Laboratory Studies
Upon initial presentation of atrioventricular node reentrant tachycardia (AVNRT), assessments of serum electrolyte levels, thyroid function, and hemoglobin are often performed.
Other laboratory studies may be performed to monitor serum levels and adverse effects in children receiving antiarrhythmic medications.
Electrocardiography
The electrocardiogram (ECG) obtained during normal sinus rhythm shows a normal PR interval and the absence of ventricular preexcitation. Some patients may exhibit a slightly shortened PR interval or increased beat-to-beat variability of the PR interval, reflecting varying conduction through the fast or slow pathways. The typical atrioventricular node reentrant tachycardia (AVNRT) is characterized as a narrow complex regular tachycardia with rates that vary from 150 to 300 beats per minute. [17] Unlike AV reciprocating tachycardia (accessory pathway mediated tachycardia [eg, Wolff-Parkinson-White syndrome (WPW)]), AVNRT may exhibit AV dissociation with block to either the atrium (1:2 conduction) or to the ventricle (2:1 conduction). [18]
The His-atrial-ventricular (HAV) pattern, in which the atrial electrogram follows the His bundle electrogram and precedes the ventricular electrogram on the catheter placed in the His position, is observed in up to 74% of pediatric patients with AVNRT during an electrophysiologic (EP) study. [19]
Slow-fast form of AVNRT
Note the following:
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The slow-fast form of AVNRT is typical.
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Initiation of tachycardia usually occurs suddenly with a premature atrial beat. Sometimes, sudden sinus slowing is followed by a junctional escape beat as a trigger for the tachyarrhythmia.
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The termination usually occurs with AV block, which can be spontaneous or induced by vagal maneuvers or medications.
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The rhythm may terminate with a P wave or QRS complex, depending on the site of block.
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Little variability in RR intervals is usually noted.
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The time that the impulse takes to reach the atrium and the ventricle from the distal node is approximately the same, which causes the retrograde P waves to be buried within the QRS or appear immediately preceding or at the terminal end of the QRS.
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The RP interval is usually less than 50-70 milliseconds, which often results in the P wave being hidden in the QRS complex.
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When the P wave is visible at the end of the QRS, it exhibits a characteristic late-positive component in ECG lead V1 (ie, pseudo-R' wave), or the retrograde P waves may simulate an S wave in the inferior leads.
Fast-slow form of AVNRT
Note the following:
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The fast-slow form of AVNRT is atypical. [20]
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The trigger is usually a premature ventricular beat that blocks in the fast pathway and is conducted in a retrograde fashion through the slow pathway and then in an antegrade fashion through the fast pathway.
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In this form, conduction to the atria takes longer than conduction to the ventricles and the RP interval is longer than the PR interval.
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Another characteristic is that the P-wave axis is superior (ie, negative P waves in the inferior leads), because the impulse is retrograde and originates in the AV node.
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Distinguishing this tachycardia from permanent form of junctional reciprocating tachycardia (PJRT) can be difficult. However, PJRT usually presents with a more incessant rather than paroxysmal pattern. [14]
Imaging Studies
Chest radiography and echocardiography are often performed to evaluate the degree of cardiopulmonary dysfunction associated with the tachyarrhythmia and to assess for structural abnormalities.
Clinical and experimental studies using electrophysiologic and electroanatomical mapping are adding to the understanding of the anatomy and physiology of this disorder.
Some studies suggest that the coronary sinus, imaged at the time of electrophysiologic study, may have a broader opening in pediatric patients with atrioventricular node reentrant tachycardia (AVNRT). [21]
Procedures
The electrophysiologic characteristics of atrioventricular node reentrant tachycardia (AVNRT) include initiation and termination of tachycardia by extrastimulus or rapid pacing; normal antegrade and retrograde AV nodal conduction (with the earliest retrograde activation at the His bundle); and termination with AV block that, although uncommon, may allow the AVNRT to persist. These characteristics can be evaluated in patients through the electrophysiologic study (EPS), which may be semi-invasive (eg, esophageal electrode behind the heart) or intracardiac.
Note the following:
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During the EPS, the presence of the two functionally distinct AV nodal pathways can usually be demonstrated with atrial extrastimulus testing in adult patients.
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As the atrial extrastimulus-coupling interval (A1-A2) is shortened by 10-millisecond decrements, the AV nodal conduction time following the atrial extrastimulus (A2-H2) increases gradually.
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At a critical atrial extrastimulus-coupling interval, a 10-millisecond decrease in A1-A2 results in a marked increase (>50 ms) in A2-H2. This abrupt increase in AV nodal conduction time is termed a jump in conduction (discontinuous AH conduction curve), and it often is associated with the appearance of atrial echo beats or initiation of AVNRT.
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Further 10-millisecond decreases in the A1-A2 interval result in small additional increases (< 50 ms) in the A2-H2 interval, or, less commonly, additional AH jumps are evident.
Some data indicate that AV nodal physiology in children is different than in adults. Based on the traditional definition of a 50-millisecond AH jump after a decrement of 10 milliseconds in the extrastimulus coupling interval, only 62% of the children in one study met criteria for dual AV node physiology. [22] However, all patients had inducible AVNRT, and most of them were successfully ablated. The clinical importance of this finding is that children may not always fit the classic electrophysiologic criteria as it applies to adults; therefore, the endpoints for catheter ablation need to be readdressed and redefined in the pediatric population. Data from Dasgupta et al suggest that single echo beats without sustained slow pathway conduction or inducible AVNRT may be an acceptable endpoint for catheter ablation in the pediatric population. [23]
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Atrioventricular Node Reentry Supraventricular Tachycardia. Nonsustained atrioventricular node reentry tachycardia (AVNRT). This electrocardiogram is from a 10-year-old who is in sinus rhythm until a junction escape beat initiates a 5-beat run of supraventricular tachycardia. The heart rate is quite slow at 130 beats per minute, likely due to his resting state (higher vagal tone) and treatment with the beta-blocker atenolol. Note the pseudo R' waves in lead V1. These deflections represent retrograde atrial activation. Some patients may also exhibit pseudo S waves in the inferior leads. The R' waves are lost when the tachycardia ends, demonstrating that the R' wave is not associated with ventricular depolarization. The terminal QRS has no R' wave, indicating that the tachycardia terminated in the retrograde limb of the circuit (fast AV nodal pathway).
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Atrioventricular Node Reentry Supraventricular Tachycardia. Low voltage bridge in atrioventricular node reentry tachycardia (AVNRT). The images are a three-dimensional electroanatomic voltage map of the right atrium in the left anterior oblique projection with caudal angulation. The purple regions represent areas of high ("normal") atrial electrogram voltage, whereas gray and red regions have lower amplitude signals. The red region projecting from the tricuspid annulus (cutout) posteriorly toward the coronary sinus (thin purple cylinder) is a potential target for slow pathway ablation. The white spherical images are locations where cryotherapy of lesions were performed. The lesion highlighted in yellow represents the location of the successful slow pathway ablation. The others are "insurance" lesions.
Tables
| Type of Tachycardia | Treatment (Grade) | Not Mentioned in 2019 Guidelines |
|---|---|---|
| Narrow QRS tachycardias | Verapamil and diltiazem; beta-blockers (now all are grade IIa) | Amiodarone, digoxin |
| Wide QRS tachycardias | Procainamide, adenosine (both grade IIa); amiodarone (IIb) | Sotalol, lidocaine |
| Inappropriate sinus tachycardia | Beta-blockers (IIa) | Verapamil/diltiazem, catheter ablation |
| Postural orthostatic tachycardia syndrome | Salt and fluid intake (IIb) | Head-up tilt sleep, compression stockings, selective beta-blockers, fludrocortisone, clonidine, methylphenidate, fluoxetine, erythropoietin, ergotaminel octreotide, phenobarbitone |
| Focal atrial tachycardia | Acute: beta-blockers (IIa); flecainide/propafenone, amiodarone (IIb) | Acute: procainamide, sotalol, digoxin |
| Chronic: beta-blockers; verapamil and diltiazem (all IIa) | Chronic: amiodarone, sotalol, disopyramide | |
| Atrial flutter | Acute: ibutilide (I); verapamil and diltiazem, beta-blockers (all IIa); atrial or transesophageal pacing (IIb); flecainide/propafenone (III) | Acute: digitalis |
| Chronic: — | Chronic: dofetilide, sotalol, flecainide, propafenone, procainamide, quinidine, disopyramide | |
| Atrioventricular nodal reentrant tachycardia (AVNRT) | Acute: — | Acute: amiodarone, sotalol, flecainide, propafenone |
| Chronic: verapamil and diltiazem; beta-blockers (all IIa) | Chronic: amiodarone, sotalol, flecainide, propafenone, “pill-in-the-pocket” approach | |
| Atrioventricular reentrant tachycardia (AVRT) | Beta-blockers (IIa); flecainide/propafenone (IIb) | Amiodarone, sotalol, “pill-in-the-pocket” approach |
| SVT in pregnancy | Verapamil (IIa); catheter ablation (IIa when fluoroless ablation is available) | Sotalol, propafenone, quinidine, procainamide |
| Adapted from Brugada J, Katritsis DG, Arbelo E, et al, for the ESC Scientific Document Group. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2019 Aug 31;ehz467. https://academic.oup.com/eurheartj/advance-article/doi/10.1093/eurheartj/ehz467/5556821 | ||
