1. Introduction

Prompt termination of supraventricular tachycardia (SVT) is essential to restore atrioventricular synchrony, optimize cardiac output, and prevent hypotension, ischemia, or organ hypoperfusion.

Goals of Management

• Restore sinus rhythm or control ventricular rate to maintain adequate perfusion.
• Choose pharmacologic agents that balance efficacy with the risk of adverse effects such as hypotension or bradycardia.

Safety Considerations

A thorough assessment of the patient’s hemodynamic status, presence of underlying conduction disease, and relevant comorbidities is crucial before selecting any pharmacologic agent.

2. Non-Pharmacologic Interventions

Vagal maneuvers are safe, readily available bedside techniques that increase parasympathetic tone to transiently block AV nodal conduction. They may terminate AVNRT or AVRT.

A. Valsalva Maneuver

• Standard Technique: Patient strains (e.g., blows into a 10mL syringe to move the plunger) for 15-20 seconds while in a supine or semi-recumbent position. Efficacy is approximately 20-30%.
• Modified Technique: Patient strains in a semi-recumbent position, followed by immediate repositioning to supine with passive leg raise to 45 degrees for 15-30 seconds. This modification can boost conversion rates to around 40%.

B. Carotid Sinus Massage

Apply firm, steady pressure unilaterally over the carotid sinus (located at the anterior border of the sternocleidomastoid muscle at the level of the cricoid cartilage) for 5-10 seconds. Auscultate for carotid bruits before attempting; contraindicated in patients with known carotid stenosis or recent TIA/stroke.

C. Diving Reflex

Immersion of the face in ice-cold water for up to 30 seconds. This maneuver is more commonly used and effective in the pediatric population.

3. Pharmacotherapy in Typical SVT (AVNRT/AVRT)

In hemodynamically stable patients with typical SVT (AVNRT/AVRT) refractory to vagal maneuvers, intravenous adenosine is the first-line pharmacologic agent. If adenosine is ineffective or contraindicated, calcium channel blockers (diltiazem) or beta-blockers may be used. Hemodynamically unstable patients require urgent synchronized electrical cardioversion.

A. Adenosine

• Mechanism: Activates A1 receptors in the AV node, leading to potassium efflux, hyperpolarization, and transient AV nodal block, interrupting reentrant circuits involving the AV node.
• Indication: First-line therapy for termination of regular, narrow-complex SVT (AVNRT, AVRT) refractory to vagal maneuvers.
• Dosing & Administration: Initial dose is 6 mg administered as a rapid IV push over 1–2 seconds via a proximal large-bore IV, immediately followed by a 20 mL saline flush. If there is no response within 1–2 minutes, a second dose of 12 mg may be given once.
• Pharmacokinetics/Pharmacodynamics: Ultra-short half-life (<10 seconds) due to rapid uptake by erythrocytes and endothelial cells. Efficacy is highly dependent on rapid delivery to central circulation.
• Monitoring: Continuous ECG and blood pressure monitoring. Observe for transient AV block, sinus bradycardia, or asystole. Be prepared for potential arrhythmia recurrence.
• Contraindications: Second- or third-degree AV block or sick sinus syndrome (unless a functional pacemaker is present), known hypersensitivity, severe bronchospastic lung disease (e.g., severe asthma).
• Pearls & Pitfalls:
  • If SVT does not terminate, adenosine may unmask underlying atrial activity (e.g., atrial flutter waves, atrial tachycardia).
  • Common transient side effects include flushing, chest discomfort or pressure, and dyspnea. These are usually very short-lived.
  • Use with caution in patients with transplanted hearts (may have denervated hearts and exaggerated response; consider lower initial doses like 3 mg). Larger doses may be needed in patients taking a P1 receptor antagonist (e.g., theophylline, caffeine). Smaller doses may be needed in patients taking a nucleoside transport inhibitor (e.g., dipyridamole, carbamazepine).

B. Diltiazem

• Mechanism: Non-dihydropyridine calcium channel blocker (CCB) that slows AV nodal conduction and prolongs the AV nodal refractory period.
• Indication: Termination of SVT refractory to adenosine, or when adenosine is contraindicated or ineffective. Can also be used for rate control in atrial fibrillation/flutter.
• Dosing: Initial bolus of 0.25 mg/kg actual body weight (commonly 15–20 mg for an average adult) IV over 2 minutes. If the response is inadequate after 15 minutes, a second bolus of 0.35 mg/kg (commonly 20–25 mg) may be given. A continuous infusion of 5–15 mg/hour can be used for ongoing rate control.
• Pharmacokinetics/Pharmacodynamics: Onset of action is 2–5 minutes; duration of action is 1–3 hours. Metabolized hepatically via CYP3A4.
• Monitoring: Blood pressure (q5min during bolus/titration), PR interval, and continuous ECG. Watch for hypotension and bradycardia.
• Contraindications: Severe hypotension (SBP <90 mmHg), cardiogenic shock, decompensated heart failure with reduced ejection fraction (HFrEF), second- or third-degree AV block or sick sinus syndrome (without a pacemaker), Wolff-Parkinson-White (WPW) syndrome, ventricular tachycardia.
• Pearls & Pitfalls:
  • Has a longer duration of action than adenosine; use a lower initial bolus or exercise caution in patients with borderline blood pressure.
  • Negative inotropic effects may precipitate or worsen heart failure in susceptible individuals. Be mindful of drug interactions (e.g., with beta-blockers, digoxin).

C. Beta-Blockers (Esmolol, Metoprolol)

• Mechanism: Block β1-adrenergic receptors in the AV node, slowing AV nodal conduction and increasing the AV nodal refractory period.
• Agent Selection:
  • Esmolol: Ultra-short-acting (half-life ~9 minutes), allowing for rapid titration and quick offset if adverse effects occur. Preferred in critically ill patients or when hemodynamic instability is a concern.
  • Metoprolol: Longer-acting, administered as IV boluses. Suitable if an infusion is not desired and longer duration of action is acceptable.
• Dosing:
  • Esmolol: Loading dose of 500 mcg/kg IV over 1 minute, followed by a continuous infusion starting at 50 mcg/kg/min. Titrate by 25-50 mcg/kg/min every 4-5 minutes as needed for heart rate control, up to a maximum of approximately 200-300 mcg/kg/min.
  • Metoprolol: 2.5–5 mg IV over 2 minutes; may be repeated every 5 minutes up to a total dose of 15 mg.
• Monitoring: Heart rate, blood pressure, continuous ECG, signs of bronchospasm (especially in patients with reactive airway disease).
• Contraindications: Severe asthma or bronchospastic disease, acute decompensated heart failure, severe bradycardia, second- or third-degree AV block (without a pacemaker), sick sinus syndrome (without a pacemaker), WPW syndrome.
• Pearls & Pitfalls:
  • Esmolol’s rapid onset and offset make it particularly useful in situations requiring tight control or when assessing tolerance to beta-blockade.
  • Negative inotropic effects can worsen left ventricular function; use with caution in patients with borderline cardiac function.

D. Refractory SVT & Electrical Cardioversion

• Indications: Hemodynamic instability (e.g., hypotension with signs of shock, altered mental status, acute heart failure, ischemic chest pain) due to SVT, or SVT that is refractory to appropriate pharmacologic interventions in stable patients.
• Technique: Synchronized electrical cardioversion. For narrow-complex regular SVT, initial energy is typically 50–100 Joules (biphasic). If the patient is conscious and time permits, provide sedation and analgesia (e.g., midazolam, fentanyl, propofol, etomidate).
• Post-Shock Care: Continuous ECG and hemodynamic monitoring. Identify and address any potential triggers for SVT. Consider maintenance antiarrhythmic therapy or referral for electrophysiology study if SVT is recurrent or associated with severe symptoms.

4. Management of Pre-Excited SVT (Wolff-Parkinson-White Syndrome)

In patients with Wolff-Parkinson-White (WPW) syndrome, an accessory pathway (bypass tract) allows electrical impulses to bypass the AV node. If SVT occurs (often orthodromic AVRT or pre-excited atrial fibrillation), AV nodal blocking agents are contraindicated as they can lead to preferential conduction down the accessory pathway, potentially precipitating ventricular fibrillation (VF).

A. Risks of AV Nodal Blockers in Pre-Excited Tachycardia

When an accessory pathway is present, blocking the AV node (the normal “brake” for ventricular rate during atrial tachyarrhythmias) can paradoxically accelerate ventricular response if the arrhythmia is atrial fibrillation or flutter conducting antegrade over the accessory pathway. This can lead to very rapid ventricular rates and degenerate into VF.

Prohibited Agents in Pre-Excited Atrial Fibrillation/Flutter or Undifferentiated Wide-Complex Tachycardia (possible pre-excitation):

• Adenosine
• Verapamil / Diltiazem (Non-dihydropyridine CCBs)
• Beta-blockers
• Digoxin

Note: For orthodromic AVRT (narrow complex SVT using the accessory pathway only for retrograde conduction), adenosine can be used cautiously if pre-excitation is not evident on the baseline ECG and the diagnosis is certain. However, if there’s any doubt or if atrial fibrillation with pre-excitation is suspected, these agents are best avoided.

B. Procainamide

• Mechanism: Class IA antiarrhythmic agent that blocks sodium channels, slowing conduction velocity and prolonging the refractory period in both the AV node and, importantly, the accessory pathway.
• Indication: Drug of choice for hemodynamically stable pre-excited SVT (e.g., orthodromic AVRT where accessory pathway involvement is known or suspected) or atrial fibrillation with a rapid ventricular response in patients with known WPW syndrome.
• Dosing: Administer as an IV infusion at a rate of 20–50 mg/min until the arrhythmia terminates, QRS complex widens by >50% of baseline, hypotension develops, or a total dose of approximately 17 mg/kg has been administered. Maintenance infusion: 1-4 mg/min.
• Monitoring: Continuous ECG monitoring (watch for QRS widening, QT prolongation, conversion to sinus rhythm), blood pressure every 3-5 minutes during infusion, and frequent assessment for signs of hypotension.
• Contraindications: Severe hypotension, cardiogenic shock, advanced heart failure, torsades de pointes, known procainamide or NAPA allergy, complete heart block. Use with caution in renal impairment due to accumulation of N-acetylprocainamide (NAPA), an active metabolite.
• Pearls & Pitfalls:
  • Infuse slowly and stop the infusion if significant QRS widening (>50% from baseline) or hypotension occurs.
  • Be prepared for potential proarrhythmic effects. Dose adjustment is necessary in renal impairment.

C. Electrical Cardioversion for Pre-Excited SVT

• Indications: Any hemodynamically unstable patient with pre-excited SVT (e.g., hypotension, altered mental status, signs of shock). Also indicated for stable pre-excited atrial fibrillation if procainamide is ineffective, contraindicated, or unavailable.
• Technique: Synchronized electrical cardioversion. For pre-excited atrial fibrillation or other wide-complex tachycardias in WPW, initial energy is typically 100–200 Joules (biphasic). Sedate if possible.
• Post-Shock Care: Continuous monitoring. All patients with WPW syndrome, especially those presenting with rapid tachyarrhythmias, should be referred for electrophysiology evaluation and consideration of definitive catheter ablation of the accessory pathway.

5. Clinical Decision Algorithms

Standardized algorithms enhance safety and streamline decision-making during the acute management of SVT, particularly under time pressure.

A. Algorithm for Typical SVT (AVNRT/AVRT – Narrow Complex, Regular)

B. Algorithm for Pre-Excited SVT (WPW)

6. Monitoring and Safety

Close and continuous monitoring of ECG and hemodynamic parameters is essential to detect the effectiveness of therapy and identify adverse events promptly.

• Continuous ECG Monitoring: Essential to observe for termination of SVT, recurrence, development of AV block (especially with adenosine, CCBs, beta-blockers), QRS widening (with procainamide), or other arrhythmias.
• Blood Pressure and Heart Rate: Monitor frequently (e.g., every 2-5 minutes) during IV drug administration/infusion and after each intervention. Hypotension and bradycardia are common adverse effects.
• Laboratory Monitoring: Check electrolytes (especially potassium and magnesium) as imbalances can predispose to arrhythmias. Monitor renal function if procainamide is used, as its metabolite NAPA is renally cleared.

Adverse Events and Rescue Measures

• Adenosine: Transient asystole or bradycardia is common and usually self-limiting. Bronchospasm can occur; treat supportively (e.g., inhaled beta-agonists if severe, though usually not required).
• Diltiazem / Beta-Blockers: Hypotension and/or bradycardia. Manage with IV fluids if hypotensive. Reduce or stop infusion. Atropine (0.5-1 mg IV) can be used for symptomatic bradycardia. Calcium chloride or glucagon may be considered for severe CCB or beta-blocker toxicity, respectively.
• Procainamide: Hypotension is common; slow or stop infusion. Proarrhythmia (e.g., Torsades de Pointes if QT prolongs significantly) can occur; stop infusion and manage specific arrhythmia.

7. Pearls, Pitfalls, and Practice Nuances

• Always confirm that a tachycardia is narrow-complex and regular before presumptively treating as typical AVNRT/AVRT with AV nodal blockers. If there is any doubt, especially if wide or irregular, consider expert consultation or alternative diagnostic/therapeutic approaches.
• Administer adenosine through the most proximal IV line possible (e.g., antecubital fossa) followed by a rapid saline flush to ensure it reaches the heart quickly due to its very short half-life.
• In patients with borderline hypotension, consider starting with reduced doses of calcium channel blockers or beta-blockers and titrate cautiously, or opt for agents with shorter half-lives like esmolol.
• The modified Valsalva maneuver should be attempted before pharmacologic therapy in stable patients with SVT, as it can be effective and avoids drug-related side effects.
• Synchronized electrical cardioversion remains the fastest and most reliable therapy for any SVT causing hemodynamic instability. Do not delay cardioversion in unstable patients by attempting multiple drug therapies.
• Early referral to an electrophysiologist for consideration of catheter ablation is crucial for patients with recurrent SVT, SVT associated with high-risk features (e.g., WPW with rapid conduction), or when patient preference favors a definitive cure.