Supraventricular Tachycardia

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.

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.

• 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.

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.

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.

• 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.

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.

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]

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.

1. Vagal maneuver unsuccessful: proceed to IV adenosine, confirming any prior dose was actually a true rapid push through a working, proximal IV line followed immediately by a saline flush — a slow push or a small/distal IV is the most common reason adenosine appears not to work.
2. Adenosine unsuccessful after the full 6 mg, then 12 mg, then 12 mg sequence: reassess whether this could be atrial fibrillation or flutter rather than AVNRT/AVRT (adenosine will not terminate these, though transient AV block can unmask flutter waves), then proceed to an IV calcium channel blocker or IV beta-blocker if the rhythm is confirmed to be regular narrow-complex SVT with no pre-excitation concern.
3. Second-line IV agent unsuccessful, contraindicated, or the patient becomes unstable at any point: proceed to immediate synchronized electrical cardioversion rather than trialing a third pharmacologic agent.
4. Frequent recurrence despite successful acute termination: refer for catheter ablation evaluation rather than defaulting to indefinite chronic drug therapy — ablation is a reasonable first discussion, not only a last resort.
5. Breakthrough episodes on an adequately dosed first-line chronic beta-blocker or calcium channel blocker: escalate to flecainide or propafenone (only if no coronary artery disease or structural heart disease) or sotalol, always paired with an AV-nodal-blocking agent when using a Class IC drug to prevent rapid 1:1 conduction if the rhythm organizes into atrial flutter, and revisit ablation.
6. Any episode of pre-excited atrial fibrillation, or any WPW patient with rapidly conducted SVT: refer urgently to electrophysiology for ablation regardless of how well the acute episode responded to treatment.

• 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.

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.

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.

Beta-blockers

Second-line acute agents (alternative to a calcium channel blocker); also first-line chronic suppressive therapy alongside a calcium channel blocker.

Class IA antiarrhythmic

Specific role in pre-excited atrial fibrillation with Wolff-Parkinson-White syndrome, where AV-nodal-blocking agents are dangerous.

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.

Class III antiarrhythmics

Reserve tier for chronic suppression once a beta-blocker or calcium channel blocker has failed and ablation is not being pursued.