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SVT vs Atrial Fibrillation (AF) — Complete Comparative Study

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PART 1 — DEFINITIONS

Supraventricular Tachycardia (SVT)

• AV Nodal Reentry Tachycardia (AVNRT) — most common (60%)
• AV Reentry Tachycardia (AVRT) using an accessory pathway (e.g., WPW)
• Focal Atrial Tachycardia (AT)

"Supraventricular arrhythmias that result in an elevated heart rate (>100 beats/min) are broadly defined as supraventricular tachycardias (SVTs)." — Harrison's Principles of Internal Medicine 22E

Atrial Fibrillation (AF)

• No organized atrial contraction
• Irregularly irregular ventricular response
• Absent P waves on ECG replaced by fibrillatory (f) waves

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PART 2 — PATHOGENESIS

SVT Pathogenesis

• Requires two pathways with different conduction velocities and refractory periods
• In AVNRT: dual AV nodal pathways (fast & slow) form the circuit entirely within the AV node region
• In AVRT: accessory pathway (bypass tract) creates a macro-reentrant circuit using atrium → AV node → ventricle → accessory pathway → atrium

"Reentry is a common electrophysiologic mechanism that predisposes to most ventricular arrhythmias and to most supraventricular tachyarrhythmias." — Harrison's 22E

AF Pathogenesis

• Other trigger sites: posterior left atrial wall, superior vena cava sleeves, coronary sinus, vein of Marshall

• Risk factors (HTN, obesity, age, diabetes, alcohol, sleep apnea, structural heart disease) → atrial remodeling
• Electrical remodeling: shortening of atrial effective refractory periods ("AF begets AF")
• Structural remodeling: atrial fibrosis, left atrial enlargement, heterogeneous conduction

• Multiple simultaneous wandering wavelets propagate through partially refractory atrial tissue
• No fixed circuit — unstable, chaotic, self-perpetuating

"There is evidence that functional reentry is the underlying mechanism for perpetuation and maintenance of both atrial fibrillation and ventricular fibrillation. Multiple wavefronts resulting from multiple functional reentrant circuits appear to drive arrhythmia." — Harrison's 22E

• Each stage involves progressively more severe structural/electrical remodeling

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PART 3 — CLINICAL FEATURES / PATIENT PRESENTATION

SVT Clinical Presentation

AF Clinical Presentation

• Pulmonary disease (COPD, PE)
• Ischemic/structural heart disease
• Rheumatic heart disease (especially mitral stenosis)
• Alcohol ("holiday heart")
• Thyroid disease (hyperthyroidism)
• Electrolyte imbalance
• Surgery (post-cardiac surgery in up to 50%)

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PART 4 — ECG / DIAGNOSIS / LAB REPORTS

SVT ECG Features

• AVNRT: P waves buried in or just after QRS ("pseudo R' in V1", "pseudo S in II/III/aVF")
• AVRT (orthodromic): narrow QRS, retrograde P in ST segment (RP < PR)
• AVRT (antidromic / WPW): wide QRS, delta wave during SR, short PR

AF ECG Features

Key ECG Comparison Table

Lab Investigations

• Electrolytes (K+, Mg2+, Ca2+) — hypokalemia/hypomagnesemia precipitate/worsen both
• Thyroid function tests (TSH, fT4) — hyperthyroidism major cause of AF; can worsen SVT
• CBC — anemia as precipitant
• Renal function (BUN, Cr) — guides drug dosing (DOACs, digoxin)
• Liver function — affects drug metabolism (amiodarone, DOACs)
• Blood glucose — electrolyte disturbances in DM
• Cardiac enzymes (Troponin) — rule out ACS as trigger

• INR/PT — for warfarin monitoring
• CHA₂DS₂-VASc score — thromboembolic risk assessment
• HAS-BLED score — bleeding risk assessment
• BNP/NT-proBNP — assess for heart failure with AF
• Echocardiogram — LA size, LV function, valve disease, thrombus (TEE for left atrial appendage)
• Holter monitor / event recorder / implantable loop recorder — detect paroxysmal AF

• EP Study (Electrophysiology Study) — definitive mapping of reentry circuits before ablation
• Holter/event monitor — document paroxysmal SVT episodes

After Treatment ECG Changes

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PART 5 — LAB AND TREATMENT RELATION

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PART 6 — TREATMENT PROTOCOL

SVT Treatment Protocol

1. Vagal maneuvers (Valsalva, carotid sinus massage, diving reflex in children, modified Valsalva) — first-line, success rate 20–50%
2. Adenosine (6 mg IV rapid push → 12 mg → 18 mg) — first-line drug; terminates >90% of AVNRT/AVRT
   • Give into antecubital vein, flush rapidly; half-life 10 seconds
   • Contraindicated in: asthma, WPW with pre-excited AF, heart transplant
3. IV calcium channel blockers — Verapamil 5–10 mg IV or Diltiazem IV (if adenosine fails)
4. IV beta-blockers — Metoprolol 5 mg IV; Esmolol infusion
5. Synchronized cardioversion — if hemodynamically unstable or drug failure (50–100 J biphasic)

AF Treatment Protocol

Pillar 1 — Anticoagulation (Stroke Prevention)

• CHA₂DS₂-VASc ≥2 (men) or ≥3 (women) → mandatory anticoagulation
• All patients ≥75 years → CHA₂DS₂-VASc ≥2 automatically → anticoagulate
• Anticoagulate ≥3 weeks before elective cardioversion (or TEE to exclude LA thrombus) + 4 weeks post-cardioversion

Pillar 2 — Rate Control

Pillar 3 — Rhythm Control

• Flecainide IV/oral — rapid, effective in absence of structural disease
• Propafenone — similar to flecainide
• Amiodarone IV/oral — use in structural heart disease, HF
• Ibutilide IV — in-hospital use

• Synchronized 120–200 J biphasic (200 J monophasic)
• Require adequate anticoagulation (≥3 weeks before or TEE exclusion of LAA thrombus)
• Continue anticoagulation ≥4 weeks post-cardioversion ("electrical stunning" of atria)

• Electrically isolates pulmonary veins (primary trigger source) from left atrium
• First-line in symptomatic paroxysmal AF; increasingly used in persistent AF
• In EAST-AFNET 4 trial — early rhythm control (including ablation) reduced CV death, stroke, and hospitalization vs. rate control alone
• In patients with HFrEF — catheter ablation superior to pharmacotherapy (improves EF)
• Success rate: ~70–80% single procedure for paroxysmal AF; lower for persistent

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PART 7 — PROGNOSIS & CURABILITY

SVT Prognosis

AF Prognosis

"AF tends to be a progressive condition, with, at this point, no definitive cure that will completely eliminate AF durably in a predictable fashion." — Harrison's 22E

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PART 8 — DISEASE STUDY (Overview Summary Table)

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PART 9 — LAB CORRELATION

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PART 10 — SYNDROME STUDY

Key Associated Syndromes

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PART 11 — TREATMENT CHANGING PROTOCOLS: DO'S AND DON'TS

DO'S ✅

• Do perform vagal maneuvers first before any drug administration
• Do use modified Valsalva (semi-recumbent, leg elevation) — improves success rate
• Do give adenosine as rapid IV bolus close to the heart (antecubital) with rapid flush
• Do ablate if SVT is recurrent, poorly tolerated, or patient prefers cure
• Do stratify WPW patients for SCD risk — ablate if high-risk features (short R-R in AF <250ms, syncope)
• Do monitor ECG during adenosine administration

• Do anticoagulate before cardioversion (≥3 weeks or TEE to exclude LAA thrombus)
• Do continue anticoagulation ≥4 weeks after cardioversion (atrial stunning)
• Do treat reversible causes first (thyroid, infection, alcohol)
• Do prefer DOACs over warfarin in non-valvular AF (fewer interactions, no INR monitoring)
• Do consider early rhythm control in newly diagnosed AF (EAST-AFNET 4 trial)
• Do offer PVI ablation to symptomatic patients failing one antiarrhythmic drug
• Do use amiodarone in AF with structural heart disease / HFrEF

DON'TS ❌

• Don't use verapamil/diltiazem in wide-complex tachycardia (may be VT — risk of VF)
• Don't use adenosine in asthma (severe bronchospasm)
• Don't use adenosine in pre-excited AF/WPW (blocks AV node → all conduction down accessory pathway → VF)
• Don't use verapamil in WPW with pre-excited tachycardia
• Don't give AV nodal blockers for wide-complex tachycardia without diagnosis

• Don't use flecainide or propafenone in structural heart disease / HF / CAD (proarrhythmic)
• Don't use verapamil/diltiazem in AF with HFrEF (EF <40%) — negative inotropic effect
• Don't use verapamil in pre-excited AF (WPW + AF) — absolute contraindication (→ VF)
• Don't stop anticoagulation just because patient is in sinus rhythm after ablation (AF may recur asymptomatically)
• Don't rely on aspirin alone for stroke prevention in AF — it is inferior to anticoagulation
• Don't cardiovert AF of unknown duration without adequate anticoagulation (3 weeks) or TEE
• Don't use dronedarone in permanent AF (increases mortality)
• Don't use amiodarone without monitoring TFTs, LFTs, PFTs (pulmonary fibrosis, thyroid toxicity, hepatotoxicity)

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PART 12 — DIAGNOSIS & DIFFERENTIAL DIAGNOSIS (DD)

SVT Differential Diagnosis

AF Differential Diagnosis

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PART 13 — DRUG STUDY / COMBINATIONS

Antiarrhythmic Drug Classification (Vaughan-Williams)

Key Drug Combinations

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PART 14 — पथ्य व अपथ्य (Pathya-Apathya) Study

पथ्य (Beneficial — Do's)

• Low-sodium diet — reduces hypertension-driven AF substrate
• Mediterranean diet — reduces AF recurrence and cardiovascular events
• High-potassium foods (bananas, leafy greens, avocado) — maintains electrolyte balance
• Magnesium-rich foods (nuts, seeds, dark leafy greens) — reduces atrial irritability
• Omega-3 fatty acids (fish, walnuts, flaxseed) — anti-inflammatory; reduces AF substrate
• Adequate hydration — dehydration can trigger SVT/AF
• Green tea (light) — antioxidant properties; however, avoid excess (caffeine)

• Moderate aerobic exercise — reduces AF burden, improves vagal tone
• Weight loss (obesity management) — reduces LA size, AF recurrence (LEGACY trial: weight loss >10% → 46% AF-free)
• Sleep hygiene — treat obstructive sleep apnea (CPAP reduces AF recurrence)
• Stress management — yoga, meditation, pranayama reduce SVT/AF triggers
• Alcohol cessation — holiday heart syndrome; alcohol is a direct AF trigger
• Smoking cessation — reduces cardiovascular risk and atrial inflammation
• Regular INR monitoring (if on warfarin) — strict compliance
• Medication compliance — take antiarrhythmics and anticoagulants as prescribed

अपथ्य (Harmful — Avoid)

• Caffeine excess (coffee, energy drinks, cola) — triggers SVT and AF in susceptible patients
• Alcohol — even moderate intake triggers AF; binge drinking = holiday heart
• High-fat, processed, fried foods — promote inflammation and metabolic syndrome
• Excessive salt — worsens hypertension → AF substrate
• Vitamin K–rich foods in excess (spinach, kale) if on warfarin — destabilizes INR
• Grapefruit / grapefruit juice — inhibits CYP3A4 → increases levels of some antiarrhythmics and some DOACs (rivaroxaban, apixaban)
• Liquorice (mulethi) — causes pseudohyperaldosteronism → hypokalemia → worsens arrhythmia

• Strenuous competitive exercise without cardiac clearance (WPW — SCD risk)
• Sleep deprivation — increases sympathetic tone, AF triggers
• Emotional stress / anger — catecholamine surge triggers reentrant circuits
• Self-medication / herbal remedies without physician guidance — many contain ephedrine-like compounds (e.g., ma huang, bitter orange) → potent arrhythmogenic
• Over-the-counter decongestants (pseudoephedrine, phenylephrine) — trigger SVT/AF
• NSAIDs (ibuprofen, diclofenac) — increase AF risk; increase bleeding risk with anticoagulants
• Obesity — independent risk factor for AF; worsens SVT frequency
• Tobacco / smoking — directly proarrhythmic; increases cardiovascular burden
• Driving / operating machinery during recurrent uncontrolled SVT/AF episodes
• Missed doses of anticoagulants — catastrophic stroke risk in AF

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Summary Comparison Table

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