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International Journal of Arrhythmia 2011;12(2): 7-13.
심실상성 빈맥의
감별진단을 위한 방법

인제대학교 의과대학 내과학교실 박 경 민
Kyoung-Min Park, MD, PhD
Department of Internal Medicine, Sanggye-Paik Hospital, University of Inje College of Medicine, Seoul, Korea


   The goals of electrophysiologic (EP) testing in patients with supraventricular tachycardias (SVTs) include the following: ① evaluation of baseline cardiac electrophysiology; ② induction of SVT; ③ evaluation of the mode of initiation of the SVT; ④ definition of atrial activation sequence during the SVT; ⑤ definition of the relationship of the P wave to the QRS at the onset and during the SVT; ⑥ evaluation of the effect of BBB on the tachy cardia cycle length and ventriculoatrial (VA) interval; ⑦ evaluation of the SVT circuit and requirement of the atria, His bundle (HB), and/or ventricles in the initiation and maintenance of the SVT; ⑧ evaluation of SVT response to programmed electrical stimulation and overdrive pacing from the atrium and ventricle; and ⑨ evaluation of the effects of drugs and physiological maneuvers on the SVT. Discussion in this section will focus on differential diagnosis of narrow QRS complex paroxysmal SVTs, including AT, ORT, and AVNRT divided into Baseline findings, Tachycardia characteristics, and Maneuvers during tachycardias.

1. Baseline Findings

   There are several baseline findings to differentiate these three SVTs. We have to confirm three evidences of baseline findings i.e. evidence before the induction of SVT. First, we have to find evidence of an accessory pathway (AP), second, evidence of a dual AV nodal pathway, and third, evidence of intra atrial conduction delays or scars.

First, evidence of an accessory pathway (AP)

1) Ventricular preexcitation

   The definition of preexcitation is below 35 msec of an HV interval it can be measured using the earliest intracardiac ECG. The degree of preexcitation depends on AV nodal conduction time and the location of the accessory pathway. Although the prevalence is low, the positive predictive value may be 86%.

Second, evidence of a dual AV nodal pathway

2) Dual AV nodal physiology

   The evidence of a dual AV nodal physiology during atrial extra stimuli and decremental ventriculoatrial (VA) conduction are the substrate for AVNRT. The definition of AH jump (atrio-his jump) is prolongation of the AH interval ≥50 msec with a 10 msec decrease in extra-atrial stimulus interval (A1A2).

3) Decremental VA conduction

   Decremental VA conduction makes an accessory pathway unlikely, but does not exclude a retrograde block in the pathway with conduction up the AV node and a decremental accessory pathway.
  Third, evidence of intra atrial conduction delays or scars with the information of past medical history and endocardial electrograms.

Other baseline findings

4) VA block cycle length >600 msec

   Absence of VA conduction makes AVRT unlikely. However, rare accessory pathways are catecholamine dependent. Consequently, there is about 5% chance of AVRT if the VA block cycle length is over 600 msec at baseline.

5) VA block with adenosine

   VA block with adenosine during ventricular pacing suggests the absence of an AP. Absence of VA block is always not diagnostic of an AP because retrograde conduction couldn't be blocked in some fast AV nodal pathways with adenosine. Retrograde fast pathway conduction is not blocked by 12 mg of adenosine in 38% of patients with typical AVNRT.1

6) Para-Hisian pacing2

   Accessory pathway response during para-Hisian pacing favors ORT with high predictive value (Figure 1).

(1) Methods

   Para-Hisian pacing uses right ventricular pacing close to the His bundle or proximal right bundle branch. The pacing output is altered to produce ventricular capture with an intermittent His bundle or right bundle branch capture to selectively alter the timing of His-bundle activation without changing the timing of local ventricular activation. With retrograde AV nodal conduction, the delay in timing of retrograde His bundle activation should produce an equal delay in the timing of retrogradeatrial activation without changing the retrograde atrial activation sequence (Figure 1A). With retrograde conduction over an AP, the loss of His bundle capture should not change the timing of retrograde atrial activation or the retrograde atrial activation sequence (Figure 1B). A mixture of these two responses (delay in the timing of atrial activation in the His bundle electrogram with a change in the retrograde atrial activation sequence) would be expected with retrograde conduction over both an AP and the AV node (Figure 1C). The degree of contribution to atrial activation by the AP and the AV node (atrial fusion) should depend on the distance of the AP from the para-Hisian pacing site and the retrograde conduction times over the AP and AV node.

(2) Measures

   The response to para-Hisian pacing is determined by the change in the following variables between HB-RB capture and HB-RB non-capture and measures the ① atrial activation sequence; ② the S-A interval in each electrogram, including an electrogram recorded close to the site of the earliest retrograde atrial activation during tachycardia; and ③ H-A interval in the His bundle electrogram. These variables are examined before and after AP ablation.

2. Tachycardia Characteristics

1) Septal ventriculoatrial (VA) interval

   If the VA interval during tachycardia is below 70 msec, it favors AVNRT with more than 99% positive predictive value.

2) Eccentric atrial activation

   Early atrial activity in the proximal coronary sinus electrodes suggests a posteroseptal pathway or AV node slow pathway conduction. Eccentric atrial activation is any atrial activation that does not activate the AV node and the area around the AV node first. This is frequently seen with retrograde ventricular stimulation, when the retrograde impulse finds the AV node refractory. The site of earliest atrial activation is then the distal CS and not in the proximal area closer to the AV node/His bundle.3,4

3) SVT termination with VA block

   Spontaneous termination of an atrial tachycardia (without an atrial premature depolarization) would not be expected to be followed by AV block.

4) Coumel's law (increase VA time >20 ms with bundle branch block [BBB])

   An increase in the VA time >20 ms with BBB is diagnostic of ORT using an AP that is ipsilateral to the side of BBB. Beware that a compensatory decrease in the AH or HV may not cause a change in the tachycardia cycle length.

5) LBBB aberration during PSVT

   The mere development of LBBB is more common during ORT regardless of change in the VA interval. There are two reasons for this. First, the ORT tends to be faster (however, LBBB is more common during ORT association independent of rate) and second, LBBB facilitates induction of ORT using a left-sided accessory pathway by allowing more time for the pathway to recover

6) Induction dependent on a critical AH

   AVNRT is more likely when the induction is dependent on a critically long AH interval (i.e. anterograde block in the fast pathway). Similarly, AVNRT is more likely when the termination is dependent on a critically short AH interval. The same principal applies to ORT, which is the most likely mechanism when the induction depends on an anterograde block in an accessory pathway.

7) SVT cycle length = 500 msec

   AVNRT tends to be slower than ORT, but there is considerable overlap. However, very slow tachycardias are more likely to be AVNRT

8) AV block during SVT

   AV block during SVT excludes ORT. Although AV block is more common during AT than AVNRT, AVNRT is so common that when AV block occurs, the tachycardia is still more likely to be AVNRT. AV block during AVNRT is usually 2:1, is infranodal and functional, and resolves during ventricular pacing.

3. Maneuvers during Tachycardias

  * Atrial pacing
    1. Pace the A during SVT at a CL 10~40 ms < SVT CL
    2. Pace the A during SVT at the AV block CL
    3. Scan diastole with a premature atrial extrastimulus
  * Ventricular pacing
    1. Pace the V during SVT at a CL 10~40 ms < SVT CL
    2. Pace the V during SVT at a CL 200~250 ms for 3~6 beats
    3. Scan diastole with a premature ventricular extrastimulus

1) Atrial overdrive pacing maneuvers

   Dependence of tachycardia termination or continuance on last AH interval

(1) Pacing Maneuver

   Pace atrium during SVT at longest cycle length (CL) resulting in AV block

(2) Observation

   Is SVT termination dependent on last AH interval?

(3) Interpretation

   AVNRT usually terminates after pacing when the last AH interval is short relative to the AH of the tachycardia, and continues after pacing when the last AH interval is long.

2) Ventricular overdrive pacing maneuvers

   Response to ventricular pacing just faster than the tachycardia

(1) Pacing Maneuver

   Pace the V during SVT at a CL 10~40 ms < SVT CL

(2) Observation

   Can the atrial 'A' rate be accelerated to the ventricular 'V' pacing rate? (Entrainment)

  Entrainment can be defined when the atrial cycle length accelerated to the pacing cycle length, without change in the atrial activation sequence, and the tachycardia continued after pacing was discontinued.

A. If not entrained,
① can SVT be terminated with a PVC during His bundle refractoriness?
② can atrial activation be advanced with a PVC during His bundle refractoriness?
③ can SVT be terminated with a PVC without depolarizing the atrium?

# Interpretation
  Tachycardia termination with a PVC delivered during His refractoriness is diagnostic of ORT.
  To conclude that the His bundle was refractory, the ventricular extrastimulus must result in ventricular capture and not precede the expected time of the His bundle depolarization by more than the baseline HV interval.
  ① Advancement of atrial activation with a PVC delivered during His refractoriness is diagnostic of an AP, but not of an ORT. If atrial activation has been advanced but caused a different activation, then the AP may not participate in the tachycardia. Inability to advance A with a PVC does not exclude an AP. You may not see advancement if an extrastimulus is delivered far from the AP.
  ② If SVT terminated with a PVC without depolarizing the atrium, there is no possibility of atrial tachycardia.

B. If entrained,
① is the response or cessation of pacing 'A-A-V' or 'A-V'?
② is the PPI (post-pacing interval) - TCL (tachycardia cycle length) > or < 115 msec?

# Interpretation
  ① If the response or cessation of pacing during tachycardia is 'A-A-V', it favors AT and if 'AV', it favors AVNRT or ORT. If the tachycardia mechanisms are atypical AVNRT, pseudo' A-AV'patterns may be observed because of longer retrograde atrial conduction times through slow pathways of AV node.
  ②The S-A (stimulus-atrial interval) VA (ventriculoatrial interval) and PPI-TCL are useful in distinguishing atypical AVNRT from ORT using a septal accessory pathway. Consequently, patients with QRT using a septal accessory pathway have an S-A-VA < 85 msec and PPI-TCL < 115 msec5 (Figure 2).

4. Differential Diagnosis of PSVT in the EP Laboratory

   In most cases of SVT, a combination of baseline findings, tachycardia characteristics, and pacing maneuvers are needed to make a diagnosis (Figure 3). The combination of atrial activation sequence, septal VA interval, and response after entrainment from the ventricle provides a diagnosis in 65% of cases and excludes one mechanism in an additional 27%.


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