Supraventricular Tachycardia
Clinical Snapshot
Supraventricular tachycardia (SVT) is a general term for any tachyarrhythmia arising from atrial tissue or the atrioventricular (AV) node — that is, from above the ventricles — typically producing a narrow QRS complex (120 ms or less) unless aberrant conduction or a pre-existing bundle branch block widens it. The two most common re-entrant forms, AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant tachycardia (AVRT, using a congenital accessory pathway), usually occur in a structurally normal heart, start and stop abruptly, and are typically benign though often distressing to the patient. Because atrial fibrillation and atrial flutter are technically also supraventricular in origin but carry a real thromboembolic risk and a fundamentally different management approach — a rate-or-rhythm-control strategy plus a stroke-risk-based anticoagulation decision, not vagal maneuvers and adenosine — this chapter focuses specifically on regular narrow-complex SVT (AVNRT, AVRT, and focal atrial tachycardia) while addressing the acute differential from atrial fibrillation/flutter and the distinct danger of AV-nodal-blocking drugs in Wolff-Parkinson-White (WPW) syndrome with pre-excited atrial fibrillation.
Recognize the Condition
Typical presentation
Regular narrow-complex SVT characteristically starts and stops abruptly — patients often describe a sudden "switch flipping" sensation rather than a gradual speeding up, which is itself a useful clue distinguishing it from sinus tachycardia. Common symptoms include rapid, regular palpitations, lightheadedness, dyspnea, and chest tightness or discomfort during the episode. Rapid, visible pulsations in the neck (sometimes called the "frog sign") can occur in AVNRT specifically, caused by the atria contracting against a closed tricuspid valve at the same time as the ventricles. Polyuria shortly after an episode ends is a recognized feature, related to atrial stretch and natriuretic peptide release during the tachycardia. More severe episodes can cause pre-syncope or syncope, particularly with a very rapid ventricular rate or underlying structural heart disease.
The 3 mechanisms behind regular narrow-complex SVT
AV nodal re-entrant tachycardia (AVNRT)
The most common form in adults, more frequent in women. A re-entrant circuit forms using two functionally distinct pathways within the AV node itself (a "fast" and a "slow" pathway) rather than any accessory structure outside the node. The heart is usually structurally normal.
AV re-entrant tachycardia (AVRT)
Uses a congenital accessory pathway connecting the atria and ventricles outside the AV node as one limb of a re-entrant circuit, with the AV node as the other limb. When the accessory pathway also conducts antegrade during sinus rhythm, it produces the delta wave and short PR interval of Wolff-Parkinson-White syndrome on a resting ECG (manifest pre-excitation); when it conducts only retrograde, the resting ECG is normal (concealed pathway).
Focal atrial tachycardia
Arises from a localized area of atrial tissue capable of rapid automatic or triggered firing, rather than a re-entrant circuit. Usually benign, but can cause a reversible tachycardia-induced cardiomyopathy if it persists, unrecognized, for a prolonged period.
Risk Factors
- Female sex — AVNRT in particular is more common in women.
- A congenital accessory pathway (manifest or concealed) predisposing to AVRT.
- Caffeine, alcohol, or stimulant medication/recreational drug use as an episode trigger in some patients — though many patients have no consistent identifiable trigger.
- Structural heart disease, more relevant to focal atrial tachycardia and to SVT occurring after cardiac surgery.
- Thyroid dysfunction and other systemic causes of an atrial arrhythmia, particularly for focal atrial tachycardia.
- Digoxin toxicity is a classic, specific cause of certain atrial tachycardias and should be considered in any patient taking digoxin who develops a new atrial arrhythmia.
Red Flags & Refer
Any tachyarrhythmia causing hemodynamic compromise is itself a red flag requiring immediate synchronized cardioversion rather than continued pharmacologic escalation.
- Hemodynamic instability during the tachycardia — hypotension, altered mental status, signs of shock, or acute pulmonary edema — requires immediate synchronized electrical cardioversion, not a further trial of pharmacotherapy.
- Chest pain or syncope occurring during the tachycardia episode, which raises concern for underlying structural or ischemic heart disease and warrants prompt evaluation beyond simple rhythm termination.
- An irregularly irregular, wide-and-variable-complex tachycardia in a patient with known or suspected Wolff-Parkinson-White syndrome (pre-excited atrial fibrillation) — do not give adenosine, an IV calcium channel blocker, an IV beta-blocker, or digoxin; these can precipitate ventricular fibrillation in this specific setting.[1]
- A wide-complex tachycardia of uncertain origin in a hemodynamically unstable patient should be treated as ventricular tachycardia until proven otherwise — do not assume it is SVT with aberrancy.
- Any patient with newly discovered or previously known pre-excitation (delta wave) who has had a documented episode of rapidly conducted SVT or atrial fibrillation needs urgent electrophysiology referral for ablation.
Assessment & Diagnosis
Differentiating regular narrow-complex SVT from atrial fibrillation and atrial flutter
Because atrial fibrillation and flutter are technically supraventricular but need a fundamentally different management approach — a rate-or-rhythm-control strategy plus a stroke-risk-based anticoagulation decision, rather than vagal maneuvers and adenosine[2] — confirming which rhythm is present matters as much as recognizing that a tachyarrhythmia is occurring at all.
| Feature | Regular narrow-complex SVT (AVNRT/AVRT/focal AT) | Atrial fibrillation | Atrial flutter |
|---|---|---|---|
| Rhythm on ECG | Regular | Irregularly irregular | Regular, or regularly irregular with variable AV conduction |
| Atrial activity | P waves often hidden within or just after the QRS complex, or distorting the ST segment | No discrete P waves; a fibrillatory baseline | Sawtooth flutter waves |
| Response to vagal maneuvers/adenosine | Typically terminates completely | Does not terminate; ventricular rate may transiently slow | Does not terminate; transient AV block can unmask flutter waves, which is diagnostically useful even though not curative |
| Thromboembolic/stroke risk | Not increased by the arrhythmia itself | Increased — needs a separate stroke-risk-based anticoagulation decision | Increased, managed the same as atrial fibrillation |
| Typical underlying heart | Usually structurally normal | Often has structural heart disease, but can occur without it | Often has structural heart disease, but can occur without it |
Treat any irregularly irregular tachycardia, or one showing flutter waves, as atrial fibrillation or flutter rather than as AVNRT/AVRT — their acute and long-term management, including the anticoagulation decision, diverges sharply from the regular narrow-complex SVT covered in the rest of this chapter.
History
- Characterize onset and offset — abrupt in AVNRT/AVRT, more gradual in sinus tachycardia and often in focal atrial tachycardia.
- Ask about duration, frequency, and any identifiable trigger (caffeine, alcohol, stimulants, exertion, emotional stress).
- Ask specifically about associated chest pain, syncope, or near-syncope during episodes, and about a family history of sudden cardiac death or known pre-excitation.
- Review the current medication list for any AV-nodal-blocking agent already on board, and for digoxin specifically if an atrial tachycardia is suspected.
Examination
- Vital signs, with specific attention to blood pressure and mental status to identify hemodynamic instability.
- Look for visible rapid neck pulsations (suggestive of AVNRT specifically).
- Assess for signs of heart failure or structural heart disease.
Investigations
- A 12-lead ECG captured during the tachycardia is the single most useful test — obtain one before any treatment is given whenever the patient's stability allows, since the rhythm often cannot be reproduced once it has terminated.[3]
- If the diagnosis remains uncertain, adenosine given during continuous ECG recording can be diagnostically useful even when it does not cure the arrhythmia: the transient AV block it produces can unmask flutter waves or atrial-tachycardia P waves that were hidden within the QRS/T wave at the faster rate.[4]
- Once sinus rhythm is restored, obtain a resting 12-lead ECG specifically to screen for a delta wave/pre-excitation pattern that may have been masked during the tachycardia.
- Ambulatory monitoring (Holter, or an event/patch monitor) for episodes not captured on a standard ECG, chosen based on how frequently episodes occur.
- Echocardiography to assess left ventricular function and structural heart disease — most useful when chronic antiarrhythmic therapy is being considered, when a re-entrant tachycardia has been present for a prolonged period (screening for tachycardia-induced cardiomyopathy), or when focal atrial tachycardia is suspected.
- Routine echocardiography is not required for a single, brief, self-terminated episode of typical AVNRT in an otherwise healthy patient with a normal examination and a normal ECG in sinus rhythm.
Treatment Targets
- Restore sinus rhythm during an acute episode — rhythm control is achievable in essentially all re-entrant SVT (AVNRT/AVRT) and is always the acute goal.
- Avoid harm from AV-nodal-blocking drugs in a patient with pre-excited atrial fibrillation/Wolff-Parkinson-White syndrome.
- Reduce or eliminate recurrent episodes with chronic suppressive therapy or, preferably, curative catheter ablation.
- Identify and refer appropriate candidates for catheter ablation rather than defaulting to indefinite drug therapy.
- Screen incidentally discovered pre-excitation (WPW pattern) for risk and refer for specialist evaluation.
Choose Initial Treatment
1st line Vagal maneuvers — modified Valsalva (preferred technique) or carotid sinus massage — for every hemodynamically stable episode of regular narrow-complex SVT, attempted before any drug is given.
1st-line pharmacotherapy — use when vagal maneuvers fail IV adenosine 6 mg as a rapid push immediately followed by a saline flush is the preferred agent; if the arrhythmia has not terminated within 1-2 minutes, give 12 mg the same way, and may repeat 12 mg once more if still unsuccessful.[4]
2nd line — use when adenosine fails after both repeat doses, recurs immediately, or is contraindicated (e.g. severe reactive airway disease) an IV nondihydropyridine calcium channel blocker (diltiazem or verapamil) in a patient with normal LV function, or an IV beta-blocker (metoprolol or esmolol) — do not combine both classes together.
Special situation — pre-excited atrial fibrillation in Wolff-Parkinson-White syndrome avoid adenosine, IV calcium channel blockers, IV beta-blockers, and digoxin entirely; use IV procainamide, or proceed directly to synchronized cardioversion if there is any hemodynamic instability.[1]
Stop trialing further drugs escalate to immediate synchronized electrical cardioversion for any hemodynamically unstable patient at any point in this sequence, rather than cycling through additional pharmacologic agents.
Non-Pharmacologic Treatment
Vagal maneuvers
- Modified Valsalva (preferred technique): have the patient exhale forcefully against a closed glottis, as if straining, for 15 seconds while semi-recumbent at roughly a 45-degree angle, then immediately assist the patient supine with the legs passively raised to roughly 45 degrees for a further 15 seconds — this modified sequence increases venous return and vagal tone more effectively than a standard Valsalva alone and should be attempted first.
- Carotid sinus massage: apply firm pressure to one carotid sinus for 5-10 seconds under continuous ECG and blood pressure monitoring; auscultate for a carotid bruit first and avoid in patients with known carotid stenosis or a history of stroke/TIA — massage one side at a time, never both simultaneously.
- Facial cold-water immersion (diving reflex): an alternative vagal maneuver used particularly in infants and young children who cannot cooperate with a Valsalva maneuver.
- Coach patients with recurrent, well-characterized episodes on how to self-perform a modified Valsalva maneuver at home as a first response before seeking care.
Electrical cardioversion
Synchronized direct-current cardioversion delivers a shock timed to the R wave to avoid inducing ventricular fibrillation, and is the definitive acute treatment whenever a patient becomes hemodynamically unstable during SVT, or when pharmacologic therapy fails or is inappropriate (e.g., pre-excited atrial fibrillation with instability). A biphasic defibrillator is preferred over a monophasic one given a lower required energy dose; begin with anterior-apex pad placement and switch to an antero-posterior position if the first attempt is unsuccessful.
Catheter ablation
Catheter ablation delivers targeted radiofrequency or cryothermal energy to the specific re-entrant circuit or accessory pathway responsible for the arrhythmia, permanently eliminating it in most patients. Given its high cure rate and low complication rate for AVNRT, AVRT, and focal atrial tachycardia relative to indefinite antiarrhythmic drug therapy, ablation is considered a reasonable first-line option — not just a fallback after drug failure — for patients with recurrent symptomatic episodes, and is strongly recommended for any patient with Wolff-Parkinson-White syndrome and rapidly conducted pre-excited SVT given the real risk of sudden death in that specific population.[3] Discuss ablation as an option at the first specialist visit for a patient with recurrent, documented AVNRT/AVRT, rather than only after drug therapy has already failed.
Lifestyle counselling
Identify and counsel on reducing individual triggers where present — caffeine, alcohol, stimulant medications or recreational drugs, and sleep deprivation — though many patients have no consistent identifiable trigger, and this alone does not replace definitive management.
Special Populations
Pregnancy
Vagal maneuvers remain first-line and are safe throughout pregnancy. IV adenosine is considered the preferred pharmacologic agent for acute termination in pregnancy given its extremely short half-life and lack of demonstrated fetal harm.[3] IV beta-blockers and IV calcium channel blockers can be used if adenosine fails, with standard maternal hemodynamic monitoring. For chronic suppressive therapy, an oral beta-blocker is generally preferred; catheter ablation can be deferred until after delivery when possible, though it is not absolutely contraindicated during pregnancy for refractory recurrent episodes when performed with a radiation-minimizing technique.
Breastfeeding
Adenosine's effect is confined to the moment of administration and is compatible with breastfeeding. Beta-blockers and nondihydropyridine calcium channel blockers used for chronic suppression are also generally considered compatible with breastfeeding; monitor the infant for excess sedation or poor feeding if a maternal beta-blocker is used.
Pediatrics
SVT, usually AVRT via a concealed or manifest accessory pathway, is the most common significant arrhythmia in infants and children. Vagal maneuvers are first-line, with facial cold-water/ice immersion preferred over carotid sinus massage or Valsalva coaching in infants who cannot cooperate. IV adenosine remains first-line pharmacotherapy, weight-based (0.05-0.1 mg/kg initial, increasing by 0.05-0.1 mg/kg if needed to a maximum of 0.3 mg/kg for patients under 50 kg; standard adult dosing at 50 kg or above). Refer all children with SVT to pediatric cardiology, since natural history, drug selection, and ablation timing differ substantially from adults.
Older adults
Use lower initial doses of IV and oral AV-nodal-blocking agents given a higher prevalence of sinus node dysfunction and conduction system disease; precede carotid sinus massage with auscultation for a bruit and use it cautiously given a higher prevalence of carotid disease in this population.
Wolff-Parkinson-White syndrome and pre-excitation
In Wolff-Parkinson-White (WPW) syndrome, a congenital accessory pathway connects the atria directly to the ventricles, bypassing the AV node; when this pathway conducts antegrade during sinus rhythm it produces the classic delta wave and short PR interval on a resting ECG. A regular tachycardia in a WPW patient using this pathway as one limb of a re-entrant circuit (orthodromic AVRT) is managed the same way as any other regular narrow-complex SVT, including with adenosine.[3]
The genuine danger arises specifically when a WPW patient develops atrial fibrillation that conducts, at least partly, down the accessory pathway (pre-excited atrial fibrillation) — this typically appears as an irregularly irregular, wide-and-variable-complex tachycardia, often at a very rapid ventricular rate. Adenosine, IV calcium channel blockers, IV beta-blockers, and digoxin all act primarily by slowing conduction through the AV node; in this specific setting they do not slow the accessory pathway, and can preferentially block the only limb that was protecting the ventricle from the full atrial rate — paradoxically accelerating ventricular conduction and precipitating ventricular fibrillation.[1]
Manage suspected pre-excited atrial fibrillation with procainamide, which does slow accessory-pathway conduction, or with immediate synchronized cardioversion in any hemodynamically unstable patient — never with an AV-nodal-blocking agent. Catheter ablation is strongly recommended for any patient with WPW and documented rapidly conducted pre-excited SVT/atrial fibrillation, and should also be discussed for asymptomatic pre-excitation found incidentally on a resting ECG, since risk stratification (and often ablation) is warranted even before symptoms occur.[3]
Monitoring & Follow-Up
Obtain a 12-lead ECG once sinus rhythm is restored to confirm resolution and specifically screen for a delta wave/pre-excitation pattern that may have been masked by the tachycardia — a newly found WPW pattern changes both the drug selection for any future episode and the referral pathway. For episodes not captured on a standard ECG, arrange ambulatory monitoring (a Holter for daily/near-daily symptoms, an event or patch monitor for infrequent episodes) to document the rhythm before committing to chronic therapy. Patients started on chronic antiarrhythmic therapy need drug-specific monitoring — QT interval and electrolytes for sotalol, QRS duration for flecainide/propafenone, and periodic reassessment of the ongoing need for the drug at all, since many patients on long-term suppressive therapy are, in retrospect, good candidates for a curative ablation instead. Reassess symptom burden and quality of life at every follow-up — this, not simply whether episodes occurred, is what should trigger a referral or therapy-change discussion.
Common Errors to Avoid
- Giving adenosine as a slow push, through a small or distal IV, or without an immediate saline flush — its half-life is under 10 seconds, so anything less than a true rapid push directly into a proximal vein followed by a rapid flush will be metabolized before it reaches the heart.
- Using an AV-nodal-blocking drug (adenosine, an IV calcium channel blocker, an IV beta-blocker, or digoxin) in an irregularly irregular, wide-and-variable-complex tachycardia suspicious for pre-excited atrial fibrillation in WPW.
- Trialing a sequence of drugs in a hemodynamically unstable patient instead of proceeding immediately to synchronized cardioversion.
- Combining an IV beta-blocker and an IV calcium channel blocker — both are AV-nodal blocking, and the combination carries a real additive bradycardia, hypotension, and arrest risk.
- Assuming any irregular narrow-complex tachycardia is simply "SVT" and treating it with adenosine — adenosine will not terminate atrial fibrillation, and while it can transiently unmask flutter waves for diagnostic purposes, it is not a treatment for atrial flutter or fibrillation.
- Missing a delta wave/pre-excitation pattern on a post-conversion ECG, and therefore missing its implications for future drug selection and referral.
- Using oral diltiazem or verapamil in a patient with a wide-complex tachycardia of uncertain origin — if it is actually ventricular tachycardia, an AV-nodal-blocking calcium channel blocker can cause hemodynamic collapse.
- Not identifying candidates for curative catheter ablation and leaving them on indefinite chronic drug therapy instead of discussing ablation as a first-line option.
Clinical Decision Algorithm
Drug Tables
How to use this table: Doses are adult doses and require patient-specific confirmation (renal/hepatic function, weight, allergy history). Pediatric dosing is weight-based per the current product monograph unless stated. Drug pricing is intentionally omitted. Select any drug name to open its complete Pharmasist Drug Database page.
Purine nucleoside
First-line acute pharmacotherapy after vagal maneuvers fail.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Adenosine | Initial dose: 6 mg rapid IV push over 1-2 seconds, immediately followed by a 20 mL saline flush If unsuccessful at 1-2 minutes: 12 mg rapid IV push with flush; may repeat 12 mg once more if still unsuccessful Pediatrics (under 50 kg): 0.05-0.1 mg/kg rapid IV push, increasing by 0.05-0.1 mg/kg if needed to a maximum of 0.3 mg/kg Pediatrics (50 kg or more): Standard adult dosing | Transient flushing, chest tightness/dyspnea, transient high-grade AV block or asystole (expected and self-limited given the ultra-short half-life), bronchospasm | Theophylline/caffeine antagonize the effect (a larger dose may be needed); dipyridamole potentiates the effect (reduce the dose); carbamazepine may worsen heart block | Must be given as a true rapid IV push directly followed by a rapid saline flush via a proximal, large-bore IV — the half-life is under 10 seconds, so anything slower will be metabolized before reaching the heart. |
Nondihydropyridine calcium channel blockers
Second-line acute agents (in a patient without pre-excited atrial fibrillation and without decompensated heart failure); also used chronically for suppression.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Diltiazem | Acute IV: 0.25 mg/kg IV over 2 minutes; may give an additional 0.35 mg/kg IV after 15 minutes if needed Chronic oral: 180-360 mg/day in divided or extended-release dosing, per current product-specific titration | Hypotension, bradycardia, constipation | Do not combine with an IV beta-blocker; inhibits the metabolism of several CYP3A4 substrates | Use with caution in reduced LV ejection fraction. |
| Verapamil | Acute IV: 5-10 mg IV over 2 minutes; may give an additional 10 mg IV after 30 minutes if needed Chronic oral: 120-480 mg/day, per current product-specific titration | Hypotension, bradycardia, constipation, flushing | Do not combine with an IV beta-blocker; inhibits the metabolism of several CYP3A4 substrates | Use with caution in reduced LV ejection fraction. |
Beta-blockers
Second-line acute agents (alternative to a calcium channel blocker); also first-line chronic suppressive therapy alongside a calcium channel blocker.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Metoprolol | Acute IV: 2.5-5 mg IV over 2 minutes, may repeat every 5 minutes to a total of 3 doses Chronic oral: 50-200 mg/day in 1-2 divided doses, per current product-specific titration | Hypotension, bradycardia, bronchospasm, fatigue | Do not combine with an IV calcium channel blocker | |
| Esmolol | Acute IV: Loading 0.5 mg/kg IV over 1 minute, then a maintenance infusion starting at 0.05 mg/kg/min, titrated per response | Hypotension, bradycardia | Contraindicated within 24 hours of IV verapamil/diltiazem | Ultra-short half-life (about 9 minutes) allows rapid reversal if not tolerated. |
| Propranolol | Acute IV: 1-3 mg IV, given no faster than 1 mg/minute, may repeat once after several minutes Chronic oral: 80-240 mg/day in divided doses, per current product-specific titration | Hypotension, bradycardia, bronchospasm, fatigue, depression | Do not combine with an IV calcium channel blocker | Non-selective; use with more caution in reactive airway disease than a beta-1-selective agent. |
| Bisoprolol | Chronic oral: 2.5-10 mg once daily | Bradycardia, hypotension, fatigue | Additive bradycardia with a calcium channel blocker or digoxin | Beta-1-selective; chronic oral use only. |
| Atenolol | Chronic oral: 50-150 mg once daily | Bradycardia, hypotension, fatigue | Additive bradycardia with a calcium channel blocker or digoxin | Beta-1-selective; chronic oral use only. |
Class IA antiarrhythmic
Specific role in pre-excited atrial fibrillation with Wolff-Parkinson-White syndrome, where AV-nodal-blocking agents are dangerous.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Procainamide | IV loading (direct injection): 100 mg IV every 5 minutes (rate not exceeding 50 mg/minute) until the arrhythmia is suppressed or a total of 1 g has been given IV loading (infusion alternative): 500-600 mg infused over 25-30 minutes IV maintenance: 2-6 mg/minute, adjusted for body weight, circulatory status, and renal function | Hypotension (can be precipitous with IV use), QRS widening, torsades de pointes, granulocytopenia (rare) | Additive QT prolongation with other QT-prolonging drugs; amiodarone reduces its clearance | Chosen specifically because it slows conduction through the accessory pathway itself, unlike adenosine, calcium channel blockers, beta-blockers, or digoxin. Requires continuous ECG and blood pressure monitoring during IV administration. |
Class IC antiarrhythmics
Second-line chronic suppressive therapy, or single-dose pill-in-the-pocket use in carefully selected patients. Contraindicated in coronary artery disease or structural heart disease.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Flecainide | Chronic oral: 50 mg PO every 12 hours initial, titrate based on QRS interval to a maximum of 200 mg every 12 hours Pill-in-the-pocket: 300 mg PO single dose if 70 kg or more; 200 mg PO single dose if under 70 kg | Blurred vision, tremor, proarrhythmia, heart failure | Metabolized by CYP2D6 — many potential interactions | Always co-prescribe an AV-nodal-blocking agent (beta-blocker or nondihydropyridine calcium channel blocker) to prevent rapid 1:1 conduction if the rhythm organizes into atrial flutter. |
| Propafenone | Chronic oral: 150 mg PO every 8 hours initial, titrate based on QRS interval to a maximum of 300 mg every 8 hours Pill-in-the-pocket: 600 mg PO single dose if 70 kg or more; 450 mg PO single dose if under 70 kg | Constipation, headache, metallic taste, proarrhythmia | Reduces digoxin levels by 25-50%; metabolized by CYP2D6 — many potential interactions | Always co-prescribe an AV-nodal-blocking agent for the same reason as flecainide. Monitor QRS duration carefully. |
Class III antiarrhythmics
Reserve tier for chronic suppression once a beta-blocker or calcium channel blocker has failed and ablation is not being pursued.
| Drug | Dosage | Adverse effects | Drug interactions | Comments |
|---|---|---|---|---|
| Sotalol | Chronic oral: 80 mg PO twice daily initial, titrate every 2-3 days to a usual range of 160-320 mg/day in 2 divided doses | Torsades de pointes, bradycardia, bronchospasm, worsening heart failure | Additive QT prolongation with other QT-prolonging drugs; additive bradycardia with a calcium channel blocker, digoxin, or another beta-blocker | Initiate and up-titrate only in hospital with continuous ECG/QT monitoring. |
| Amiodarone | Chronic oral: Per current heart-rhythm-specific product-monograph titration; requires baseline and periodic thyroid/liver/pulmonary monitoring | Thyroid dysfunction, pulmonary fibrosis, hepatotoxicity, photosensitivity, corneal deposits | Reduces the clearance of digoxin, warfarin, and procainamide — reduce their doses when combined | Reserve for recurrent focal atrial tachycardia when a beta-blocker/calcium channel blocker has failed and ablation is being deferred — consider ablation before committing to long-term amiodarone given its extracardiac toxicity burden. |
References
- Pre-Excited Atrial Fibrillation in Wolff-Parkinson-White (WPW) Syndrome: A Case Report and a Review of the Literature — Reviews in Cardiovascular Medicine (Schiavone M, Filtz A, Gasperetti A, Zhang X, Forleo GB, Santangeli P, Di Biase L). Rev Cardiovasc Med 2024;25(4):125
- The 2020 Canadian Cardiovascular Society/Canadian Heart Rhythm Society Comprehensive Guidelines for the Management of Atrial Fibrillation — Canadian Journal of Cardiology, Canadian Cardiovascular Society/Canadian Heart Rhythm Society (Andrade JG, Aguilar M, Atzema C, et al.). Can J Cardiol 2020;36(12):1847-1948
- 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia — Circulation, American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society (Page RL, Joglar JA, Caldwell MA, et al.). Circulation 2016;133(14):e506-e574
- Adenosine for paroxysmal supraventricular tachycardia: dose ranging and comparison with verapamil. Assessment in placebo-controlled, multicenter trials — Annals of Internal Medicine (DiMarco JP, Miles W, Akhtar M, et al.). Ann Intern Med 1990;113(2):104-110
Professional reference only. Apply clinical judgment and verify patient-specific decisions against current authoritative guidance and product information.