What are the different types of supraventricular tachycardia (SVT) and their treatments?

Types of Supraventricular Tachycardia and Their Management

Supraventricular tachycardia encompasses three main types: atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and atrial tachycardia (AT), each requiring specific diagnostic and therapeutic approaches. 1

Main Types of SVT

1. Atrioventricular Nodal Reentrant Tachycardia (AVNRT)

AVNRT is the most common form of SVT, accounting for the majority of cases, typically occurring in young adults without structural heart disease, with over 60% of cases in women. 1

Clinical Characteristics

• Heart rate typically ranges from 180-200 bpm but can vary from 110 to >250 bpm 1
• Patients present with sudden onset palpitations, shortness of breath, dizziness, and characteristic neck pulsations 1
• The arrhythmia is usually well tolerated and rarely life-threatening, with syncope being uncommon 1
• Triggers include exertion, coffee, tea, or alcohol 1

ECG Features

• Typical AVNRT shows a pseudo R' wave in lead V1 and pseudo S waves in inferior leads due to P waves hidden within or immediately after the QRS complex 1
• The reentrant circuit involves anterograde conduction over a slow AV nodal pathway and retrograde conduction over a fast pathway, creating a short RP tachycardia 1
• Atypical AVNRT demonstrates a long RP interval with retrograde P waves (negative in inferior leads) 1

2. Atrioventricular Reentrant Tachycardia (AVRT)

AVRT involves a reentrant circuit utilizing an accessory pathway between the atria and ventricles, distinct from the AV node. 2, 3

Clinical Characteristics

• Orthodromic AVRT (most common form) conducts anterograde through the AV node and retrograde through the accessory pathway, producing narrow QRS complexes 1
• Antidromic AVRT conducts anterograde through the accessory pathway and retrograde through the AV node, producing wide QRS complexes 1
• Wolff-Parkinson-White syndrome represents a specific subset with pre-excitation on baseline ECG 2

ECG Features

• P waves appear in the ST segment, separated from the QRS by >70 ms in orthodromic AVRT 1
• Wide QRS with left bundle branch block morphology suggests anterograde conduction over the accessory pathway 1

3. Atrial Tachycardia (AT)

Atrial tachycardia originates from a focal source or reentrant circuit within the atrial tissue, independent of the AV node. 2, 3

Clinical Characteristics

• AT can occur with or without structural heart disease 2
• The rhythm may be regular or irregular depending on the mechanism 3
• Multifocal atrial tachycardia (MAT) represents a specific subtype often associated with pulmonary disease 1

Acute Management Algorithm

For Hemodynamically Stable Patients

Step 1: Vagal Maneuvers (First-Line)

• Perform vagal maneuvers immediately as first-line intervention, with the patient in supine position 1, 4
• Modified Valsalva maneuver: bearing down against closed glottis for 10-30 seconds at 30-40 mm Hg pressure 1
• Carotid sinus massage: apply steady pressure for 5-10 seconds after confirming absence of bruit 1
• Ice-cold towel to face or facial immersion in 10°C water activates diving reflex 1
• Overall success rate is approximately 27.7%, with Valsalva being more effective than carotid massage 1, 4

Step 2: Adenosine (Second-Line)

• Administer adenosine if vagal maneuvers fail, with 90-95% success rate for terminating AVNRT and orthodromic AVRT 1, 4
• Adenosine serves both therapeutic and diagnostic purposes, unmasking atrial activity in non-AV node dependent rhythms 1
• Expect brief side effects in approximately 30% of patients 4

Step 3: IV Calcium Channel Blockers or Beta Blockers (Third-Line)

• Administer IV diltiazem, verapamil, or beta blockers if adenosine fails, with 80-98% success rates 1, 4
• These agents are particularly effective for AVNRT conversion 1
• Critical caveat: Never use in suspected VT, pre-excited atrial fibrillation, or systolic heart failure due to risk of hemodynamic collapse or ventricular fibrillation 1, 4

Step 4: Synchronized Cardioversion

• Perform synchronized cardioversion if pharmacological therapy fails or is contraindicated 1

For Hemodynamically Unstable Patients

Immediate synchronized cardioversion is first-line management for patients with hypotension, altered mental status, signs of shock, chest pain, or acute heart failure. 1, 4

Special Consideration: Pre-Excited Atrial Fibrillation

Use IV ibutilide or procainamide for stable patients with pre-excited AF; avoid AV nodal blocking agents (adenosine, calcium channel blockers, beta blockers) that may enhance conduction over the accessory pathway and precipitate ventricular fibrillation. 4

Long-Term Management

Catheter Ablation (Preferred)

Catheter ablation is the most effective first-line therapy for preventing recurrent symptomatic SVT, with success rates of 94.3-98.5% and recurrence rates <5%. 4, 5

Pharmacological Suppression (Alternative)

For patients declining ablation or unsuitable candidates:

• Oral beta blockers, diltiazem, or verapamil serve as first-line pharmacological options 4
• Flecainide or propafenone are effective in patients without structural heart disease for preventing paroxysmal SVT 4, 6, 7
• Flecainide is FDA-approved for prevention of PSVT including AVNRT, AVRT, and other SVTs of unspecified mechanism 6
• Propafenone reduces attack rates significantly, with 47-67% of patients remaining attack-free 7

Critical Pitfalls to Avoid

Never administer verapamil or diltiazem for wide-complex tachycardia unless SVT with aberrancy is definitively proven, as these agents may cause hemodynamic collapse in ventricular tachycardia. 1

Never use AV nodal blocking agents in patients with pre-excited atrial fibrillation (Wolff-Parkinson-White with AF), as this may accelerate ventricular rate and precipitate ventricular fibrillation. 1, 4

Avoid flecainide and propafenone in patients with structural heart disease or recent myocardial infarction due to proarrhythmic risk. 6

All patients treated for SVT require referral to a heart rhythm specialist for consideration of definitive therapy. 3