Advanced Concepts in Arrhythmias

by Nicholas G. Tullo, MD, FACC, FHRS


Supraventricular Tachycardia

Supraventricular tachycardia (SVT) includes atrial fibrillation and flutter, atrial tachycardias, and a group of disorders known as paroxysmal supraventricular tachycardia (PSVT). Paroxysmal supraventricular tachycardia is characterized by a regular, narrow QRS complex tachycardia of sudden onset and termination.  The most common variety of PSVT arises from the AV nodal complex and is known as AV Nodal Reentry Tachycardia (AVNRT).  This is responsible for over 60% of PSVT in adults. The rate can vary between 120 and 220 beats per minute. At faster rates, a rate-related bundle branch block can result in a wide QRS tachycardia.  Characteristically, P-waves are not visible on the surface ECG since they are buried in the QRS complex.  Hence, the older term for this rhythm disturbance was “junctional tachycardia.”  AVNRT occurs because of reentry over the slow and fast AV nodal pathways (transitional fibers) and so it does not originate from within the AV node.  The AV node is part of the circuit, however, which is why this arrhythmia can be terminated abruptly by AV nodal blocking agents such as adenosine, verapamil, and beta blockers.  There are several varieties of AVNRT.  “Common” AVNRT (seen above) is caused by a reentry wavefront that travels down the slow pathway and back up the fast pathway.  This is also known as “slow-fast” AVNRT.  Uncommon AVNRT is also referred to as “fast-slow” AVNRT. As can be deduced from the name, the antegrade limb in uncommon AVNRT is the fast pathway and the retrograde pathway is the slow pathway.  Atypical AVNRT (“slow-slow”) can occur in a small number of patients who have multiple slow AV nodal pathways.  Patients who have AVNRT can often terminate the tachycardia by increasing vagal tone with the Valsalva maneuver and carotid massage.  On occasion, sustained tachycardia will result in an emergency room visit.  IV adenosine or verapamil are both very effective in terminating this tachycardia since they both cause transient AV block that stops the circus movement.  Long-term pharmacologic therapy aimed at slowing AV node conduction (such as beta blockers, verapamil, or diltiazem) can reduce the frequency and severity of attacks. However, these medications are often ineffective, they frequently result in significant side effects, and they may be pro-arrhythmic (the arrhythmia can occur more frequently, albeit at a slower and perhaps more tolerable rate).  Definitive (curative) therapy includes electrophysiologic testing and catheter ablation of the slow AV nodal pathway.  This procedure can permanently eliminate the arrhythmia in over 95% of patients with only a 1-2% risk of complete AV block requiring a permanent pacemaker.  Catheter ablation is the treatment of choice in most symptomatic patients, particularly young ones who would otherwise need long-term medical therapy.

The second most common type of PSVT is known as AV Reentry Tachycardia or AV Reciprocating Tachycardia (AVRT). AVRT results from reentry caused by an accessory AV pathway, which is a second electrical connection between the atrium and the ventricle.  In some patients, the accessory pathway is capable of conducting the electrical signal in an antegrade direction (from the atria to the ventricles), bypassing the AV node. This deforms the QRS complex in a characteristic manner, resulting in a short PR, a wide QRS, and a slurred onset of the QRS (known as a “delta wave”) with secondary ST/T wave abnormalities. This pattern of pre-excitation is diagnostic of the Wolff-Parkinson-White (WPW) Syndrome.  A premature atrial or ventricular beat can initiate AVRT if its conduction is blocked in one of the pathways. Most often, reentry occurs down the AV node, thorough the ventricular myocardium, up the accessory pathway, and back to the atrial myocardium, where it is free to go down the AV node again, thus completing the circuit.  This is known as “orthodromic” AVRT and results in a narrow QRS tachycardia with retrograde P-waves (inverted in leads II, III, and aVF) that begin just after each QRS complex.  The tachycardia behaves like AVNRT in that it is rapid and regular, with sudden onset and termination. In young patients it may occur at rates up to 250 beats per minute. Rarely, antidromic AVRT occurs due to reentry down an accessory pathway and back up the AV node or even a second accessory pathway. This results in a wide QRS complex because antegrade conduction down the accessory pathway causes “maximal pre-excitation.”  Unfortunately, the majority of patients with orthodromic AVRT do not exhibit the classic findings of WPW Syndrome on their ECG because these patients have a “concealed” accessory pathway that is only capable of retrograde conduction.  These concealed accessory pathways can easily cause orthodromic AVRT.  Thus, all patients with AVRT have an accessory pathway (concealed or overt), and AVRT is responsible for up to 30% of all PSVT in adults and the majority of PSVT in children.  Patients with overt WPW Syndrome can also develop atrial fibrillation with very rapid conduction (approaching 300 beats per minute) down the accessory pathway.  This arrhythmia can result in ventricular fibrillation. Patients with WPW and rapid conduction of atrial fibrillation down the accessory pathway appear to be at increased risk of sudden death. A significant portion of young children and adults who die suddenly while playing competitive sports do so because of this condition.

The acute treatment of sustained AVRT is the same as AVNRT. Since the AV node is part of the circuit, AVRT should terminate with intravenous adenosine or verapamil.  To prevent recurrent episodes, AV nodal blocking agents can be used.  In addition, Class IA, Class IC and Class III antiarrhythmic agents have been used to affect conduction in the accessory pathway (which is sodium-dependent).  Atrial fibrillation with rapid conduction down an accessory pathway in a patient with WPW Syndrome should never be treated with verapamil, since this can actually increase the rate of conduction down to the ventricles and may result in ventricular fibrillation. Although medical therapy has been used to treat AVRT, the treatment of choice is catheter ablation of the accessory pathway. This procedure is over ninety-five percent successful at permanently eliminating the problem with only a 1-2% risk of serious complications.  Catheter ablation is preferable to long-term medical therapy in most patients. Catheter ablation should be performed in patients with recurrent symptomatic PSVT, patients with WPW and rapidly conducting accessory pathways, and in asymptomatic patients with WPW who are in a position of responsibility (e.g. airplane pilot, bus driver), where the occurrence of symptoms could place others in jeopardy.