What is the treatment for supraventricular tachycardia (SVT)?

Treatment of Supraventricular Tachycardia

For hemodynamically stable SVT, begin with vagal maneuvers (particularly the modified Valsalva maneuver), followed immediately by intravenous adenosine if vagal maneuvers fail; for hemodynamically unstable patients, proceed directly to synchronized cardioversion. 1

Acute Management Algorithm

Step 1: Assess Hemodynamic Stability

Determine if the patient shows signs of hemodynamic instability including hypotension, altered mental status, signs of shock, chest pain, or acute heart failure symptoms. 2, 1

If hemodynamically unstable: Proceed immediately to synchronized cardioversion—this successfully restores sinus rhythm in all patients and must be performed promptly. 2, 3

If hemodynamically stable: Continue to Step 2.

Step 2: Vagal Maneuvers (First-Line for Stable Patients)

• Modified Valsalva maneuver is the most effective technique with a 43% success rate for converting SVT to sinus rhythm. 1, 4
• Overall, vagal maneuvers have approximately 27.7% success rate across all techniques. 1
• Critical pitfall: Never apply pressure to the eyeball—this practice is dangerous and has been abandoned. 3

Step 3: Adenosine (Second-Line for Stable Patients)

If vagal maneuvers fail, adenosine is highly effective with 90-95% success rates for terminating AVNRT and orthodromic AVRT. 1, 4, 5

Dosing protocol: 2

• Initial dose: 6 mg rapid IV bolus (injected as proximal to the heart as possible), administered over 1-2 seconds, followed by rapid saline flush
• If no response within 1-2 minutes: 12 mg rapid IV bolus
• Can repeat 12 mg dose one additional time if needed

Expected side effects: Approximately 30% of patients experience brief transient effects including flushing, chest pain, hypotension, dyspnea, or transient AV block—these resolve within seconds due to adenosine's extremely short half-life. 2, 1

Critical warnings: 2, 6

• Adenosine can precipitate atrial fibrillation or cause decompensation in patients with pre-excitation (Wolff-Parkinson-White syndrome)
• Rare cases of ventricular fibrillation have been reported, even in structurally normal hearts
• Mandatory requirement: Prompt access to resuscitation, defibrillation, and transcutaneous pacing equipment must be immediately available with every adenosine administration

Step 4: Alternative IV Medications (If Adenosine Fails or Is Contraindicated)

Calcium channel blockers (Class IIa recommendation): 2

• IV diltiazem: 0.25 mg/kg IV bolus over 2 minutes, followed by infusion at 5-10 mg/h (up to 15 mg/h)
• IV verapamil: 5-10 mg (0.075-0.15 mg/kg) IV bolus over 2 minutes; if no response, can give additional 10 mg 30 minutes after first dose
• Success rates: 80-98% for conversion to sinus rhythm 2, 1
• Slow infusion up to 20 minutes may lessen potential for hypotension 2

IV beta-blockers (Class IIa recommendation): 2

• Esmolol: 500 mcg/kg IV bolus over 1 minute, followed by infusion at 50-300 mcg/kg/min
• Metoprolol: 2.5-5.0 mg IV bolus over 2 minutes; can repeat every 10 minutes up to 3 doses
• Propranolol: 1 mg IV over 1 minute; can repeat at 2-minute intervals up to 3 doses

Critical contraindications for calcium channel blockers and beta-blockers: 2, 3

• Do NOT use in wide-complex tachycardia unless SVT with aberrancy is definitively proven—these agents may cause hemodynamic collapse in ventricular tachycardia
• Avoid in patients with suspected VT, pre-excited atrial fibrillation, or systolic heart failure
• Contraindicated in patients with AV block greater than first degree or SA node dysfunction

Step 5: Synchronized Cardioversion (If Medications Fail)

For hemodynamically stable patients whose SVT is refractory to pharmacological therapy or when medications are contraindicated, synchronized cardioversion is highly effective and should be performed after adequate sedation or anesthesia. 2

Special Considerations for Pre-Excited Atrial Fibrillation

For stable patients with pre-excited AF: Use ibutilide or IV procainamide—avoid AV nodal blocking agents (adenosine, calcium channel blockers, beta-blockers, digoxin) as these may enhance conduction over the accessory pathway and precipitate ventricular fibrillation. 1

For unstable patients with pre-excited AF: Immediate synchronized cardioversion is indicated. 2

Long-Term Management

Catheter Ablation (First-Line for Prevention)

Catheter ablation is the most effective therapy to prevent recurrent SVT, with success rates of 94.3-98.5% and recurrence rates <5%. 1, 3, 4

• All patients treated for SVT should be referred for heart rhythm specialist opinion to discuss ablation. 7
• Ablation is recommended as first-line therapy for preventing symptomatic recurrent SVT. 1, 3

Pharmacological Options (For Patients Declining or Not Candidates for Ablation)

First-line oral medications: 2, 1

• Beta-blockers, diltiazem, or verapamil (Class I recommendation in absence of pre-excitation)
• These reduce frequency and duration of SVT episodes

Second-line options for patients without structural heart disease: 2, 1

• Flecainide or propafenone (Class IIa recommendation)
• Critical warning: Flecainide can cause proarrhythmic effects in 4% of supraventricular arrhythmia patients, including exacerbations of SVT and rare ventricular arrhythmias. 8
• Contraindicated in patients with structural heart disease, ischemic heart disease, or history of myocardial infarction

Third-line options: 2

• Amiodarone, dofetilide, or sotalol (Class IIb recommendation)
• Digoxin in absence of pre-excitation (Class IIb recommendation)

Critical Pitfalls to Avoid

• Never use calcium channel blockers or beta-blockers for wide-complex tachycardia unless SVT with aberrancy is definitively proven on ECG. 3
• Never use AV nodal blocking agents (adenosine, verapamil, diltiazem, beta-blockers, digoxin) in patients with pre-excited atrial fibrillation—this can accelerate ventricular rate and precipitate ventricular fibrillation. 2, 1
• Always have resuscitation equipment immediately available when administering adenosine. 6
• Ensure proper ECG diagnosis before treatment to distinguish SVT from ventricular tachycardia. 3