Nodal reentrant tachycardia

Premise: the heart contracts regularly due to the existence of specialized cellular structures that generate electric impulses and that regulate the distribution into the heart.
Normally, the electric impulse originates in the sinus node, propagates into the atria and reaches the atrio-ventricular node, that is the only normal electric comunication between atria and ventricles; for the atrio ventricular node the impulse propagates along the His fascicle to the intraventricular conduction system.


Atrioventricular nodal reentry tachycardia (AVNRT) is the most common type of reentrant supraventricular tachycardia (SVT), Often it would be also described with the nonspecific term paroxysmal supraventricular tachycardia.  With the improving in knowledge of the electrophysiology of reentrant SVT, more specific nomenclature based on the mechanism of reentry has been proposed. AVNRT occurs in 60% of patients (with a female predominance) presenting with paroxysmal SVT  and it is more common in young adults.


Clinical presentation


AVNRT is characterized by an abrupt onset and termination of episodes. Episodes may last from seconds to minutes to days. In the absence of structural heart disease, it is usually well tolerated. Common symptoms include palpitations, nervousness, anxiety, lightheadedness, neck and chest discomfort, and dyspnea. Polyuria can occur after termination of the episode (due to the release of atrial natriuretic factor). AVNRT may cause or worsen heart failure in patients with poor left ventricular function. It may cause angina or myocardial infarction in patients with coronary artery disease. Syncope may occur in patients with a rapid ventricular rate or prolonged tachycardia due to poor ventricular filling, decreased cardiac output, hypotension, and reduced cerebral circulation. Syncope may also occur because of transient asystole when the tachycardia terminates, owing to tachycardia-induced depression of the sinus node.



The AV node in these patients behaves functionally as if there were two separate pathways through the node. The two pathways (alfa and beta pathways ) are differentiated by their characteristic electophysiologic prAVNRT 1operties. The alfa pathway or slow pathway usually has a relatively short ERP and conducts slowly.


The beta pathway or fast pathway instead has a relatively long ERP and conducts more rapidly. Patients with these characteristics are said to have dual AV nodal pathways. In patients with dual AV nodal pathways, a norma lly timed sinus impulse will conduct through the AV node via beta pathway, since the beta conducts more rapidly than the alfa pathway. However a premature atrial impulse can arrive at the AV node at such a time that the beta pathway (with a relatively long ERP) is still refractory from the previous normal beat, but the alfa pathway  is no longer refractory. This early impulse will then traverse  the alfa pathway, reaching the His bundle after a prolonged conduction time through the AV node ( since the alfa pathway conduct slowly) this AV nodal conduction delay is manifested by a prolonged PR interval on the surface ECG. If the beta pathway recovers by the time the impulse reaches the distal portion of the alfa pathway, the impulse may conduct retrogradely up the beta pathway (producing an atrial echo beat). If this retrograde impulse is then able to reenter the alfa pathway , a continuously circulating impulse can be established within the AV node.




Management of an acute attack depends on the symptoms, the presence of underlying heart disease, and the natural history of previous episodes. Rest, reassurance, and sedation may terminate the attack. To terminate the tachycardia,  vagal maneuvers (eg, carotid sinus massage, exposure of the face to ice water, Valsalva maneuver) could be tried  before initiating drug treatment. Vagal maneuvers are unlikely to work and should not be tried if hypotension is present. Sometimes, putting the patient in the Trendelenburg position facilitates termination with a vagal maneuver. Drugs that can be used to terminate an attack include adenosine, calcium channel blockers, beta-blockers and digitalis. Direct current (DC) synchronized cardioversion is used to terminate an attack if the patient has hemodynamic compromise or if drug conversion fails and the patient continues to be symptomatic. DC cardioversion is rarely necessary for atrioventricular nodal reentry tachycardia (AVNRT). Competitive atrial or ventricular pacing may be used if DC cardioversion is contraindicated (eg, if high doses of digitalis have been administered). Preventive therapy is needed for frequent, prolonged, or highly symptomatic episodes that do not terminate spontaneously or those that cannot be easily terminated by the patient. Drugs that are used for prevention of recurrence include long-acting beta-blockers, calcium channel blockers, and digitalis. Radiofrequency catheter ablation of the reentrant circuit should be considered in patients with frequent symptomatic episodes who do not want drug therapy, who cannot tolerate the drugs, or in whom drug therapy fails.


RF ablation

The AV node results froAVNRT 2m the coalescence of two tracts of atrial fibers. These two tracts not only have a different EP features but seem to be two discrete anatomical structures: the anterior tract corresponds to the fast pathway while the posterior tract  corresponds to slow pathway. To visualize the dual AV nodal pathways is very important to know the anatomy of Koch’s triangle. The three sides of Koch’s triangle are defined by the tricuspid annulus ( the portion of annulus adjacent to the septal leaflet of the tricuspid valve), the tendon of Todaro and the Os of coronary sinus. The His bundle is located at the apex of triangle. It is important to recognize that the apex of Koch’s triangle ( where the AV node and the His bundle reside) is an anterior structure, while  the coronary sinus is a posterior structure, and defines the posterior portion of the atrial septum. In patient with AV nodal reentrant tachycardia, the fast and the slow pathway can be visualized as two tracts of atrial fibers: the fast pathway is an AVNRT 3anterior and superior tract located along the tendon of Todaro; the slow pathway is posterior and inferior and located along the tricuspid annulus near the os of coronary sinus. Because the two pathways can be discretely localized, they can be  ablated. The initial ablation target  was the fast pathway. However this approach yielded a relatively  high incidence of complete heart block and this because the proximity of AV node and  His bundle. Because of this, the definitive ablation target shifted to slow pathway. Slow pathway is posterior and relatively distant from the AV node, and the ablation of this structure yields to a low incidence of complete heart block (less than 1%). In general two approaches are commonly used for ablation of the slow AV nodal pathway: the mapping approach and the anatomic approach . Both approaches begin by first identifying then anatomic limits of Koch triangle, by placing one catheter in the His position and one in CS. The ablation catheter is then advanced from the femoral vein to the tricuspid annulus, near the os of coronary sinus. With the mapping approach, the ablation catheter is carefully manipulated along the tricuspid annulus, searching for discrete slow potential that presumably represent depolarization of the slow pathway itself. This slow potential is located between the atrial and ventricular deflection of the intracardiac electrogram. When a slow potential is identified, a RF application is delivered to ablate the slow pathway. With the anatomic approach the slow pathway ablation, is identified only by fluoroscopy. Generally, the length of the tricuspid annulus between the os of coronary sinus and the His bundle is virtually divided into three segments – posterior ( near to the os of CS), middle and anterior (near to the his bundle).The catheter is positioned across the tricuspid valve  posteriorly  and gradually withdrawn until both atrial and ventricular deflection are recorded, with the ventricular deflection larger than the atrial deflection. An RF application is delivered untill accelerated junctional tachycardia occurs.  If no tachycardia occurs after 10 or  15 seconds of RF application , the RF should be terminated and the catheter repositioned. If tachycardia does occur, 30 to 60 seconds of RF energy should be applied. Succesfull ablation is documented by confirming that the physiology of dual AV nodal pathways is no longer present.




Related Articles:

Paroxysmal Supraventricular Tachycardia Caused by 1:2 Atrioventricular Conduction in the Presence Of Dual Atrioventricular Nodal Pathways

Aureliano Fraticelli, Gabriele Saccomanno, Carlo Pappone and Giuseppe Oreto
Journal of Electrocardiology Vol. 32 No. 4 1999