Wide QRS, AV dissociation	Cardioversion if unstable; amiodarone/ICD
6	Ventricular Fibrillation	Chaotic, no QRS	Immediate defibrillation + CPR
7	Complete Heart Block	AV dissociation, slow escape	Permanent pacemaker
8	Wenckebach	Progressive PR lengthening, dropped beat	Observation/treat cause
9	Mobitz II	Fixed PR, sudden dropped QRS	Permanent pacemaker
10	LBBB	Wide QRS, M-shaped R in lateral	Treat cause; CRT if HF
11	RBBB	RSR' in V1, wide S in lateral	Usually no treatment; treat cause
12	SVT/AVNRT	Narrow QRS tachycardia, P in QRS	Adenosine; catheter ablation
13	WPW	Short PR, delta wave	Catheter ablation; avoid AV nodal blockers in AF
14	HFrEF	LVH, LBBB, non-specific changes	ACEi/ARNi + beta-blocker + MRA + SGLT2i
15	HCM	Deep Q waves lateral, LVH	Beta-blockers; mavacamten; ICD if high-risk
16	DCM	LBBB, low voltage, AF	HFrEF regimen; ICD/CRT
17	Acute Pericarditis	Diffuse saddle ST elevation, PR depression	Aspirin + colchicine 3 months
18	Pulmonary Embolism	Tachycardia, S1Q3T3, RBBB	Anticoagulation; thrombolysis if massive
19	Sick Sinus Syndrome	Sinus pauses, bradycardia-tachycardia	Permanent pacemaker
20	Long QT Syndrome	QTc >450-460 ms, torsades	Beta-blockers; ICD; avoid QT-prolonging drugs

Sources:

Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 12th Edition
Guyton & Hall Textbook of Medical Physiology, 14th Edition
Goldman-Cecil Medicine, International Edition
Harrison's Principles of Internal Medicine, 22nd Edition (2025)
The Washington Manual of Medical Therapeutics

Clinical Note: ECG interpretation must always be integrated with clinical context, patient history, and other investigations. Drug dosages and guideline recommendations should be verified against current institutional protocols. This content is for educational purposes.

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