An unusual complication of adenosine administration in supraventricular tachycardia.

Introduction

Adenosine is an atrioventricular (AV) nodal blocking agent and is most commonly used drug for acute termination of AV node dependent tachycardias. We report a case where a patient with narrow complex tachycardia (NCT) developed wide QRS complex tachycardia after adenosine administration.

Case report

45 years age female presented with acute onset palpitation. On examination she had tachycardia and a blood pressure of 116/70. ECG was suggestive of NCT (Fig. 1). On administration of 6 mg of intravenous adenosine she developed transient AV block followed by irregular wide complex tachycardia (Fig. 2) and systemic hypotension, requiring DC cardioversion. Electrocardiogram in sinus rhythm showed evidence of preexcitation (Fig. 3). Electrophysiological evaluation documented left free wall accessory pathway with inducible atrioventricular reentrant tachycardia. Radiofrequency ablation of the accessory pathway was performed through trans-septal approach. After delta wave disappeared following radiofrequency ablation, intravenous adenosine was given to see the completeness of ablation and a self-terminating episode of atrial fibrillation (AF) occurred following transient AV block (Fig. 4).

Fig. 1

12 lead ECG showing narrow complex tachycardia.

Fig. 2

12 lead ECG showing irregular wide QRS complex tachycardia due to pre excited atrial fibrillation.

Fig. 3

12 lead ECG in sinus rhythm showing delta waves consistent with left sided pathway.

Fig. 4

Post radiofrequency ablation ECG after adenosine administration showing atrial fibrillation following transient AV block and no evidence of preexcitation. There are atrial pacing spikes, but atrial fibrillation is induced probably just before the first atrial pacing spike based on P wave morphology.

Discussion

Adenosine can terminate AV node dependent reentrant tachycardias (AVNRT and AVRT) by blocking the AV node. Due to short half-life and safety profile it is widely accepted as treatment of choice for narrow complex supraventricular tachycardia [1]. Common transient arrhythmias during adenosine administration include transient complete heart block and sinus arrest [2]. Ventricular and atrial premature complex and transient nonustained ventricular tachycardia have also been reported. Adenosine can also induce atrial fibrillation. The frequency of adenosine induced atrial fibrillation may vary from 1% to 12% depending on dosage [3,4]. Mechanism of adenosine induced AF includes directs effect on atrial myocyte, sympathoexcitatory effects and effect on pulmonary vein tissue [4,5]. The drug shortens the atrial repolarization by activating efflux of potassium current through IKAdo channel [5]. Shortening of atrial repolarization is associated with shortening of atrial refractory period. Due to heterogeneous distribution of A1 receptors in atrial myocardium, adenosine induced APD shortening is non-homogeneous across atria [6] (greater shortening in RA than LA). This repolarization heterogeneity perpetuates initiation and maintenance of AF. Adenosine also results in a reflex increase in circulating catecholamine levels and sympathetic nerve traffic. Increase in circulating catecholamine level promotes atrial premature complex and atrial fibrillation has been shown to be induced with long short atrial sequence, similar to the mechanism that causes the development of ventricular fibrillation when a ventricular premature complex falls on the vulnerable portion of the T wave. Study by Ip JE et al. [5] showed that adenosine induced AF was reproducibly initiated from the RSPV and they postulated that AF occurs due to direct effect of adenosine on pulmonary vein.

We report a case where accessory pathway mediated atrioventricular tachycardia was converted to pre excited atrial fibrillation by administration of adenosine. Although adenosine has been reported to induce atrial fibrillation in 10% cases of accessory pathway mediated AVRT [4], conversion from AVRT to pre excited atrial fibrillation is rare. The commonest mechanism of pre excited AF is transient AV block, so the AF is propagated through accessory pathway if the refractory period of the AP is short. Though adenosine has no direct effect on AP, it can shorten the refractory period by sympatho-excitatory effect. Adenosine has also been reported to induce ventricular fibrillation in patients with pre-excited atrial fibrillation [7], especially if the shortest preexcitation R-R interval is more than 240 beats per minute [8]. Hence administration of adenosine should be limited to medical facilities with emergency resuscitation because of the potential for conversion of a simple NCT to life threatening pre-excited atrial fibrillation, especially if the mechanism of NCT is not clear. In such situations, intravenous beta-blockers or calcium channel blockers should be better alternatives.