Introduction

Supraventricular tachycardia (SVT) is a broad term encompassing all tachyarrhythmias that originate at or above the His bundle. This condition is characterized by atrial and/or ventricular rates exceeding 100 beats per minute (bpm) in adults and over 200 bpm in children.[1] The most common SVT subtypes in adults include atrial fibrillation and atrial flutter. Other common subtypes, which will be the focus of this activity, include atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reciprocating tachycardia (AVRT), and atrial tachycardia. In contrast, junctional tachycardia is encountered less frequently.

SVTs have a moderate prevalence, occurring at a rate of 2.25 cases per 1000 adults, and with an estimated incidence of 0.1% to 0.4% in the pediatric population.[2][3] Since the introduction of catheter ablation, the tools and technologies for this procedure have continued to advance and expand. Despite these innovations, successful management fundamentally depends on achieving an accurate diagnosis. This activity focuses on the methods used to differentiate SVT in the electrophysiology laboratories.

Anatomy and Physiology

The normal cardiac conduction system initiates with an electrical impulse generated by the sinoatrial (SA) node. This impulse then travels through the His-Purkinje system, which functions as an electrical highway, facilitating the depolarization of the heart. SVT can occur from various conduction abnormalities, such as dual pathways within the atrioventricular (AV) node, as seen in AVNRT, or from the presence of accessory pathways.

Accessory pathways are bundles of muscle with electrical properties that connect the atria and ventricles. They may be located near the His-Purkinje system or more remotely, forming macroreentrant circuits.[4] Specifically, accessory AV pathways traverse through the fibrofatty tissue of the AV groove (sulcus tissue) and the fibrous annulus (hinge lines) of the heart valves.[5] These pathways are believed to result from incomplete fusion between the sulcus and cushion tissues during embryonic development.[6]

Indications

The European Society of Cardiology (ESC) guidelines categorize recommendations into 3 main categories, as outlined below:

• Class I

  • Strongly recommended based on solid evidence
• Class II

  • This class is divided into 2 subcategories:

    • IIa

      • Benefits outweigh risks, supported by moderate evidence
    • IIb

      • May be considered useful, but the evidence is less conclusive
• Class III

  • Not recommended due to ineffectiveness or potential harm

Additionally, the recommendations are graded according to levels of evidence, as outlined below. These classifications provide a structured approach to making clinical decisions.

• Level A

  • High-quality evidence from multiple trials
• Level B

  • Moderate-quality evidence from a single trial or non-randomized studies
• Level C

  • Based on expert opinion or limited data from smaller studies

The 2019 ESC guidelines recommend an electrophysiology study for patients with recurrent symptomatic SVT when the arrhythmia mechanism is unclear, and for those with syncope suspected to be due to SVT when noninvasive testing is inconclusive (Class I and IIa recommendations).

Catheter ablation is recommended for symptomatic SVT patients who desire definitive treatment or have not responded to medical therapy. This procedure is also indicated for those with severe symptoms, such as syncope (Class I). Additionally, catheter ablation should be considered for asymptomatic patients with preexcitation who have experienced arrhythmic syncope, rapid atrial fibrillation, or left ventricular (LV) dysfunction due to electrical dyssynchrony (Class IIa).

Catheter ablation may also be considered for patients with infrequent but severe episodes of SVT in whom medical therapy is not preferred or is contraindicated, as well as for those with asymptomatic preexcitation and low-risk accessory pathways (Class IIb). The benefits of catheter ablation include reduced hospitalizations and an improved quality of life.[7]

Contraindications

Although there are no absolute contraindications to performing electrophysiology maneuvers for differentiating SVTs, caution is warranted due to the potential risks associated with electrophysiology studies, particularly those related to anesthesia and the patient's underlying comorbidities.

Technique or Treatment

Preparation

Although electrophysiology studies can vary in approach, the fundamental principles are consistent. Typically, 4-electrode catheters are inserted for electrical recording and pacing, including:

• High right atrium
• HIS bundle
• Right ventricle (RV)
• Coronary sinus 

A fifth catheter is used for radiofrequency or cryoablation.

Electrophysiology Study

Observations and maneuvers are typically categorized based on whether they are performed during sinus rhythm or tachycardia.

Clinical Significance

Observations and Pacing Maneuvers During Sinus Rhythm

Anterograde conduction during sinus rhythm is assessed at baseline and during atrial pacing, with a focus on identifying ventricular preexcitation and dual AV node physiology. Ventricular preexcitation on a baseline electrocardiogram in a patient with narrow complex SVT suggests AVRT as the likely mechanism. However, preexcitation does not exclude other causes of narrow-complex tachycardia.

Atrial Pacing During Sinus Rhythm

Atrial pacing during sinus rhythm helps identify dual AV nodal physiology and the presence of ventricular preexcitation. During atrial extrastimuli pacing, an “atrium to His (A-H) jump” is observed when a 10-millisecond decrease in the S1S2 coupling interval causes a greater than 50-millisecond increase in the A-H interval, which indicates the presence of dual AV nodal physiology. Additionally, decremental atrial pacing or atrial extrastimuli pacing can increase the degree of ventricular preexcitation or, in rare cases, uncover previously unrecognized ventricular preexcitation, especially from a left lateral accessory pathway.

Ventricular Pacing During Sinus Rhythm

Ventricular pacing during sinus rhythm is a valuable tool for assessing the presence and location of concealed accessory pathways. This technique also aids in identifying nonseptal accessory pathways by revealing eccentric retrograde atrial activation patterns.

When retrograde ventriculoatrial (VA) conduction is concentric—meaning the earliest atrial activation occurs along the septum—differential ventricular pacing can help identify a septal accessory pathway. This technique distinguishes retrograde conduction via the AV node from conduction through a septal accessory pathway, thereby differentiating nodal from extranodal responses.

Differential ventricular pacing is performed from both the RV apex and the RV base. The RV apex is located near the exit of the right bundle branch (RBB) fibers. In contrast, the RV base is closer to the typical insertion site of ventricular septal accessory pathways. During pacing, the stimulus-to-atrial (Stim-A or V-A) intervals are compared between the 2 pacing sites (see Image. Differential Ventricular Pacing Responses).

In cases where a septal accessory pathway is absent and ventricular activation conduction occurs exclusively through the AV node, pacing from the RV apex results in a shorter Stim-A or V-A interval than pacing from the RV base. This finding indicates retrograde conduction via the AV node only. Conversely, a shorter Stim-A (V-A) interval during pacing from the RV base compared to the RV apex suggests retrograde conduction through a septal accessory pathway or another extranodal pathway.[8]

Observations and Pacing Maneuvers During SVT

Observations During SVT

The following observations can be seen during SVT:

• Ventricular-to-atrial activation relationship

  • This refers to the ratio of ventricular to atrial activation electrograms during the tachycardia. The presence of A-V dissociation during the tachycardia excludes AVRT, which involves A-V bypass tracts.
• Ventricular beats exceeding atrial beats

  • This finding excludes both atrial tachycardia and AVRT. In atrial tachycardia, the atria initiate and maintain the tachycardia, so the number of atrial activations should be equal to or greater than the ventricular activations. In AVRT, atrial and ventricular activations occur in a 1:1 ratio due to the reentrant circuit involving the AV node and 1 or more accessory pathways.
• Atrial beats exceeding ventricular beats

  • When atrial beats outnumber ventricular beats, AVRT can be excluded. In AVRT, each atrial beat is usually followed by a ventricular beat. A higher number of atrial beats suggests an alternate mechanism, such as atrial flutter or atrial fibrillation.
• Ventricular activation interval (septal time)

  • This interval measures the time between ventricular activation and the subsequent atrial activation at the septum. A septal V-A interval shorter than 70 milliseconds suggests that the SVT is unlikely to be caused by AVRT involving typical bypass tracts, which generally produce longer V-A intervals. In these cases, AVNRT is more likely to occur.
• Atrial activation sequence

  • This refers to the pattern of atrial activation during tachycardia. A concentric pattern begins at the AV node and spreads outward. In contrast, an eccentric pattern—where the earliest activation occurs away from the septum—suggests the presence of a concealed accessory pathway. 

Observations During Transitions

The following observations can be seen during transitions:

• Initiation

  • How SVT begins can offer insights into its underlying mechanism. An A-H jump—a sudden increase in the interval from atrial to His bundle activation—indicates AV node involvement. This makes atrial tachycardia less likely, as it originates in the atria and does not depend on the AV node for its initiation.
• Bundle branch block (BBB)

  • The presence of the BBB during tachycardia extends the ventricular activation interval in AVRT. Specifically, a prolongation of the ventricular activation interval of more than 35 milliseconds occurring alongside the appearance of BBB indicates orthodromic AVRT, especially when a free wall accessory pathway is ipsilateral to the BBB.
• Termination

  • If the SVT terminates with an atrial event, it suggests atrial tachycardia, as atrial tachycardia originates in the atria and is characterized by atrial impulses driving the tachycardia. Consequently, when atrial tachycardia terminates, it usually does so with an atrial event. 
  • Conversely, AVNRT and AVRT may terminate with either an atrial or a ventricular event, depending on where the reentrant circuit is interrupted. If the circuit is interrupted on the ventricular side (for example, due to a change in ventricular conduction), the tachycardia may cease with a ventricular event. Alternatively, if the circuit is interrupted at the atrial level, termination may occur with an atrial event. The key distinction is that these forms of SVT are not solely dependent on atrial activity, allowing for termination through either atrial or ventricular event.
  • The term "wobble" in the context of tachycardia refers to spontaneous variations in the tachycardia cycle length (TCL). These fluctuations often result from variations in conduction velocity along different pathways that participate in the tachycardia circuit. In AVNRT, a wobble in the R-R interval suggests the presence of a "slow pathway" within the AV node. This finding also helps exclude atrial tachycardia, as atrial tachycardia typically causes variations in the A-A interval rather than the R-R interval.[9]

Pacing Maneuvers During SVT

Ventricular overdrive pacing (VOP) is a crucial technique for differentiating various types of SVT. To ensure accurate interpretation, specific conditions must be met during the maneuver, including:

• Ventricular pacing is performed at a rate 10 to 30 milliseconds faster than the TCL, and it must be confirmed that the atrial rate advances to match the ventricular pacing rate.
• The same tachycardia should continue after pacing stops.
• No significant fluctuations, or “wobbles,” in the TCL should be present during pacing.

When these criteria are fulfilled, the maneuver’s results can be interpreted based on 2 key features, described below:

• Cessation response

  • After the conclusion of ventricular overdrive pacing (VOP), the final atrial beat that has been advanced to the pacing cycle length is identified and represents the initial “A” in the cessation response. The pattern of this response helps distinguish the type of supraventricular tachycardia, as mentioned below.

    • In AVNRT and AVRT, an A-(H)-V response is observed.
    • In atrial tachycardia (AT), an A-A-(H)-V response is observed.
  • This response reflects the underlying mechanism of tachycardia. In both AVNRT and AVRT, atrial activation during ventricular pacing occurs via the retrograde limb of the reentrant circuit, leaving the anterograde limb available for conduction. As a result, the last retrograde atrial beat (A) from the final ventricular (V) pacing stimulus triggers the subsequent His bundle (H) and ventricular (V) activation, producing the characteristic A–H–V response.
  • On the other hand, during atrial tachycardia, ventricular pacing renders the AV conduction pathway immediately refractory, so the last retrograde atrial (A) beat from the final ventricular pacing stimulus is not conducted to the ventricle. Therefore, when overdrive pacing stops, the first beat of the atrial tachycardia initiates AV conduction, resulting in an A–A–H–V response (see Image. Ventricular Overdrive Pacing Responses in Atrial Tachycardia).
• Quantification in arrhythmia diagnosis

  • Additional measurements are essential to differentiate between the mechanisms underlying an A-(H)-V response seen in AVNRT or AVRT. Specifically, the difference between the PPI and the TCL (referred to as PPI−TCL) can provide valuable insight.
  • The PPI is measured from the last ventricular pacing stimulus to the return of the next ventricular beat at the same site. Generally, the closer the tachycardia circuit is to the ventricular pacing site, the smaller the PPI−TCL value will be. To distinguish between orthodromic AVRT and AVNRT, a value of less than 115 milliseconds indicates a higher likelihood of AVRT.
  • AVRT is also likely when the corrected PPI−TCL is under 110 milliseconds; the corrected PPI accounts for the difference between the A-H interval of the last paced beat and the tachycardia A-H interval (ΔAH is subtracted from the PPI). In AVRT, the PPI tends to be shorter due to ventricular involvement in the reentrant circuit.
  • Notably, quantification criteria for VOP are most predictive when pacing occurs closest to the accessory pathway, for example, at the base of the RV, allowing for significant interval differences. Although a PPI−TCL value less than 115 milliseconds (or a corrected PPI−TCL value less than 110 milliseconds) supports the diagnosis of AVRT, a higher value does not exclude it. This situation can occur in orthodromic AVRT cases where the accessory pathway is located far from the pacing site, such as with left-sided pathways. In these situations, pacing closer to the lateral pathway—either from the LV or a ventricular branch of the coronary sinus—can provide more definitive information.
  • An additional useful measurement for diagnosing orthodromic AVRT involving a septal pathway is the difference between the V-A interval during ventricular pacing (Stim-A interval) and the corresponding ventricular activation interval during tachycardia, known as ΔVA. A ΔVA value less than 85 milliseconds further supports the diagnosis of AVRT.

His-Synchronous or His-Refractory Premature Ventricular Contraction During SVT

When VOP is not feasible or diagnostic, a His-refractory premature ventricular contraction (HR-PVC) can provide additional information during tachycardia.[10] This procedure involves delivering a ventricular extrastimulus, a PVC, timed to coincide with His bundle refractoriness, either exactly at the time of His recording or within 35 to 55 milliseconds after His depolarization. Confirmation of His refractoriness is achieved by analyzing the surface QRS, which will show a fused beat, representing fusion between a fully paced QRS morphology and the QRS morphology seen during SVT. As a result, any ventriculoatrial conduction occurring after the HR-PVC cannot be mediated through the His-Purkinje system, suggesting the presence of an accessory pathway if the timing of the subsequent atrial beat following the HR-PVC is affected.

Three scenarios can arise if the timing of the immediate atrial beat is altered, as mentioned below:

• Advancement of the subsequent atrial activation

  • An atrial activation that occurs earlier than expected following an HR-PVC strongly suggests the presence of an accessory pathway, as the only way the impulse can reach the atrium prematurely in this context is via an alternative route that bypasses the His bundle. However, this finding alone does not confirm the accessory pathway’s involvement in the tachycardia. If the atrial activation sequence remains consistent with that observed during tachycardia, it strongly supports—but does not definitively prove—the accessory pathway’s participation in the tachycardia mechanism.
• Delay of the subsequent atrial activation

  • A delay in atrial activation following an HR-PVC strongly suggests the presence of an accessory pathway and its participation in the tachycardia circuit.
• Termination of the tachycardia without conduction to the atrium

  • Observing tachycardia termination without atrial conduction provides strong evidence for the presence and involvement of an accessory pathway. In this scenario, the His bundle is refractory and cannot conduct to the atrium, so the HR-PVC resets the rhythm only via the accessory pathway. However, in rare cases, an HR-PVC can delay or terminate AVNRT in the presence of a concealed nodoventricular or fasciculoventricular pathway. Here, the PVC blocks conduction through the His bundle but still reaches the ventricles via the accessory pathway, interrupting the reentrant circuit. This maneuver helps diagnose these concealed pathways.[11]

Atrial Overdrive Pacing during SVT

Atrial overdrive pacing (AOP) can be performed during SVT to differentiate atrial tachycardia from AVNRT and to distinguish AVNRT from junctional tachycardia. This maneuver involves pacing the atrium at a cycle length 10 to 40 milliseconds shorter than the TCL. The criteria for successfully interpreting an AOP response are similar to those used for VOP, as outlined below:

• Assessment of ventricular activation interval upon cessation of atrial overdrive pacing (ventricular activation linking) to differentiate atrial tachycardia from AVNRT/AVRT

  • When the first V-A interval immediately following the last atrial paced beat—measured from at least 2 different atrial pacing sites (eg, right atrium, proximal coronary sinus, and distal coronary sinus)—differs by 14 milliseconds or less, it supports a diagnosis of AVRT or AVNRT.[12] Greater differences in ventricular activation intervals support a diagnosis of atrial tachycardia.
• Assessment of the cessation response (AH-HA versus A-H-A) to differentiate AVNRT from junctional tachycardia

  • When AOP is stopped and tachycardia resumes, the electrogram displays distinct patterns depending on the type of tachycardia that has occurred. In junctional tachycardia, the response is an "Atrial-His-His-Atrial" (AH-HA) sequence (see Image. Atrial Overdrive Pacing Response in Junctional Tachycardia). This occurs because the tachycardia resumes with a junctional beat initiated by a His signal immediately after pacing stops. In contrast, in AVNRT, cessation of AOP typically results in the tachycardia resuming with an atrial beat first, producing an "atrial-His-atrial" (A-H-A) sequence on the electrogram.[13] 
• Response to atrial extrastimuli during tachycardia to differentiate AVNRT from junctional tachycardia

  • This maneuver is specifically used to distinguish between AVNRT and junctional tachycardia. An atrial extrastimulus, known as a premature atrial contraction (PAC), is delivered at various points during the TCL. Key observations are made based on the following 2 scenarios:

    • When the PAC is timed to coincide with the refractoriness of the His bundle (late PAC response)
    • When the PAC is timed before the His refractoriness (early PAC response)

If a late PAC affects the timing of the subsequent His depolarization, it strongly suggests the involvement of anterograde slow pathway conduction. This finding is typically associated with AVNRT. However, a negative response (ie, no change in His timing) is nondiagnostic. In contrast, if an early PAC advances the immediate His potential without terminating the tachycardia, it is a strong indicator of junctional tachycardia (see Image. Response to Early Premature Atrial Contraction in Junctional Tachycardia vs Atrioventricular Nodal Reentrant Tachycardia). This observation suggests that the tachycardia circuit does not depend on a retrograde fast pathway through the AV node, which is typically involved in AVNRT. Other responses, such as no change in the immediate His timing, followed by tachycardia termination, delay, or further advancement, are considered nondiagnostic.[14][15] 

Footnotes

When the pacing cycle length does not shorten or 1:1 ventricular activation conduction is absent during the VOP maneuver, the results cannot be interpreted. However, the maneuver can be reattempted with some considerations. Each attempt should involve decremental pacing, decreasing the cycle length by 10 to 20 milliseconds after each attempt that demonstrates acceleration in atrial conduction. Additionally, it is essential to confirm that the TCL returns to approximately its original value after pacing is stopped.

A pseudo-AAV response occurs when the response is mislabeled, such as selecting an “A” that precedes the actual last “A.” This situation can arise in long RP tachycardias or when isoproterenol increases junctional automaticity. To avoid this error, use calipers to measure the A-A interval and confirm it matches the pacing rate, while carefully identifying the last advanced “A.” Another scenario involves the A-H interval being shorter than the His to ventricle (H-V) interval, indicating that the impulse takes longer to conduct through the His-Purkinje system (ventricular conduction) than through the AV node. This may result from prolonged HV conduction due to conduction disease or a shortened A-H interval. This discrepancy can be addressed by comparing the AHV/AHV response with the AV/AAV response.

A summary of electrophysiology laboratory maneuvers used to differentiate between types of SVT is presented in this paper (see Table. Electrophysiology Lab Maneuvers for Differentiating Supraventricular Tachycardia).

Enhancing Healthcare Team Outcomes

Effective management of supraventricular tachycardia (SVT) in the electrophysiology laboratory relies on a well-coordinated, multidisciplinary healthcare team. This team includes physicians, advanced practitioners, nurses, pharmacists, and other healthcare professionals, each contributing distinct expertise and perspectives to support patient-centered care. Physicians and advanced practitioners lead the diagnosis and treatment of SVT, utilizing their electrophysiology training, while nurses manage patient preparation, intraprocedural monitoring, and post-procedure recovery. Pharmacists ensure the safe and effective use of medications, guiding dosing and potential drug interactions.

Clear communication among the interprofessional healthcare team members is vital for optimizing team performance and patient safety. Standardized communication tools and protocols, such as checklists and handoff templates, help streamline workflows and reduce errors. Regular team meetings and a collaborative problem-solving approach foster a culture of shared responsibility and continuous improvement. This interprofessional approach enhances efficiency, minimizes complications, and improves outcomes for patients undergoing evaluation and treatment for SVT in the electrophysiology laboratory.

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Disclosure: Abdullah Sarkar declares no relevant financial relationships with ineligible companies.

Disclosure: Maria Horenstein declares no relevant financial relationships with ineligible companies.

Disclosure: Houman Khakpour declares no relevant financial relationships with ineligible companies.