Stable, Wide-Complex Tachyarrhythmia: Should you even consider SVT with Aberrancy?

Co-authors: Paul Lavadera and Esteban Davila

Peer Editor: Alec Feuerbach

Faculty Editor: Mark Silverberg

The Case

A 65-year-old male with a history of hypertension, hyperlipidemia, diabetes, hypertrophic cardiomyopathy, recent stroke, and atrial fibrillation (AF) (+anticoagulation) presented to the ED for syncope. EMS noted a wide-complex tachycardia. EMS administered 150 mg of amiodarone, and the patient converted from wide-complex tachycardia to AF. In the ED, the patient remained in AF and at time of admission to the Coronary Care Unit (CCU), the patient had a heart rate of 61/min, blood pressure of 121/85 mm Hg, respiratory rate 16/min, and pulse oximetry 100% on room air.

The patient’s ECG at time of admission is shown below:

ECG interpretation: Atrial fibrillation at 61/min, right axis, right bundle branch block (RBBB)

Despite amiodarone infusion, the patient developed recurrent, wide-complex tachycardia while in the CCU. The patient reported palpitations but denied dyspnea, chest pain, and lightheadedness. The heart rate was approximately 160 beats/min and blood pressure was 118/83 mm Hg.

Defibrillator pads were promptly placed, and the following ECG was obtained:

ECG interpretation: regular, monomorphic, wide-complex tachycardia at 160/min

What is the differential?

The differential diagnosis for regular, monomorphic wide complex tachycardia includes ventricular tachycardia (VT), regular supraventricular tachycardia (SVT) with aberrancy, regular SVT with AV conduction over an accessory tract, and pacemaker-mediated tachycardia. “Aberrancy” occurs when conduction of a supraventricular impulse is delayed or blocked in the bundle branches or distal Purkinje system or depolarizes the ventricles through an accessory pathway. Delayed/blocked conduction can occur through pre-existing or rate-related bundle-branch block, hyperkalemia, and toxicologic causes such as sodium channel blockers. For more examples of wide-complex tachycardias, check out these posts.

Managing a patient with “stable”, regular, monomorphic, wide-complex tachycardia should start with the assumption of VT with the decision for drug or electrical therapy left to the discretion of the provider and patient. Approximately 80% of all wide complex tachycardia is VT.[1] When you add prior heart failure (reduced or preserved ejection fraction) [2], prior “angina pectoris”, or structural heart disease (as in this patient), the positive predictive value for VT is > 95%.[1,3-5]

However, if one strongly suspects SVT, specifically AV nodal reentrant tachycardia with aberrancy, one can attempt vagal maneuver or administer adenosine as both a diagnostic and therapeutic treatment. Vagal maneuvers and adenosine in VT that demonstrates retrograde VA conduction (P waves following the QRS complex) can cause retrograde P waves to disappear – this VA block can confirm the diagnosis of VT.[6] One should note that vagal maneuvers are not recommended by guidelines for regular, wide complex tachycardia.[7,8,9]

In this patient, the following diagnostic and therapeutic methods were attempted.

Attempt 1

The first attempt to convert the rhythm into sinus rhythm involved a vagal maneuver.

Result: There was no change in the rhythm.

(The modified valsalva maneuver (REVERT trial) successfully converts SVT to sinus rhythm 43% of the time compared to 17% with standard valsalva maneuver.[10])

Attempt 2

The second attempt involved 6 mg of Adenosine followed by a rapid 15 cc normal saline flush. Adenosine is a reasonable first drug treatment and is supported by the guidelines [8]; however, one should note two points. First, 10% of ventricular tachycardia cases will convert with adenosine. Therefore, although conversion with adenosine may increase the odds of SVT by a factor of 36.3,[7] it will not definitively rule in SVT. Secondly, for patients with WPW and orthodromic AVRT, adenosine could uncover an underlying AF and theoretically allow rapid conduction of AF impulses preferentially through an accessory pathway precipitating ventricular fibrillation; this is the reason for having the defibrillator pads in place.[11]

Result: The patient experienced warmth, however, there was no effect on the rhythm. Common adverse effects from adenosine should be communicated to the patient prior to administration and range from a feeling of warmth to severe chest pain.

An alternative to the method described above is the single-syringe technique, whereby 6 to 12 mg of adenosine and normal saline are drawn into one 20 ml syringe and pushed as a one-time bolus. One small, prospective study showed that a single-syringe technique may be superior to the two-syringe technique.[12]

Attempt 3

The third attempt was 12 mg of Adenosine followed by a 15 cc normal saline flush.

Result: Again, the patient felt warmth without any change in rhythm.

If the patient had AV nodal reentrant tachycardia with aberrancy or AV reciprocating tachycardia, adenosine’s effect of inhibiting the reentry pathway in the AV node theoretically should terminate the tachydysrhythmia. Given the failure of response to adenosine, the patient was thought to be in VT. The patient had no signs of end-organ hypoperfusion (and was “stable”), so cardioversion was deferred at this time.

If the wide complex tachycardia is associated with end-organ hypoperfusion, any effort to differentiate the tachydysrhythmia should “academic” and done only after treatment. The Brugada and Vereckei algorithms are most notable, but these still misdiagnose ~10% of wide complex tachycardias and inter-rater reliability is questionable.[13] Here are findings that strongly suggest VT:

AV dissociation (~100% specificity, see below)
Suggestive of AV dissociation: cannon A waves, fusion beats, capture beats
Extreme axis deviation or “northwest axis” (positive in aVR and negative in I and aVF)
Initial R or Rs wave in aVR
A very broad complex (>160 ms) with a different QRS morphology compared to the baseline QRS
RSR’ complexes with a taller left rabbit ear seen in V1
Brugada sign: Distance from onset of R wave to nadir of S wave > 100 ms in leads V1-6
Josephson sign: Notching/slurring near the nadir of the S wave

The patient had already developed liver injury presumed from prior amiodarone use, so procainamide 150 mg (class 1a antidysrhythmic) was given over ten minutes for three doses. The PROCAMIO trial found procainamide to be more successful at terminating ventricular tachycardia with fewer major cardiac adverse events [14] (doses typically 20-50 mg/min or 100 mg every five minutes (max dose of 17 mg/kg)). After transitioning to a procainamide infusion (1-4 mg/min) for two hours, the patient converted back to atrial fibrillation. The patient was transitioned to oral disopyramide (class 1a antidysrhythmic) therapy. Coronary angiography did not reveal an obstructive lesion, and an ICD was placed for secondary VT prevention. The patient was discharged with a plan for outpatient ablation therapy.