Cover Story

Ventricular Overdrive Pacing During SVT: An Opportunity for EP Techs and Allied Professionals

James Kneller, MD, PhD, FHRS, CCDS

Regional Health System,

Yakima, Washington
 

James Kneller, MD, PhD, FHRS, CCDS

Regional Health System,

Yakima, Washington
 

Efficient workflow in the electrophysiology (EP) lab involves quickly and definitively diagnosing supraventricular tachycardia (SVT). Frequently, only ventricular overdrive pacing (VOP) is needed to establish the mechanism of SVT.1 We have reviewed the concepts surrounding VOP during lab meetings, and practiced during cases. Our EP techs are now facile in performing the maneuver, making the pertinent observations and measurements needed to diagnose SVT mechanisms. This article reviews how to perform and interpret VOP during SVT, with the goal of increasing understanding and participation in other labs.

SVT Mechanisms and Ablation Strategies

SVT occurs by one of three mechanisms. The most common mechanism is AV node reentry tachycardia (AVNRT). The second most common is AV reentry tachycardia (AVRT), as occurs in patients with Wolff-Parkinson-White (WPW). SVT may also represent an atrial tachycardia (AT), which is becoming more prevalent in our aging population, with increasingly complex atrial pathology. Distinguishing between AVNRT, AVRT, and AT is critical, as the ablation strategy is very different for each form of SVT.

For AVNRT, ablation targets the slow pathway (SP) input to the AV node. The SP is a discrete anatomical region in the right atria (RA) between the tricuspid valve annulus and ostia of the coronary sinus (CS). Ablation modifies the SP so AVNRT can no longer occur. Slow junctional beats during ablation indicate effective SP modification is taking place. AVRT involves a strand of myocardium known as a bypass tract (BT), which connects the atrium to the ventricle across the annulus of the mitral (LA to LV) or tricuspid (RA to RV) valve. AVRT cycles between the atrium and ventricle using both the AVN and BT; ablation is performed where the BT crosses the valve annulus, abolishing AVRT. 

These cases can become tricky when BTs conduct in only one direction or when several BTs are present in the same patient. Finally, ATs arise from a point source or very small region of tissue, which may represent a spontaneously discharging focus or microreentrant circuit. Unlike ablation of the well-defined SP for AVNRT, or of BTs confined to the valve annulus for AVRT, ablation for AT is performed at the sight of earliest activation, which may be anywhere in the LA or RA.

Principles of SVT & VOP

In Figures 1-5, major concepts are illustrated in a single episode of AVNRT. The patient is a 55-year-old female with SVT, which was successfully terminated by adenosine in the emergency department. An EP study for SVT is routinely performed with four catheters positioned in the high right atrium (HRA), RV apex (RVa), HIS position, and CS. The catheter in the HRA is frequently swapped for an ablation catheter, which is more easily manipulated to map the origin of ATs and localize BTs. VOP distinguishes between AVNRT and AVRT by exploiting that the AVN is far from the RVa, while the RVa is within the AVRT circuit. VOP identifies AT by demonstrating an inability to participate in the tachycardia mechanism, even after accelerating atrial activation to the VOP rate. VOP impulses propagate through the tachycardia circuit during both AVNRT and AVRT, but never for AT. For this reason, successful VOP is called entrainment during AVNRT and AVRT, but not for AT.1

Induction of SVT

Prior to inducing SVT, ensure that clearly identifiable atrial (A) and ventricular (V) signals are visible on the HIS catheter. This will facilitate identification of the A and V components of overlapping signals during SVT (Figure 2A). SVT may be induced in the EP lab using decremental atrial pacing, delivery of atrial extrastimuli (S1-S2 protocols), or burst pacing. Once initiated, SVTs are typically 150-220 bpm, with QRS morphology the same as sinus rhythm since ventricular activation occurs over the AV node. The QRS during SVT differs when rate-related aberration occurs, and in AVRT when the tachycardia cycles from the atria to the ventricles over the BT (QRS is fully preexcited during SVT). Figure 1 shows induction of SVT.

Performing VOP

VOP is the process of pacing from the RV apex during SVT at a rate that is slightly faster than the tachycardia cycle length (TCL) until the paced QRS stabilizes.1 To perform VOP, first measure the TCL and ensure this is stable beat to beat (Figure 2B). Next, pace from the catheter positioned in the RVa at a rate that is 10-30 msec faster than the TCL (Figure 3). Watch as pacing changes the QRS. This is called the transition zone (TZ).2 Continue pacing until the QRS reaches a stable morphology. Usually only 15-30 paced beats are needed. Stop pacing soon after the QRS stabilizes, as no additional information is obtained and SVT is more likely to terminate with long pacing sequences. If SVT continues following VOP, simply repeat the maneuver several times at each VOP rate, then decrease the pacing CL (pace faster) by 10 msec and repeat until SVT terminates. Usually SVT terminates after decreasing the pacing CL 2-3 times. Now go back and interpret the VOP sequences.

Observations and Measurements (AVNRT)

For each VOP sequence, try to make the following observations and measurements. If SVT is terminated by VOP, enough information may still be available to establish the mechanism. SVT may be reinduced until adequate VOP sequences are obtained. Note that VOP fails to advance atrial activation in 50%-80% of ATs, which is a major clue that AT is present.1 We routinely document each relevant observation in the order of occurrence during VOP.

Step #1: At the start of a VOP pulse train, re-measure the TCL several beats prior to the onset of pacing (Figure 2B). Also measure the septal VA interval (SVAi) during SVT, which begins with the earliest onset of the surface QRS to the earliest atrial signal on the HIS or proximal CS catheter (Figure 2B). SVAi <70 msec confirms that AVNRT is present, while SVAi >70 msec is not helpful.3

Step #2: Identify the TZ during the onset of VOP (Figure 3). From the first stable paced QRS, count the paced beats required to advance atrial activation (Figure 4). Make an electronic caliper equal to the VOP cycle length. Place the caliper at the onset of atrial activation for the first stable QRS, and observe whether the caliper reaches to earliest atrial activity of the next beat. Advance the caliper to the earliest atrial activation of the next beat and measure, continuing until it is clear that the atrial rate is advanced to the pacing rate. Count how many paced beats with stable QRS were required to first advance atrial activation to the rate of VOP. Advancement during the TZ or after 1±0 stable paced QRS is consistent with AVRT, whereas 4±1 stable paced QRS complexes are needed to advance atrial activation during AVNRT.2,4 Note that in cases of AVNRT or AVRT, the atrial activation sequence observed between the HRA, HIS, and CS catheters is unchanged during VOP. This is because the paced impulses cycle through the tachycardia circuit just like the SVT beats (entrainment).1 In cases of AT when VOP successfully advances atrial activation, a discernable change in the atrial activation sequence will be observed because the VOP impulses are not using the tachycardia circuit.1,5 Only use VOP that advances atrial activation when making the  measurements described in Steps #3-5.

Step #3: Following atrial advancement during VOP, measure the paced VA interval (PVAi) from the onset of the pacing stimuli to the subsequent earliest atrial activation (Figure 4). Calculate the PVAi minus SVAi difference (∆VAi), which is 165-16=149 msec in this example. ∆VAi >85 msec is consistent with AVNRT, and <85 msec occurs with AVRT.5 ∆VAi does not apply for AT.

Step #4: Following the last pacing stimuli (VP) of VOP, identify the last atrial activation (AA) advanced to the pacing rate (Figure 5). If the next event is a sensed ventricular signal (VS) on the RVa catheter, a VPAAVS response has occurred consistent with AVNRT or AVRT.6 The observation is even more robust if a His potential is sensed (HS) prior to VS, such that a VPAAHSVS sequence is documented (as shown in Figure 5). Because the pattern of atrial activation is unchanged during VOP, the AAHSVS sequence represents the last VOP stimulus conducting through the tachycardia circuit, the same as during uninterrupted SVT. Note that if a spontaneous atrial signal (AS) follows the last advanced atrial activation (AA), aVPAAASVS response is observed, consistent with AT.6

Step #5: Review the sequence of events following VOP (Figure 5). If SVT continues after VOP, the post pacing interval (PPI) may be measured. The PPI is from the onset of the last pacing stimuli to the first VS recorded by the RVa catheter (Figure 5), which is 526 msec in this example. The TCL is now 320 msec, which is slightly faster compared to the onset of VOP. Calculate the PPI minus TCL difference (∆PPI), which is 526-320=206 msec in this example. ∆PPI >115 msec is consistent with AVNRT, and ∆PPI <115 msec occurs with AVRT.5 SP ablation abolished dual AVN physiology and SVT was no longer inducible (Figure 11A).

Observations and Measurements (AVRT)

Figures 6-8 illustrate a case of AVRT. The patient is a 58-year-old male with palpitations since childhood, and no BT seen on ECG. SVT with TCL 365 msec and SVAi 192 msec were induced in the EP lab (Figure 6), with earliest atrial activation occurring at the CS5,6 position, consistent with propagation from V to A using a BT crossing the lateral mitral valve annulus. Following the onset of VOP (Figure 7), the second paced QRS is stable, with atrial activation advanced by VOP following the second stable QRS. The PVAi is 266 msec, with ∆VAi (266-192=74 msec) <85 msec. The PPI is 472 msec, with ∆PPI (472-382=90) <115 msec (Figure 8). The atrial activation sequence is unchanged during VOP, and a VPAAHSVS sequence follows VOP. All measurements and observations are consistent with AVRT. AVRT involving a concealed (not apparent on ECG) left lateral accessory pathway was found at electrophysiology study (Figure 11B). Transseptal access was required for ablation at this location (Figure 11B).

Observations and Measurements (AT)

 

Figures 9 and 10 illustrate a case of AT. The patient is a 66-year-old female with SVT, which was successfully terminated by adenosine in the emergency department. SVT was induced in the EP lab with burst pacing, having TCL 342 msec, SVAi 182 msec (Figure 9). VOP was performed at 300 msec pacing CL. The QRS had stabilized by the second paced beat, with PVAi 120 msec, such that the ∆VAi (120-182= -62) was <85 msec, consistent with AVRT (Figure 9). However, the ∆PPI (715-343=372) was >115 msec, suggestive of AVNRT (Figure 10). This discrepancy arises because AT is present, and the ∆VAi and ∆PPI cutoffs (85 and 115 msec, respectively) do not apply for AT. 

There was a subtle but undeniable change in AAS along the CS (øøø to ###) following advancement of atrial activation to the VOP rate, which occurs with AT but not AVNRT or AVRT (Figure 9). Following VOP, a VPAAASHSVS sequence was observed (Figure 10), which only occurs with AT.6 The earliest site of activation corresponded to the posterior interatrial septum. Transseptal catheterization confirmed no earlier sites on the left side, followed by right-sided ablation for AT (Figure 11C).

Summary

SVT cases remain challenging because the diagnosis is never certain until the time of EP study, so the EP team must be prepared to pursue any SVT mechanism. VOP is the foundation of SVT assessment in the electrophysiology lab, and frequently sufficient to establish SVT mechanisms. EP techs and allied professionals may perform and interpret VOP, enhancing staff engagement and workflow in the lab.

Disclosure: The author has no conflicts of interest to report regarding the content herein. Outside the submitted work, Dr. Kneller reports speakers bureau honoraria from Biosense Webster. 

References

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  2. Rosman JZ, John RM, Stevenson WG, et al. Resetting criteria during ventricular overdrive pacing successfully differentiate orthodromic reentrant tachycardia from atrioventricular nodal reentrant tachycardia despite interobserver disagreement concerning QRS fusion. Heart Rhythm. 2011;8:2-7.
  3. Knight BP, Ebinger M, Oral H, et al. Diagnostic value of tachycardia features and pacing maneuvers during paroxysmal supraventricular tachycardia. J Am Coll Cardiol. 2000;36(2):574-582.
  4. Dandamudi G, Mokabberi R, Assal C, et al. A novel approach to differentiating orthodromic reciprocating tachycardia from atrioventricular nodal reentrant tachycardia. Heart Rhythm. 2010;7:1326-1329.
  5. Michaud GF, Tada H, Chough S, et al. Differentiation of atypical atrioventricular node re-entrant tachycardia from orthodromic reciprocating tachycardia using a septal accessory pathway by the response to ventricular pacing. J Am Coll Cardiol. 2001; 38:1163-1167.
  6. Knight BP, Zivin A, Souze J, et al. A Technique for the Rapid Diagnosis of Atrial Tachycardia in the Electrophysiology Laboratory. J Am Coll Cardiol. 1999;33:775-781.