🫀 Supraventricular Tachycardia (SVT)

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🔹 Definition

Supraventricular tachycardia (SVT) is a tachyarrhythmia originating above the bundle of His, i.e., from the sinus node, atria, or AV node.
It produces a narrow-complex (QRS <120 ms) rhythm unless aberrant conduction or pre-excitation (e.g., WPW) causes widening.

Heart rate: Usually >100–150 bpm, often paroxysmal in onset and termination.

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🔹 Mechanisms

1. Reentry (most common mechanism)

   • AV Nodal Reentrant Tachycardia (AVNRT) – dual AV nodal pathways (fast and slow).

   • AV Reentrant Tachycardia (AVRT) – macro-reentry involving an accessory pathway (e.g., in WPW syndrome).

2. Abnormal automaticity

   • Spontaneous, increased firing from ectopic atrial or junctional focus.

   • Seen in focal atrial tachycardia or junctional tachycardia.

3. Triggered activity (after-depolarizations)

   • Due to digitalis toxicity or catecholamine excess.

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🔹 Classification of Major SVTs

Type	Mechanism	ECG Findings	Comments
AVNRT	Reentry within AV node	Regular, narrow QRS; P waves hidden in or just after QRS	Most common SVT (≈60–70%)
Orthodromic AVRT	Reentry via AV node (antegrade) + accessory pathway (retrograde)	Regular, narrow QRS; retrograde P after QRS	Occurs in WPW syndrome
Antidromic AVRT	Antegrade via accessory pathway, retrograde via AV node	Regular, wide QRS (mimics VT)	Avoid AV nodal blockers
Focal Atrial Tachycardia (AT)	Ectopic atrial focus (automaticity)	Abnormal P morphology before QRS; regular rhythm	Not reentrant; may not terminate with adenosine
Multifocal Atrial Tachycardia (MAT)	≥3 different atrial foci	≥3 P-wave morphologies; irregular rhythm	Seen in COPD, hypoxia, theophylline toxicity
Atrial Flutter	Large reentry circuit in right atrium	“Sawtooth” flutter waves; regular ventricular response (2:1, 3:1)	May degenerate to AF
Atrial Fibrillation (AF)	Multiple microreentry circuits	Irregularly irregular rhythm; no P waves	Commonest sustained arrhythmia
Junctional Tachycardia	AV junction focus	Inverted P waves before/after QRS	Often due to digoxin toxicity

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🔹 Clinical Presentation

• Symptoms:

  • Sudden onset and termination of palpitations (“racing heart”)

  • Lightheadedness, dizziness, shortness of breath, chest discomfort

  • Anxiety, sweating

  • Syncope (rare; may occur in elderly or those with structural heart disease)

• Physical findings:

  • Rapid regular pulse

  • “Neck pounding” (cannon A waves in JVP → classic for AVNRT)

  • Possible hypotension during episodes

  • Heart sounds: rapid rate; may be difficult to discern individual S1/S2

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🔹 Diagnosis

1. 12-lead ECG

• Narrow complex tachycardia (QRS <120 ms) → supraventricular origin.

• Wide complex tachycardia (QRS ≥120 ms) → may still be SVT with aberrancy, but must rule out VT.

• Look for:

  • P-wave visibility (hidden, retrograde, abnormal morphology)

  • Regular vs. irregular rhythm

  • Presence of delta wave (in sinus rhythm → WPW)

2. Laboratory Tests

• Electrolytes, thyroid function, toxicology (digoxin level)

• Echocardiogram – evaluate for structural disease or heart failure

• Holter / event monitor – for intermittent SVT episodes

• Electrophysiologic (EP) study – diagnostic and therapeutic (for ablation)

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⚡ Acute Management (ACLS Algorithm)

Step 1 – Assess Stability

• Unstable: hypotension, chest pain, pulmonary edema, altered mental status
  → Immediate synchronized cardioversion

• Stable: proceed to pharmacologic management.

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Step 2 – Stable Narrow-Complex SVT

1. Vagal maneuvers

   • Valsalva maneuver, carotid sinus massage

   • Increases vagal tone → transient AV block → may terminate AVNRT/AVRT

2. Adenosine (IV, rapid push followed by flush)

   • 6 mg → if ineffective, 12 mg → may repeat once more.

   • Temporarily blocks AV conduction → diagnostic & therapeutic.

   • Contraindications: severe asthma/COPD, pre-excited AF (WPW with AF)

   • Transient effects: flushing, chest pressure, dyspnea.

3. If persistent:

   • Beta-blocker (e.g., metoprolol, esmolol)

   • Calcium channel blocker (verapamil, diltiazem)

   • Used when SVT mechanism involves AV node.

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Step 3 – Stable Wide-Complex Tachycardia

• If diagnosis uncertain → treat as VT (safer).

• If known to be antidromic AVRT → procainamide preferred.

• Avoid AV nodal blockers (may precipitate VF in WPW).

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💊 Chronic / Long-Term Management

Condition	Preferred Long-Term Therapy
AVNRT	1️⃣ Catheter ablation (curative, >95% success) 2️⃣ β-blocker or CCB for symptom control if not ablated
AVRT (WPW)	Radiofrequency ablation of accessory pathway (definitive)
Focal Atrial Tachycardia	Treat underlying cause (stimulants, hypoxia, thyrotoxicosis); β-blocker or CCB
MAT	Correct hypoxia, electrolytes; treat COPD; consider verapamil for rate control
Atrial Flutter / Fibrillation	Rate/rhythm control, anticoagulation per CHA₂DS₂-VASc score
Junctional Tachycardia	Discontinue offending drug (e.g., digoxin), β-blocker or CCB as needed

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🚫 Drugs to Avoid

• Pre-excited AF (WPW + AF):
  Avoid adenosine, verapamil, diltiazem, and β-blockers → they enhance conduction through accessory pathway → can trigger VF.
  ✅ Use procainamide or synchronized cardioversion instead.

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🔹 Key ECG Differentiators

Feature	AVNRT	Orthodromic AVRT	Antidromic AVRT	Atrial Tachycardia
P waves	Hidden in QRS or shortly after	Retrograde (after QRS)	Often not visible	Abnormal, before QRS
QRS width	Narrow	Narrow	Wide	Narrow
Mechanism	Dual AV nodal pathways	Accessory pathway	Accessory (manifest)	Ectopic focus
Response to Adenosine	Terminates	Terminates	May not	Often unaffected
Typical Rate (bpm)	150–250	150–250	150–250	100–250

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🧠 Mnemonic: "VANISH" – Steps in SVT Management

V – Vagal maneuvers
A – Adenosine
N – Narrow vs. wide QRS differentiation
I – Identify mechanism
S – Stable vs. unstable
H – Holter & ablation for long-term cure

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🧩 Prognosis

• AVNRT / AVRT: Excellent; curable with ablation.

• Focal AT / MAT: Often secondary to systemic illness → treat cause.

• Atrial flutter / AF: Chronic management with anticoagulation & rate/rhythm control.