# Supraventricular Tachycardias

## Classification and Mechanisms

### Definitions

Supraventricular tachycardia encompasses any tachyarrhythmia that requires atrial or atrioventricular nodal tissue for its initiation and maintenance. The QRS complex is typically narrow, measuring less than 120 milliseconds, unless aberrant conduction or a preexisting bundle branch block is present. The differential diagnosis for a regular narrow complex tachycardia includes sinus tachycardia, atrioventricular nodal reentrant tachycardia, orthodromic atrioventricular reentrant tachycardia, atrial tachycardia, atrial flutter, and junctional tachycardia. When the narrow complex tachycardia is irregular, the differential shifts to atrial fibrillation, multifocal atrial tachycardia characterized by three or more P-wave morphologies with variable PP, PR, and RR intervals, and atrial flutter with variable atrioventricular block.

### AVNRT (Atrioventricular Nodal Reentrant Tachycardia)

Atrioventricular nodal reentrant tachycardia is the most common regular supraventricular tachycardia, accounting for approximately 60% of all SVTs. Its mechanism depends on the presence of dual atrioventricular nodal physiology, wherein a fast pathway with a short effective refractory period and long conduction time coexists with a slow pathway that has a long effective refractory period and short conduction time, both located within or near the AV node.

Typical or slow-fast AVNRT involves antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. Because atrial and ventricular activation are nearly simultaneous, the RP interval is characteristically less than 70 milliseconds, and P waves are either buried within the QRS complex or manifest as a pseudo-r prime deflection in lead V1 or a pseudo-S wave in leads II, III, and aVF. Atypical fast-slow AVNRT conducts antegradely through the fast pathway and retrogradely through the slow pathway, producing a long RP tachycardia in which the RP interval exceeds the PR interval and P waves are visible before the next QRS complex, inverted in the inferior leads. Atypical slow-slow AVNRT uses two slow pathways and produces an intermediate RP interval.

### AVRT (Atrioventricular Reentrant Tachycardia)

Atrioventricular reentrant tachycardia requires an accessory pathway connecting the atrium and ventricle outside the normal conduction system. Orthodromic AVRT, the most common type, conducts antegradely through the AV node and retrogradely through the accessory pathway, producing a narrow QRS with a P wave visible in the ST segment and an RP interval shorter than the PR interval. Antidromic AVRT conducts antegradely through the accessory pathway and retrogradely through the AV node, producing a wide QRS that is maximally preexcited. This rare form, accounting for approximately 5% of Wolff-Parkinson-White-related tachycardias, must be differentiated from ventricular tachycardia.

A concealed accessory pathway conducts only retrogradely and therefore produces no delta wave on the resting electrocardiogram, presenting exclusively as orthodromic AVRT. A manifest accessory pathway, the Wolff-Parkinson-White pattern, conducts in both directions and produces the classic delta wave with a short PR interval on the resting ECG. These patients carry a risk of preexcited atrial fibrillation degenerating into ventricular fibrillation.

### Atrial Tachycardia

Focal atrial tachycardia originates from a single discrete site, producing a P-wave morphology that differs from sinus rhythm. It may exhibit warm-up and cool-down behavior, and the rate typically ranges from 120 to 250 beats per minute. P-wave morphology can help localize the origin: a positive P wave in V1 suggests a left atrial origin, a negative P wave in the inferior leads suggests a superior origin such as the high right atrium or right superior pulmonary vein, and a positive P wave in the inferior leads suggests an inferior origin such as the coronary sinus ostium or low right atrium.

Multifocal atrial tachycardia is defined by three or more distinct P-wave morphologies with varying PP, PR, and RR intervals. It is strongly associated with chronic obstructive pulmonary disease, acute illness, and theophylline use, and treatment should be directed at the underlying condition. Macro-reentrant atrial tachycardia involves an organized circuit that does not require the AV node and is commonly encountered after prior ablation procedures or cardiac surgery as incisional reentry.

### Atrial Flutter

Typical cavotricuspid isthmus-dependent atrial flutter follows a counterclockwise macro-reentrant circuit around the tricuspid annulus, producing the characteristic sawtooth flutter waves that are negative in leads II, III, and aVF and positive in V1. The atrial rate is approximately 300 beats per minute, and the ventricular rate with 2:1 atrioventricular block is typically 150 beats per minute. Reverse typical flutter follows a clockwise rotation and produces positive flutter waves in the inferior leads. Atypical flutter involves circuits not dependent on the cavotricuspid isthmus and may involve the left atrium, roof, mitral isthmus, or scar-related pathways. Atypical flutter is more common after atrial fibrillation ablation or cardiac surgery.

### Junctional Tachycardia

Automatic or enhanced junctional rhythm presents at a rate of 60 to 130 beats per minute with a narrow QRS and either atrioventricular dissociation or retrograde P waves. Common causes include digitalis toxicity, inferior myocardial infarction, post-cardiac surgery, and myocarditis. Junctional ectopic tachycardia is typically a pediatric arrhythmia, frequently encountered in the post-surgical setting, with rates exceeding 170 beats per minute and associated hemodynamic compromise.

| SVT Type | Mechanism | P-Wave Location | RP Interval | Response to Adenosine | Ablation Target | Success Rate |
|---|---|---|---|---|---|---|
| Typical AVNRT | Slow-fast reentry in AV node | Buried in QRS or pseudo-r' (V1) / pseudo-S (II, III, aVF) | < 70 ms | Terminates | Slow pathway | > 95% |
| Atypical AVNRT | Fast-slow reentry in AV node | Before QRS, inverted inferiorly | Long RP > PR | Terminates | Slow pathway | > 95% |
| Orthodromic AVRT | AV node (antegrade) + AP (retrograde) | In ST segment after QRS | Short RP < PR | Terminates | Accessory pathway | > 95% (left lateral) |
| Focal AT | Automatic or triggered focus | Differs from sinus P | Variable | Transient AV block, AT continues | Focal site | 85-95% |
| Typical Flutter | CTI-dependent macro-reentry | Sawtooth (neg II, III, aVF) | N/A | Slows rate, unmasked waves | CTI | > 95% |
| Junctional Tachycardia | Automaticity at AV junction | AV dissociation or retrograde | N/A | Transient slowing | -- | -- |

<image>
A six-panel comparison of SVT mechanisms. Each panel shows a simplified heart diagram with the reentrant circuit or focal origin highlighted. Panel 1 (Typical AVNRT): AV node shown with two pathways (fast pathway drawn in blue, slow pathway in red); circuit arrows showing antegrade slow, retrograde fast; ladder diagram below showing simultaneous atrial and ventricular activation (P buried in QRS). Panel 2 (Orthodromic AVRT): AV node for antegrade (blue arrow), accessory pathway on left lateral wall for retrograde (red arrow); ladder diagram showing P wave after QRS in ST segment. Panel 3 (Antidromic AVRT): AP for antegrade (red arrow, producing wide QRS), AV node for retrograde (blue arrow); wide QRS shown on ECG strip. Panel 4 (Focal Atrial Tachycardia): single star/burst at a focus (e.g., right PV) with concentric activation; warm-up pattern on ECG strip. Panel 5 (Typical Atrial Flutter): macro-reentrant circuit around tricuspid annulus (counterclockwise arrows); CTI labeled; sawtooth flutter waves on ECG strip. Panel 6 (Junctional Tachycardia): focus at AV junction; narrow QRS with AV dissociation. Each panel with clear labels and distinct color coding for circuits.
</image>

## Acute Management

### Vagal Maneuvers

The modified Valsalva maneuver, as validated by the REVERT trial, involves the patient blowing into a syringe for 15 seconds at 40 mmHg in the supine position, followed by immediate repositioning to supine with passive leg raise to 45 degrees for 15 seconds. This technique achieves a conversion rate of approximately 43%, compared to only 17% with the standard Valsalva maneuver. Carotid sinus massage is performed by applying firm, steady pressure over the carotid bifurcation for 5 to 10 seconds and should be avoided in patients with carotid bruits, recent stroke, or known carotid stenosis. The diving reflex, triggered by application of cold water or ice to the face, elicits a vagal response. These maneuvers are effective for terminating AVNRT and orthodromic AVRT but will not terminate atrial tachycardia or atrial flutter, although they may unmask flutter waves by increasing atrioventricular block.

### Adenosine

Adenosine is the first-line pharmacologic agent for regular narrow complex SVT, administered as a 6 mg rapid intravenous push followed by a rapid saline flush, with subsequent doses of 12 mg if no response, and a second 12 mg dose if necessary. Its mechanism involves transient atrioventricular nodal block, and its ultra-short half-life of 6 to 10 seconds makes it ideally suited for acute termination. Adenosine terminates AVNRT and AVRT by interrupting the circuit at the AV node. It also serves a diagnostic function, as it may transiently reveal atrial flutter waves or atrial tachycardia P waves by slowing the ventricular rate.

Adenosine is contraindicated in preexcited atrial fibrillation or Wolff-Parkinson-White syndrome with wide complex tachycardia, as it may precipitate ventricular fibrillation. It should also be avoided in patients with severe asthma due to the risk of bronchospasm and used at a reduced dose of 3 mg in heart transplant recipients due to denervation hypersensitivity. Important drug interactions include theophylline and caffeine, which are competitive antagonists requiring higher doses, and dipyridamole and carbamazepine, which potentiate the effect and necessitate lower doses. Patients should be warned about transient side effects including flushing, chest tightness, dyspnea, and brief asystole.

### IV Rate-Slowing Agents

Intravenous diltiazem is administered as a 0.25 mg/kg bolus followed by a 5 to 15 mg/hour infusion and is useful for slowing atrioventricular conduction, particularly for rate control in atrial flutter and atrial tachycardia. Intravenous verapamil at 2.5 to 5 mg over 2 minutes, with repeat doses of 5 to 10 mg after 15 to 30 minutes, should be avoided in patients with heart failure with reduced ejection fraction and Wolff-Parkinson-White syndrome. Intravenous metoprolol at 5 mg over 5 minutes, repeated up to three times, is effective for adrenergically mediated SVT. These agents terminate AVNRT and AVRT less reliably than adenosine but provide effective rate control for atrial tachycardia and flutter.

### IV Antiarrhythmics for Termination

Procainamide is administered at 10 to 17 mg/kg intravenously at a rate of 20 to 50 mg/min and slows conduction in the atrium, ventricle, and accessory pathways. It is particularly useful for Wolff-Parkinson-White syndrome with preexcited atrial fibrillation and is effective for atrial tachycardia and flutter. Ibutilide, given as 1 mg intravenously over 10 minutes with the option to repeat once, is the most effective pharmacologic agent for terminating atrial flutter, achieving conversion in approximately 60 to 80% of cases. Its use carries a risk of QT prolongation and torsades de pointes of approximately 4%, necessitating at least 4 hours of monitoring after infusion. Amiodarone, administered as intravenous loading with 150 mg over 10 minutes followed by 1 mg/min for 6 hours and then 0.5 mg/min for 18 hours, possesses both rate-slowing and conversion properties and is reserved for refractory SVT.

### Electrical Cardioversion

Synchronized cardioversion is indicated for any hemodynamically unstable SVT. Recommended biphasic energies are 50 to 100 joules for atrial flutter, 100 to 200 joules for atrial fibrillation, and 50 to 100 joules for other SVTs. Procedural sedation with propofol, etomidate, or midazolam combined with fentanyl should be administered prior to cardioversion.

## Electrophysiology Study and Ablation

### EP Study Findings

#### AVNRT

Dual atrioventricular nodal physiology is demonstrated during electrophysiology study by an AV nodal jump, defined as a greater than 50 millisecond increase in the AH interval with a 10 millisecond decrease in the atrial coupling interval during decremental atrial pacing. Tachycardia is induced through atrial extrastimulus testing, with the arrhythmia initiated when a critically timed premature atrial complex blocks in the fast pathway and conducts down the slow pathway. During tachycardia, the VA time is less than 70 milliseconds, reflecting nearly simultaneous atrial and ventricular activation, and retrograde atrial activation is concentric with the earliest activation at the His bundle region. Para-Hisian pacing differentiates AVNRT from AVRT: in AVRT, the retrograde atrial activation time remains constant regardless of His capture, whereas in AVNRT it changes.

#### AVRT

During tachycardia in AVRT, retrograde atrial activation is eccentric, with the earliest activation at the accessory pathway insertion site. The VA interval exceeds 70 milliseconds, reflecting sequential conduction through the AV node and then the accessory pathway. Accessory pathway localization can be performed pre-procedurally using delta wave morphology algorithms such as those developed by Arruda and Milstein, while intracardiac mapping provides precise localization during the procedure. In patients with a manifest accessory pathway, the shortest preexcited RR interval during atrial fibrillation of less than 250 milliseconds indicates a high-risk pathway with rapid antegrade conduction and the potential for ventricular fibrillation.

#### Atrial Tachycardia

Activation mapping during atrial tachycardia identifies the site where the earliest atrial activation precedes P-wave onset by more than 30 milliseconds. Entrainment mapping demonstrates a post-pacing interval minus tachycardia cycle length of less than 20 milliseconds at the successful ablation site. Common origins for focal atrial tachycardia include the crista terminalis, tricuspid annulus, coronary sinus ostium, pulmonary veins, mitral annulus, and left atrial appendage.

### Catheter Ablation

#### AVNRT Ablation

Ablation for AVNRT targets slow pathway modification at the posteroseptal right atrium near the coronary sinus ostium within Koch's triangle. The endpoint is elimination of slow pathway conduction, demonstrated by loss of dual AV nodal physiology, or persistent single AV nodal echo without sustained tachycardia. The success rate exceeds 95% with a recurrence rate of less than 3 to 5%. The risk of complete AV block is less than 1% with experienced operators, with risk increasing as the ablation site approaches the compact AV node.

#### AVRT/Accessory Pathway Ablation

Ablation targets the accessory pathway location, identified by the earliest retrograde atrial activation during AVRT or the earliest ventricular activation corresponding to the delta wave during sinus rhythm. Left-sided accessory pathways are approached retrogradely through the aorta across the aortic valve or through a transseptal approach. Right-sided pathways are accessed directly via the femoral vein. Septal pathways carry a higher risk of AV block due to proximity to the AV node and His bundle, and cryoablation is preferred for midseptal pathways because it allows reversible test lesions. Success rates exceed 95% for left lateral pathways and range from 85 to 90% for right-sided pathways, with lower rates for septal and epicardial locations. Class I indications for ablation include symptomatic recurrent SVT, preexcited atrial fibrillation, and high-risk accessory pathway features on electrophysiology study.

#### CTI Ablation for Typical Atrial Flutter

Ablation of the cavotricuspid isthmus between the tricuspid annulus and the inferior vena cava involves creation of a linear lesion set. The endpoint is bidirectional conduction block across the cavotricuspid isthmus. The success rate exceeds 95% with a recurrence rate of less than 5%. This is a simple, safe, and highly effective procedure that is preferred over long-term antiarrhythmic drug therapy. An important consideration is that approximately 30% of patients with typical flutter will develop atrial fibrillation within 5 years due to shared risk factors.

#### Focal AT Ablation

Focal atrial tachycardia ablation utilizes activation mapping and pace mapping to localize the focus. Success rates range from 85 to 95% depending on location, with a recurrence rate of 5 to 10%. Certain foci, including para-Hisian, deep epicardial, and aortomitral continuity locations, may be associated with lower success rates or higher procedural risk.

<image>
An illustration of Koch's triangle and the slow pathway ablation target for AVNRT. Show a detailed view of the right atrium opened and viewed from the right side. Key landmarks labeled: (1) Tendon of Todaro (running from IVC to central fibrous body), (2) Coronary sinus ostium (at the inferior base of the triangle), (3) Tricuspid valve annulus (forming the anterior border), (4) Compact AV node (at the apex of Koch's triangle near the central fibrous body, marked with a yellow circle), (5) His bundle (extending from the AV node through the membranous septum, marked with a blue line), (6) Fast pathway region (superior/anterior, near the His bundle recording site, marked in blue), (7) Slow pathway region (inferior/posterior, near the CS ostium, marked in red with ablation target symbols showing RF lesion locations). The triangle should be clearly delineated with dotted lines. Include the Eustachian ridge and IVC opening for orientation. Use anatomic tissue coloring with endocardial surface visible. Ablation catheter tip shown at the slow pathway region with RF energy illustration.
</image>

## Special Considerations

### SVT in Pregnancy

Adenosine is safe during pregnancy and remains the first-line agent. Among beta-blockers, metoprolol is preferred, while atenolol should be avoided due to its association with intrauterine growth restriction. Verapamil is generally safe but should be avoided in the first trimester if possible. Cardioversion is safe at all stages of pregnancy and does not affect the fetal heart. Catheter ablation should be avoided if possible due to radiation exposure, but when necessary in the second trimester, non-fluoroscopic mapping systems using three-dimensional electroanatomic mapping should be employed. Flecainide and propafenone have limited safety data and should only be used when the patient is refractory to first-line agents.

### SVT vs. VT: Key Differentiating Maneuvers During EP Study

Ventricular overdrive pacing during tachycardia provides critical diagnostic information. In AVNRT and AVRT, entrainment produces a VAAV response with a post-pacing interval minus tachycardia cycle length of less than 115 milliseconds and an SA-VA difference of less than 85 milliseconds. In ventricular tachycardia, entrainment produces a VVAV response with a post-pacing interval minus tachycardia cycle length exceeding 115 milliseconds. A His-refractory premature ventricular complex delivered when the His bundle is refractory will advance the next atrial activation if an accessory pathway is present, confirming AVRT, whereas failure to affect the tachycardia suggests AVNRT or atrial tachycardia. Parahisian pacing demonstrates that retrograde atrial activation via an accessory pathway shows identical VA time with and without His capture, whereas conduction via the AV node shows shorter VA time with His capture.

## Key Clinical Pearls

- Modified Valsalva (REVERT technique with leg raise) doubles the conversion rate of SVT compared to standard Valsalva -- should be first intervention in all stable SVT
- In a regular narrow complex tachycardia at rate ~150 bpm, ALWAYS consider atrial flutter with 2:1 block -- adenosine will unmask flutter waves but will not terminate flutter
- Adenosine should NEVER be given for wide complex tachycardia of uncertain origin -- if the rhythm is VT, adenosine is ineffective and delay in appropriate treatment is harmful; if preexcited AF, adenosine can cause VF
- Catheter ablation of typical atrial flutter is highly effective (>95%), low-risk, and should be offered as first-line therapy -- long-term AAD therapy for flutter is less effective and carries more side effects
- AVNRT and AVRT can both present as narrow complex tachycardia and are indistinguishable on surface ECG in many cases -- the EP study is definitive for mechanism differentiation and guides ablation strategy
- All patients with WPW and AF should be referred for EP study and ablation regardless of symptoms -- the risk of VF from rapid preexcited conduction is life-threatening

## References

- Page RL, et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients with Supraventricular Tachycardia. Circulation. 2016;133:e506-e574.
- Brugada J, et al. 2019 ESC Guidelines for the Management of Patients with Supraventricular Tachycardia. Eur Heart J. 2020;41:655-720.
- Appelboam A, et al. Postural Modification to the Standard Valsalva Manoeuvre for Emergency Treatment of SVT (REVERT). Lancet. 2015;386:1747-1753.
- Katritsis DG, et al. EHRA Expert Consensus Document on the Management of Supraventricular Arrhythmias. Europace. 2017;19:465-511.
- Orejarena LA, et al. Paroxysmal Supraventricular Tachycardia in the General Population. JACC. 1998;31:150-157.