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The differential diagnosis of supraventricular tachycardia (SVT) includes sinus tachycardia (ST), atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), atrial tachycardia (AT), junctional ectopic tachycardia (JET), atrial flutter (AFL), atrial fibrillation (AF), and multifocal atrial tachycardia (MAT) (Figure 1.1). The term paroxysmal supraventricular tachycardia (PSVT) is used to refer to regular SVTs with abrupt onset and termination, namely AVNRT, AVRT, and AT.¹ AVNRT is the most common, accounting for at least 60% of PSVTs that present to the electrophysiology (EP) laboratory. AVRT and AT account for 30% and 10% respectively (Figure 1.2). This chapter will focus on the diagnosis of AVNRT, AVRT, and AT in the EP laboratory. The discussion of AVRT will focus on orthodromic reciprocating tachycardia (ORT), a narrow complex tachycardia (in the absence of aberrant conduction) with antegrade conduction via the AV node and retrograde conduction via an accessory pathway. The diagnosis of PSVT depends on evaluation of 3 key elements: (1) baseline findings prior to tachycardia initiation; (2) tachycardia characteristics; (3) tachycardia response to atrial and ventricular pacing maneuvers.

Preprocedure Planning

Before performing an EP study on a patient with PSVT, a detailed history and physical should be performed. Clinical details, like the patient’s age at onset of PSVT, may give insight into the underlying mechanism. More than 70% of patients with AVRT present before the age of 20 (median age 23 ± 14 years). In contrast, 60% of patients with AVNRT present after the age of 20 (median age 32 ± 18 years).2 Atrial tachycardia is also influenced by age, accounting for 23% of PSVTs over the age of 70. There are also differences by gender. In a study of 1700 patients presenting with PSVT, the majority of those with AVRT were men (54%). However, the majority of patients with AVNRT and AT were women (70% and 62%, respectively).³

The baseline ECG should be assessed for evidence of manifest preexcitation. The ECG during PSVT with 1:1 atrioventricular (AV) conduction should be evaluated for the P-wave morphology and the R-P interval. A long R-P tachycardia (defined as an R-P interval > 50% of the R-R interval) could represent atypical AVNRT, AVRT, or AT. However, the P-wave morphology can be useful, as AVNRT should have a superiorly directed P wave. An inferior P-wave axis would be more consistent with AT or AVRT. A similar logic applies for short R-P tachycardias. When no P waves are discernable during SVT, the terminal portion of the QRS complex during SVT should be compared to the baseline ECG. A pseudo R in lead V₁ or pseudo S in the inferior leads, representing retrograde atrial activation, may be discernable. This finding makes AVNRT very likely. In addition, if the onset or termination of tachycardia is documented, this should be examined for clues as to the tachycardia mechanism. Tachycardia initiation with a premature atrial complex (PAC) and marked P–R prolongation usually signifies an AV nodal dependent arrhythmia. Consistent termination with AV block without a premature atrial beat makes AT extremely unlikely. However, these ECG criteria should be used with caution as studies looking at their effectiveness have shown an incorrectly classified the tachycardia 20% of the time.⁴

Vascular Access and Catheter Placement

Informed consent and labs (complete blood count, coagulation studies, and chemistries) are obtained in the cardiac surveillance unit on or before the day of the procedure. The majority of patients undergoing an electrophysiology (EP) procedure for PSVT receive intravenous sedation administered by the EP nursing staff under the direction of the attending physician. Most EP procedures for PSVT can be performed using access via a single femoral vein. Standard sheaths for an EP procedure for PSVT include 3 sheaths from the right femoral vein. After the patient is prepped and draped, access to the right femoral vein is obtained via the modified Seldinger technique. When the suspicion is high that the PSVT mechanism is AVNRT, a long guiding sheath can be placed initially, and an ablation catheter can be placed in the His bundle location and used for the diagnostic portion of the study. A standard 4-mm electrode-tip deflectable ablation catheter is typically used. A soft-tip quadripolar catheter is positioned in the RV apex. A steerable quadripolar catheter is positioned in the high right atrium (HRA). The ablation catheter or the HRA catheter can later be moved to the coronary sinus (CS) to assess for eccentric or concentric atrial activation, if needed to help with the diagnosis. After catheters are positioned, the patient receives an intravenous bolus of heparin (3000 U) followed by an additional 1000 U every hour to prevent thrombus formation. A multipolar catheter can be placed in the CS at the beginning of the procedure if there is evidence of preexcitation suggestive of a left-sided pathway. Though not technically necessary, an advanced 3D mapping system can be helpful and is usually employed.

Baseline Observations in the EP Lab

Before initiation of SVT in the EP lab, baseline observations can be made that may help guide the differential diagnosis to a particular tachycardia mechanism.⁵ Ventricular preexcitation on the surface ECG or an HV interval less than 35 ms has a positive predictive value (PPV) of 86% and a negative predictive value (NPV) of 78% that the patient will have AVRT. Dual AV nodal physiology, defined as an increase of ≥ 50 ms in the A2-H2 interval with a 10-ms decrement in the A1-A2 interval during extrastimulus pacing has a PPV for AVNRT of 86%. Despite these numbers, 10% of patients with ventricular preexcitation will have inducible AVNRT and 15% of patients with dual AV nodal physiology will have AVRT or AT. Lack of baseline VA conduction at a ventricular pacing cycle length of ≥ 600 ms makes the presence of an accessory pathway (AP) unlikely. However, 5% of patients without evidence of VA conduction at baseline will have inducible AVRT, as retrograde AP conduction may be dependent on catecholamine stimulation.6 Furthermore, evidence of decremental VA conduction with ventricular extrastimulus pacing makes the presence of an AP unlikely. However, a small percentage of pathways do exhibit decremental conduction. Evidence of intra-atrial conduction delay or atrial scar, as determined by low-voltage or fractionated atrial electrograms, may suggest atrial tachycardia as the culprit mechanism. Although administration of adenosine with atrial or ventricular pacing can help determine the presence of an extranodal pathway, 38% of patients with typical AVNRT continue to have VA conduction via the fast pathway even in the presence of adenosine.⁷

Parahisian Pacing

Parahisian pacing can be utilized at baseline to determine the presence or absence of retrograde conduction over a septal AP.⁸ To perform this maneuver, the pacing catheter is positioned at the basal RV septum. The distal pacing electrodes should record both His and ventricular electrograms. To avoid inadvertent atrial capture, atrial electrograms should be minimized at the distal pacing electrode. Pacing should initially be performed at higher outputs (5–10 mA) to ensure His bundle capture and decremented until loss of His bundle capture with QRS widening.

Parahisian pacing results in both antegrade and retrograde conduction via the His-Purkinje system (HPS). The antegrade wavefront conducts via the HPS, resulting in a relatively narrow QRS morphology. In the absence of an AP, the retrograde wavefront conducts over the His bundle, with a Stim-His (S-H) interval of 0 ms, followed by atrial activation, with a Stim-Atrial (S-A) interval equal to the His-Atrial (H-A) interval. As the pacing output is decreased, loss of His bundle capture results in widening of the QRS as a result of antegrade conduction occurring directly over slowly conducting ventricular myocardium. Retrograde His bundle capture is delayed as conduction first occurs over ventricular myocardium, followed by retrograde activation of the right bundle with resultant activation of the His bundle. This delayed His activation results in prolongation of the S-A interval, which is a sum of the S-H and H-A interval. This is typical of a nodal response to parahisian pacing (Figure 1.3A). In the setting of a septal AP, the S-A interval remains constant, with loss of His bundle capture as atrial cproperties of the AP connecting the ventricular myocardium to the atrium (Figure 1.3B).

In order to properly interpret the results of parahisian pacing, the retrograde atrial activation sequence (RAAS) must be closely observed.⁹ When there is evidence of loss of His bundle capture with the same S-A interval and no change in RAAS, conduction is via only an AP. However, if there is a change in the RAAS after loss of His bundle capture, conduction is likely occurring either via multiple APs, simultaneous conduction up the fast and slow AV nodal pathways, or concomitant conduction up the AV node and an AP. To differentiate among these possibilities, close attention is needed to determine if changes occur in the S-A interval or H-A interval and if there is evidence of fusion on a multipolar CS catheter.¹⁰ The sensitivity of the extranodal response to parahisian pacing for detecting the presence of an AP is 46%. This likely reflects the fact that an extranodal response is less likely to be elicited for pathways farther from the AV nodal (i.e., lateral pathways). The specificity of this finding is 96%.

Differential RV Pacing

Another maneuver utilized to determine the presence of a septal AP is to perform differential RV pacing.11 Ventricular pacing is performed at both apical and basal RV sites at the same pacing cycle length (CL) and the interval from the RV pacing stimulus to the high right atrial (HRA) electrogram (V-A interval) is measured. In the absence of an AP, the V-A interval is longer when pacing basally compared to pacing apically, because conduction from the base must proceed over the septal myocardium before entering the HPS at the RV apex. However, in the presence of a HRA AP, the V-A interval is shorter when pacing basally compared to apically, as retrograde atrial activation is dependent on conduction via the basally located AP. The V-A index can be calculated, which is the difference in the V-A intervals apically compared to basally (VA_apical – VA_basal). A V-A index of > 10 ms had a sensitivity, specificity, and PPV of 100% for detecting the presence of a posteroseptal AP.

Tachycardia Characteristics

After initiation of SVT, there are several observations that can be made to determine the tachycardia mechanism. The tachycardia cycle length (TCL) gives insight into the mechanism of the tachycardia, although there is significant overlap. In general, AVNRT tends to be slower than AVRT. Slow tachycardias (CL > 500 ms) tend to be AVNRT, with a PPV of 83%. The first measurement made at the initiation of the tachycardia is the septal V-A interval, measured from the beginning of the surface QRS to the earliest septal atrial electrogram. In adults, a septal V-A interval of less than 70 ms excludes AP-mediated tachycardias and makes typical AVNRT highly likely. Less than 1% of ATs will exhibit a V-A interval of less than 70 ms.

When tachycardia is initiated, spontaneous oscillations (“wobble”) in the TCL should be noted. If changes in the A-A interval precede changes in the H-H interval (the As are driving the Vs), the most likely mechanism is AT. However, if changes in the H-H interval precede changes in the A-A intervals, the most likely mechanism is AVNRT or ORT.

If the septal V-A time is greater than 70 ms, the CS catheter can be used to determine whether the RAAS during tachycardia is concentric or eccentric. During typical AVNRT, the RAAS is concentric, as the area of earliest atrial activation is near the fast pathway that inserts near the His bundle at the apex of the triangle of Koch. With atypical AVNRT, the earliest atrial activation is near the CS ostium. With the exception of paraseptal AVRT and AT, AVRT and AT will demonstrate varying degrees of eccentric atrial activation, depending on the pathway or foci locations relative to the AV node. Evidence of eccentric activation excludes most all forms of AVNRT as the tachycardia mechanism. However, a small number of patients with ANVRT have evidence of eccentric atrial activation and can only be successfully ablated from within the CS or along the mitral annulus, related to the leftward extensions of the slow pathway.

Initiation, termination, and zones of perturbation during tachycardia can give insight into the mechanism of the arrhythmia. When tachycardia induction is reproducibly dependent on a prolongation of the A-H interval with atrial pacing, the most likely diagnosis is AVNRT, with a PPV of 91%. This prolongation is related to block in the fast pathway and “jumping” to the slow pathway, usually with a change in the A-H interval of at least 50 ms with an atrial extrastimulus. Initiation of AVRT may also demonstrate some AV delay, but delay can also occur anywhere within the circuit, including intramyocardial conduction delay. As AT is independent of the AV node, AV nodal delay is not required for tachycardia induction.

The development of LBBB is more commonly seen with ORT, with a PPV of 92%. There are several reasons for this phenomenon. The faster rate of ORT likely favors the development of aberrant conduction. The occurrence of LBBB aberration also promotes the development of ORT by allowing the AP time to recover to allow for retrograde conduction to occur. Furthermore, as induction of AVNRT is dependent on the development of AV nodal delay, resulting in a longer H1-H2 interval, the development of aberration is unlikely. In contrast, a critical A-H delay is not required for initiation of ORT. Therefore, the short A-H interval during tachycardia initiation encroaches on the refractoriness of the HPS, resulting in aberration. An increase in the V-A interval by greater than 20 ms with bundle branch block (BBB) is diagnostic of ORT using an AP that is ipsilateral to the side of block, with a PPV of 100%. This increase in the V-A interval is related to relatively slower intramyocardial conduction caused by the BBB. This increase in the V-A interval may result in a corresponding increase in the TCL. However, the increased VA time may also result in a compensatory decreased in the A-H interval, resulting in no apparent change in the TCL (Figure 1.4).

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