Atrioventricular Nodal Reentrant Tachycardia

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common form of supraventricular tachycardia (SVT).1 Although its treatment does not usually require admission to the hospital, it is a common tachycardia seen in the emergency department. Evidence from the specialty of electrophysiology has and is still changing the way that the arrhythmia is diagnosed, described, and treated. It is important that acute and critical care nurses have current information regarding physiology, symptoms, electrocardiographic features, other diagnostic criteria, and treatment of this arrhythmia. Thorough knowledge of AVNRT provides a framework to compare and contrast with other tachycardias to enhance the accuracy of rhythm interpretation, which is the prerequisite for optimal patient management.More than 60% of cases of AVNRT are reported in women.2 The mean age for the first presentation is 32 years (SD, 18 years), and it typically occurs in persons without structural or ischemic heart disease.1,3 AVNRT affects quality of life; however, it is rarely life threatening. AVNRT can occur spontaneously or can be provoked by exertion or substance exposure including alcohol and caffeine.1 Palpitations are the most common symptom, and patients may also report shortness of breath, dizziness, and neck palpitations.1 Patient reports of “shirt flapping” and/or “neck pounding” have been associated with AVNRT and are most likely related to reversed pulsatile flow when the right atrium contracts against a closed tricuspid valve.4,5 The finding of a flapping or bulging appearance of neck veins on physical examination is referred to as the “frog sign.”6 Polyuria is also common in AVNRT related to higher right atrial pressures and release of atrial natriuretic peptide.7AVNRT is a result of dual atrioventricular nodal physiology consisting of 2 distinct pathways usually referred to as the “fast” and “slow” pathways.1 These 2 pathways have the potential to form a reentrant circuit. It is most common for the fast pathway to be located near the apex of the Koch triangle (an anatomical area located in the endocardium of the right atrium that has the coronary sinus at 1 angle, and the tendon of Todaro and the septal leaflet of the triscupid valve as the 2 sides). The entire atrial component of atrioventricular conduction lies within this triangle.1 The slow pathway is located inferior and posterior to the atrioventricular node tissue.1 Right and left inferior extensions of the atrioventricular node contribute to the substrate of the slow pathway.8 Variant pathways can also exist.8 An accessory pathway is an extra conduction pathway that connects an atrium to a ventricle, allowing conduction to bypass the atrioventricular node and directly stimulate ventricular depolarization. The fast and slow pathways of AVNRT are not accessory pathways as seen in patients with Wolff-Parkinson-White syndrome. The accessory pathways of Wolff-Parkinson-White syndrome are responsible for atrioventricular reentrant tachycardia (AVRT).In typical AVNRT, a premature atrial contraction can serve as the trigger if the fast pathway is still refractory from the previous sinus beat. If so, the premature atrial contraction will be conducted only down the slow pathway, resulting in a long PR interval. By the time the premature atrial contraction reaches the atrioventricular node, the fast pathway is no longer refractory. If the fast pathway allows retrograde conduction, the impulse will travel retrograde up the fast pathway at the same time as ventricular conduction is traveling antegrade through the His-Purkinje system. This process results in nearly simultaneous atrial and ventricular depolarization. Retrograde conduction up the fast pathway results in atrial depolarization and conduction back down the slow pathway to the atrioventricular node. The cycle continues to repeat because each time the impulse reaches the atrioventricular node via the slow pathway there is simultaneous atrial depolarization (via the retrograde fast pathway) and ventricular depolarization (via the normal His-Purkinje depolarization).AVNRT is typically a narrow-complex SVT because of the normal His-Purkinje depolarization. Exceptions include a preexisting conduction defect or the development of a rate-dependent bundle branch block (aberrancy). Right bundle branch block is the more common form of aberrant conduction.1,8 The heart rate is commonly between 180/min and 200/min but can vary from 110/min to more than 250/min. Rarely the rate will be slower than 110/min.1 The R-R interval typically is regular; however, some R-R variation may exist because of variations in reentrant circuits.9 AVNRT typically conducts 1:1 except in rare cases of 2:1 conduction or variable atrioventricular block.1 Atrioventricular dissociation is not usually present, although it is possible because the atria and the ventricles are not responsible for the reentrant circuit.8In typical AVNRT, called slow-fast, conduction approaches the atrioventricular node via the slow pathway, and from the atrioventricular node, the ventricles and atria are depolarized at essentially the same time as just described. Atrial activation can occur before, at the onset of, or just after the QRS complex.1,8 The almost simultaneous depolarization of ventricles and atria result in P′ waves being very close to or merging with the QRS complex and altering the morphology of the normal QRS complex. (P′ wave is defined as representing origination from atrial depolarization, not from the sinus node.) There will be pseudo s waves in leads II, III, and aVF (see Figure) and a pseudo r′ wave in lead V1.1,8 In typical AVNRT, the P′ wave is closer to the previous QRS complex and the tachycardia is therefore referred to as short RP tachycardia.1Atypical AVNRT occurs in 5% to 10% of cases.8 In atypical AVNRT, called fast-slow, conduction approaches the atrioventricular node via the fast pathway. The ventricles are depolarized via the His-Purkinje system, and the atria are depolarized via retrograde conduction up the slow pathway. The retrograde atrial activation occurs after ventricular activation, resulting in a ventricular-atrial interval of more than 60 milliseconds.8 P′ waves are clearly visible because of atrial depolarization via the slow pathway. Because of retrograde atrial depolarization, the P′ waves are negative in leads II, III, aVF, and V6, and will be positive in lead V1.1,8 If atypical AVNRT is started by an ectopic atrial beat, the morphology of the P′ waves will differ from the initial ectopic beat.1 In atypical AVNRT, the P′ wave is closer to the subsequent QRS complex and it is referred to as long RP tachycardia.1 Another form of atypical AVNRT is slow-slow, where both pathways involved in the reentry circuit have slow conduction.Differential diagnoses for regular narrow-complex SVT include atrial tachycardia, junctional tachycardia, and orthodromic AVRT. Orthodromic AVRT is seen in patients with an accessory pathway. The Table outlines features of narrow complex tachycardias important for differential diagnosis. Differentials for an irregular SVT include atrial fibrillation, multifocal atrial tachycardia, and atrial flutter with variable conduction. It is important to remember that it is more difficult to differentiate the irregularity of the ventricular rate with a very rapid ventricular response.Ventricular tachycardia must be excluded as the cause of any wide complex tachycardia. The treatment of ventricular tachycardia with certain medications used to treat SVTs (eg, verapamil and diltiazem) can be harmful.1 After ventricular tachycardia has been excluded, remaining differentials include AVNRT with aberrant conduction, atrial tachycardia or atrial flutter with aberrant conduction, AVNRT with the presence of a bystander accessory pathway (an accessory that is present but not part of the reentrant circuit), or antidromic AVRT (which involves antegrade conduction over the accessory pathway [producing direct ventricular stimulation] and retrograde conduction up through the atrioventricular node).Both the fast and slow conducting pathways are known to be heterogeneous, and as a result AVNRT may have atypical retrograde activation of the atria.8,10 All forms of AVNRT may display anterior, posterior, and middle retrograde conduction patterns, and several forms of AVNRT may be inducible in a single patient during an electrophysiology study.8,11 Additionally, electrocardiographic (ECG) features in AVNRT may mimic what is seen in patients with accessory pathways. For example, retrograde atrial depolarization in atypical AVNRT can mimic a left lateral posterior accessory pathway.12 Patients with AVNRT may also have a bystander accessory pathway.8 These complex anatomical and physiological variations result in potential differences in ECG recordings during AVNRT. Pacing maneuvers and programmed electrical stimulation during electrophysiology study are used to aid in the definitive diagnosis of SVTs.1,8In AVNRT, the initial decrease in blood pressure is greatest during the first 10 to 30 seconds despite a consistent heart rate.13,14 Heart rate alone is not responsible for the degree of hemodynamic compromise. Shorter ventriculoatrial intervals are associated with a greater decrease in blood pressure.14 In 1 study, patients with typical AVNRT had a partial recovery in initial hypotension that resulted in stable hypotension and an associated decreased cardiac output. In patients with atypical AVNRT, the initial drop in blood pressure was less, recovery was complete, and cardiac output showed no clinically significant change.15 Syncope or near syncope is not common; however, older patients are at higher risk.1The goal of AVRNT treatment is to slow conduction through the atrioventricular node and allow the sinus node to regain control. A Valsalva maneuver is the first-line treatment for AVNRT, and all patients with AVNRT should be taught to perform such maneuvers. If a Valsalva maneuver is not effective, rapid-acting adenosine is the drug of choice to slow conduction through the atrioventricular node.1 Long-term antiarrhythmic therapy is not effective in most patients, and therefore catheter ablation of the slow pathway is the definitive treatment for both typical and atypical AVNRT.1For patients who decline ablative therapy, β-blockers or one of the calcium channel blockers diltiazem or verapamil are used as first-line pharmacological agents to slow atrioventricular node conduction. If β-blockers and calcium channel blockers are ineffective, class I and class III antiarrhythmic agents can be used. Flecainide or propafenone (class I agents) are preferred over class III agents but can be used only in patients with no structural heart disease. Amiodarone, dofetilide, and sotalol (class III agents) and digoxin can also be considered.1Cardiac mapping with specialized multielectrode catheters or electromagnetic mapping systems is performed during electrophysiology study to identify target areas for ablation. With advances in technology, ablation for AVNRT can be done with minimal or no fluoroscopy.1 Energy sources used in AVNRT ablation include radiofrequency and cryoablation. Cryoablation has the potential advantage of lower risk of permanent block through the atrioventricular node but has also been associated with higher recurrence rates of AVNRT.16 Ablation lesions are made in the inferior or middle part of the triangle of Koch.1 Initial success rates are greater than 95%.17 Complications include a 0.4% to 1.0% risk of atrioventricular block requiring a permanent pacemaker17,18 and a 5% risk of recurrence of AVNRT.19 Older age is not a contraindication for the procedure; however, a preexisting first-degree atrioventricular block carries a higher risk for the development of late atrioventricular block.20 In these patients, slow pathway modification rather than ablation is favored.8,20AVNRT is the most commonly occurring SVT, and nurses should be skilled in recognizing the ECG features associated with this arrhythmia as well as ECG features associated with other narrow complex SVTs that are part of the differential diagnosis. Accurate interpretation of cardiac arrhythmias is an important component of patient safety. A thorough understanding of the physiology of AVNRT and its treatment options also prepares nurses to educate patients about signs and symptoms, medications, electrophysiology studies, and ablation procedures.