AVNRT Slow/Fast

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

Main article AVNRT

Differential Diagnosis

The differential of a narrow complex tachycardia with a short RP interval includes Low Atrial Tachycardia, AVRT with Septal Bypass Tract, or accelerated Junctional Tachycardia

Induction of AVNRT

There are several ways to induce AVNRT.

1. The most common way is through the introduction of atrial or ventricular premature depolarizations (APDs and VPDs) beats. You may also need to use double atrial stimuli is you are on the slow pathway.
2. Continuous burst pacing or rapid incremental pacing in the right atrium (RA), the coronary sinus (CS) may induce the tachycardia
3. Decremental ramp atrial extrastimuli has also been shown to effectively induce AVNRT. to perform this you must set the total number in S1 drive train to one. Turn on S1, S2, S3, S4, S5, and S6 at following cycle lengths: S1—600 ms, S2—550 ms, S3—500 ms, S4—450ms, S5—400 ms, and S6—350 ms. Thus, a train consisting of a total of six APDs at decremental coupling interval of 50 ms from previous APDs are delivered from the HRA. If no SVT is induced, then S1 is programmed at 550 ms and cycle lengths of the subsequent APDs were also decreased by 50 ms, to a minimum of 300 ms.
4. If you have no success with the above pacing protocols then you can start pharmacological agents such as isoproterenol or atropine.
5. Esmolol has also been reported as useful because it changes the conduction over fast pathway and shortens the refractory period.
6. Non-pharmacological maneuvers such as hyperventilation and 45 degree headup upright posture during pacing have also been studied to facilitate induction of AVNRT.

Criteria for Support for AVNRT

• Critical prolongation of the AH interval initiates tachycardia

AH interval of 230 ms at Drive train of 400ms and S2 of 230 ms

AH interval Jumps to 376 ms at Drive train of 400ms when the S2 is decreased by 10 ms. This figure shows the jump with a single echo beat

• Concentric Activation of the atria with the earliest atrial activation at the His bundle or proximal CS and the Septal VA < 65-70 msec.

Initiation of AVNRT with double extrastimuli from the CS resulting initiation of a tachycardia with a jump to the slow pathway and concentric retrograde activation. The earliest atrial activation is marked with an arrow

• Ventricular Overdrive Maneuver results in a value greater than 115 ms

The Post Pacing Interval is 508 ms and the Tachycardia Cycle Length is 328 ms. So the PPI-TCL equals 180 ms supporting evidence for AVNRT

• Delta HA Interval, more postive than -10.
• Development of a BBB with initiation
• Parahisian Pacing results in a Nodal Response
• Decremental VA conduction during programmed Ventricular Stimulation
• Termination by a PVC that was delivered early when the His bundle was not refractory.

Against AVNRT

1. Rare to be induced with V pacing

Maneuvers

1. PACs. Fail to advance even when early
2. PVCs. Fail to advance a when His is refractory
3. Ventricular Overdrive Maneuver (PPI-TCL>115)
4. V pacing at TCL. Measure VA

Ablation

To ablate AVNRT using an anatomic strategy, you must position your catheter anterior to CS os and have an A/V electrogram proportion of 1/4. The atrial component is usually has multiple components (fractionated) and is rarely sharp. Initial power of 50 W for 60 seconds. With target temperature of 60 degrees. Terminate if no accelerated junctional rhythm occurs after 15 seconds. If junctional rhythm occurs look for VA block and check for antegrade conduction and PR prolongation with rapid atrial pacing (400-500 ms). If unsuccessful may need to ablate superior to the CS os or in CS os. Also can ablate in. Recheck with programmed atrial stimulation after each ablation

Medical Treatment

• Beta Blocker
• Verapamil
• Flecainide 50-200 mg bid
• Propafenone 150 to 300 TID

EKG Findings

• 
  This is an extremely rare tachycardia which occurs when a single sinus impulse conducts down an AV node with both a slow and fast pathway. When most impulses reach the AV node they conduct down both the slow and fast pathway. Since conduction is faster down the fast pathway it beats out the slow pathway conduction and depolarizes the ventricle. The impulse traveling down the slow pathway either collides with the impulse from the fast pathway that is now traveling back up the slow or the impulse traveling down the slow pathway reaches the ventricle and finds the ventricle refractory. In the above EKG the sinus impulse represented by the P wave in the beginning of the rhythm strip conducts down the fast pathway resulting in the first QRS complex; the impulse from the slow pathway also depolarizes the ventricle seen as the second QRS complex. You will notice that there is no p wave between the first and second QRS complexes. Therefore the first sinus beat results in a doubling of the ventricular sinus rate. This sequence is repeated again in the 7th and 8th QRS complex. It is an extremely rare tachycardia and is resistant to multiple antiarrhythmic medications. The above patient underwent ablation of their slow pathway and no further episodes were observed.

References

1. Josephson ME. Supraventricular tachycardia. In: Josephson ME (ed.): Clinical Cardiac Electrophysiology—Techniques and Interpretations,3rd Ed. Philadelphia, Lippincott-Williams and Wilkins, 2002
2. Tachycardia and Other Supraventricular Tachycardias BHARAT K. KANTHARIA, M.D., FAROOQ A. PADDER, M.D.,and STEVEN P. KUTALEK, M.D. PACE 2006; 29:1096–1104