Irregular Narrow Complex Tachycardia in a 29-Year-Old Woman
- 1 to 2 atrioventricular conduction
- atrioventricular nodal reentrant tachycardia
- dual atrioventricular nonreentrant tachycardia
A 29-year-old woman without known medical illness was evaluated for incessant palpitations. She presented to an emergency department multiple times, where various diagnoses were made, including junctional tachycardia, atrial tachycardia, and atrial fibrillation. Therapy with propafenone, metoprolol, and rivaroxaban was initiated, but her symptoms continued. Echocardiography did not show evidence of structural heart disease. The patient was then referred to our hospital for further treatment and potential ablation for atrial fibrillation. At her clinic visit, a 12- ECG revealed an irregular narrow complex tachycardia with group beating pattern (Figure 1).
What is the rhythm shown in Figure 1?
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Response to ECG Challenge
P waves arising from the sinus node are seen at a rate of 66 beats per minute. Each P wave is followed by 2 QRS complexes until the tachycardia terminates, followed by reinitiation of tachycardia with the same pattern. The double ventricular response to a single atrial activation, called 1 to 2 atrioventricular conduction or dual ventricular response, occurs when activation from each sinus beat first proceeds down the fast pathway (FP) to create a QRS complex with a short PR interval, followed by activation down the slow pathway (SP) to create another QRS complex with a longer PR interval1 (Figure 2). This repeats itself for each sinus beat, leading to a nonreentrant tachycardia named dual atrioventricular nonreentrant tachycardia.2,3 The occurrence of 1 to 2 atrioventricular conduction during sinus rhythm requires the absence of retrograde concealment into the SP by antegrade activation down the FP (Figure 3). It also requires slow enough conduction down the SP to allow recovery of the His-Purkinje system to produce another QRS complex. Also notable is the occurrence of Wenckebach phenomenon in the SP, such that there is progressive prolongation of the PR interval for the second QRS complex (arising from SP conduction), followed by block leading to temporary termination of the tachycardia.1 In Figure 2, the PR interval associated with SP conduction progressively prolongs from 600 to 680 milliseconds after the 4th, 5th, and 6th sinus beats, followed by complete block in the SP after the 7th sinus beat.
Differential diagnosis for this ECG includes single junctional extrasystole after each sinus beat. However, the repetitive group beating pattern makes this less likely. The presence of regular sinus rhythm with no other apparent atrial activity excludes other common causes of irregular narrow complex tachycardia, such as atrial fibrillation, atrial flutter, and multifocal atrial tachycardia.
The patient underwent an electrophysiology study that confirmed the presence of dual atrioventricular nodal physiology and 1 to 2 atrioventricular conduction during sinus rhythm and with premature atrial contraction (Figure 4A). In addition, 1 to 2 atrioventricular conduction resulted in induction of typical atrioventricular nodal reentrant tachycardia (AVNRT), an unusual form of AVNRT initiation (Figure 4B). AVNRT is most commonly initiated by a premature atrial contraction that encounters a refractory FP, resulting in conduction down the SP. If conduction in the SP is slow enough, then the FP repolarizes and can conduct in the retrograde direction, thus initiating a reentrant rhythm. In this case, however, the 1 to 2 atrioventricular conduction results in conduction down the FP, followed by the SP to produce 2 QRS complexes. The FP recovers refractoriness by the time that SP conduction is completed, resulting in its retrograde activation to initiate AVNRT. AVNRT is a reentrant tachycardia, unlike dual atrioventricular nonreentrant tachycardia. Radiofrequency ablation of the SP in the triangle of Koch resulted in elimination of both forms of tachycardia. The patient did not have recurrent tachycardia 6 months after the ablation.
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- © 2017 American Heart Association, Inc.