Examine the single lead EMS rhythm strip carefully. What is in your DD of regular wide complex tachy?
A 60-year-old male with hyperlipidemia who is otherwise healthy and active without cardiac comorbidities experienced acute onset of rapid regular palpitations after his usual daily workout. He developed associated diaphoresis and dizziness and EMS was notified. Initial rhythm strip obtained by EMS revealed a wide complex tachycardia (WCT) (Figure 1).
Figure 1: Continuous single lead EMS rhythm strip
Question 1: What is the differential diagnosis of the observed wide complex tachycardia (WCT)?
Answer: The differential diagnosis of a regular WCT includes ventricular tachycardia (VT), supraventricular tachycardia (SVT) with aberrancy, and antidromic atrioventricular reentrant tachycardia (AVRT). It is difficult to make a definitive diagnosis using this single lead rhythm strip and VT would seem to be the reflexive diagnosis, but several observations can narrow the differential.
The rhythm strip shows a narrow complex tachycardia (NCT) that transitions to a WCT without a change in QRS axis (direction of dominant QRS vector) as would be seen in VT. Specifically, the first 10 beats on the recording show a NCT at approximately 150 beats per minute (bpm). Recall that atrial flutter (AFL) is a macro-reentrant right atrial circuit occurring at approximately 300 bpm, therefore a regular NCT at 150 bpm should raise suspicion for AFL with 2:1 atrioventricular (AV) conduction.
Figure 2. Annotated rhythm strip. The upper strip shows a narrow QRS complex representing conduction via the
AV node, with the bottom strip showing a wide QRS which may represent bundle branch aberration or preexcitation
due to conduction via an accessory pathway.
Close analysis of R-R wave intervals of these first 10 beats does show subtle irregularity; the other possible interpretation of this initial rhythm would be atrial fibrillation/flutter which may coexist. Subsequently the rhythm accelerates to a very regular NCT at approximately 300 bpm, initially with a narrow QRS for the duration of the upper strip until a widened QRS morphology develops at the same heart rate for the remainder of the recording.
This may represent a transition of ongoing AFL from 2:1 conduction to 1:1 conduction (or organization of atrial fibrillation to 1:1 atrial flutter) with subsequent QRS widening due to bundle branch aberration or alternatively pre-excitation due to antegrade conduction over an accessory pathway. Indeed, close analysis of atrial activity in the rhythm strip does reveal negative sawtooth flutter waves occurring at ~300 bpm (Figure 2, above).
Question 2: EMS finds the patient to be hemodynamically stable in this persistent WCT. What possible interventions would you consider?
ACLS guidelines recommend that in a patient in a hemodynamically stable (normotension, no symptoms of ischemia or heart failure) WCT suspicious for VT medical therapy with amiodarone should be instituted. (In a case of hemodynamic instability, direct current cardioversion should be performed in both wide and narrow complex tachycardias.) The alternating wide and narrow complex rhythm may not be VT, but likely represents SVT with bundle branch aberration or atrial fibrillation/flutter with pre-excitation.
Because ongoing pre-excited atrial fibrillation/flutter is a possibility, pushing adenosine would not be prudent as AV node blockade can provoke increasingly rapid conduction across an accessory pathway with subsequent ventricular fibrillation/flutter and hemodynamic collapse.
IV procainamide would be a reasonable option as it preferentially blocks accessory pathway conduction. In this case, the patient spontaneously converted to sinus rhythm without intervention.
Question 3: The patient is admitted to telemetry and overnight has no further arrhythmias. What is the best next step in his management?
An electrophysiology study (EPS) with radiofrequency (RFA) catheter ablation would be both diagnostic and likely curative. EPS involves advancing mapping electrode catheters via the femoral veins into the cardiac chambers which allows induction of arrhythmia with programmed electrical stimulation, delineation of the arrhythmia focus, and focal ablation.
The patient underwent EPS and was found to have easily inducible atrial fibrillation that would organize into the following regular wide complex rhythm (Figure 3, below).
Figure 3: Surface 12-lead ECG of induced wide complex tachycardia.The surface 12 lead of the induced clinical arrhythmia does not elucidate whether the rhythm is VT, antidromic AVRT, or SVT with bundle branch aberration or preexcitation. Placement of a 20-pole mapping electrode around the tricuspid annulus (TA) in the right atrium revealed counterclockwise wavefront of atrial activation at a cycle length of approximately 300 bpm consistent with typical AFL.
Catheter ablation from the tricuspid valve to the inferior vena cava along the cavotricuspid isthmus disrupted the AFL circuit with subsequent conversion to sinus rhythm.
Post-ablation, programmed electrical stimulation of the atrium was performed and showed no evidence of inducible typical AFL and no evidence of AVRT. Induction of atrial fibrillation (AF) with rapid atrial pacing, however, did show intermittent beats with preexcitation, suggesting a “bystander” accessory pathway, ie, one that is not involved in an AVRT circuit but can conduct in antegrade fashion. Ablation of the accessory pathway therefore is indicated to mitigate future risk of rapid preexcited AF. A left lateral accessory pathway was mapped along the mitral annulus and focal ablation of the bypass tract was performed with success. Post-ablation, the patient had no further evidence of preexcitation and programmed electrical stimulation of the atrium and ventricle showed no recurrent wide complex tachycardia. The patient was discharged the following day and has done well without recurrent arrhythmia.
Additional reading material: http://lifeinthefastlane.com/ecg-library/pre-excitation-syndromes
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