Saturday, April 3, 2021

AV Nodal Reentrant Tachycardia Case File

Posted By: Medical Group - 4/03/2021 Post Author : Medical Group Post Date : Saturday, April 3, 2021 Post Time : 4/03/2021
AV Nodal Reentrant Tachycardia Case File
Eugene C. Toy, Md, Michael d . Faulx, Md

Case 13
A 24- ear-o d woman with no prior medical history presents to your clinic with a complaint of sporadic episodes of intermittent palpitations and mild shortness of breath lasting 1–2 hours at a time over the past 6–8 months, about twice per week. She has not experienced any episodes of syncope, chest pain, lower extremity edema, orthopnea, or dyspnea with exertion; she reports that the mild shortness of breath occurs only when she is experiencing her palpitations. 

She exercises for 30 minutes, 4 times per week, without limitations. With regard to her palpitations, she states that they occur spontaneously without clear provocation. Once started, the palpitations are constant until they abruptly stop, usually about 1-2 hours later; when most severe, she lies down and tries to relax, but the palpitations continue. During a few of her episodes. she or one of her fiends pal pated her pulse, with a consistent reading at approximately 150-160 bpm. She has not presented earlier for evaluation because the episodes resolve before she can present for evaluation, and she has been “very busy” with her graduate school work. Her general appearance is normal and she is in no distress. Vital signs include blood pressure 110/60 mmHg and heart rate of 65 bpm. Physical exam is unrevealing; no JVP is noted, and there are normal lung findings and no cardiac murmurs, gallops, or rubs. Heart sounds are normal, with regular rate and rhythm. A baseline ECG is obtained in office and shows normal sinus rhythm. After discussion with her, further workup is scheduled for her return visit to the clinic at a later date. However, 2 days later, you get a call from her that she just began having palpitations. She comes to the clinic urgently. and a repeat ECG is obtained for review (Figure 13-1). While tachycardic, she has subjective palpitations. but remains hemodynamically stable with systolic blood pressure of 105 mmHg.
  • What is the differential diagnosis of this patient’s condition?
  • What is the most likely diagnosis?
  • What is the best next step in management?
ECG of AV Nodal Reentrant Tachycardia

Figure 13-1. ECG for the main subject of this case.

Answer to Case 13:
AV Nodal Reentrant Tachycardia

Summary: A 24-year-old woman with no medical history presents with intermittent episodes of palpitations lasting 1–2 hours at a time, about 2 days per week, for several months. Initial assessment was negative, but before completion of further testing, she had another episode with documented ECG showing a narrow complex tachycardia. The tachycardia is regular, with a short RP interval, and a pseudo-R′ appearance in lead V1, which is actually the retrograde P wave (atrial activation from the AV node) occurring nearly simultaneously with the QRS (ventricular activation).
  • Differential diagnosis: AVNRT, AVRT, atrial fibrillation, atrial flutter, atrial tachycardia.
  • Most likely diagnosis: Atrioventricular nodal reentrant tachycardia (AVNRT).
  • Next step in management: Maneuvers to confirm rhythm (carotid sinus massage, adenosine).


  1. Know how to interpret an electrocardiogram (ECG) to classify narrow complex tachycardia (NCT) to help form a differential diagnosis.
  2. Learn maneuvers–both physical and with medications–to help definitively diagnose the arrhythmia.
  3. Learn treatment strategies for NCT, including catheter ablation.

This 24-year-old woman presents with intermittent, symptomatic tachycardia with palpitations. As is often the case, on her first presentation to your office she is asymptomatic and in normal rhythm. But on her return, while experiencing palpitations, she is tachycardic, with ECG showing a NCT with rate of ~150 beats per minute. The first step in her management is to diagnose her arrhythmia. Immediate conversion (either medical or electrical) to sinus rhythm is not necessary here as she is tolerating her tachycardia well and is hemodynamically stable. While ECG is necessary for diagnosis, often the multiple different types of NCT can appear similar. Differentiation of NCT starts with separation into long-RP-interval (atrial tachycardia, sinus tachycardia, AVRT, atrial flutter) and short-RP-interval (AVNRT most common) tachycardias, although considerable overlap is present (atrial tachycardia, AVRT, and atrial flutter can be either). A pseudo-R′ is identified in lead V1 (short RP interval), making AVNRT the most likely arrhythmia; however, it is still possible that it could be AVRT, atrial tachycardia, or atrial flutter. Therefore, maneuvers, both physical and medical, can be applied to help differentiate her rhythm.

The purpose of vagal maneuvers is to slow AV nodal conduction, thereby allowing a slower ventricular rhythm with ongoing atrial arrhythmia, or to ascertain whether the rhythm is dependent on the AV node as part of a reentrant loop, in which case the arrhythmia will terminate. The first of these steps consists in performing vagal maneuvers. Valsalva or coughing can be employed but can interfere with ECG if the patient moves or strains too much. Therefore carotid sinus massage (CSM) may be best, and should be performed while running a continuous rhythm strip or ECG. If CSM is not feasible (carotid bruit present, patient body habitus, central venous catheters in the inpatient setting, etc), then pharmacologic assessment can be achieved with adenosine. Adenosine acts to slow or block AV nodal conduction, and provides the same diagnostic answers as vagal maneuvers. Comparison with other AV nodal blocking agents (beta-blockers, calcium channel blockers), reveals adenosine to have the advantage of an extremely short half-life. (Its t1/2 is so short, in fact, that if it is injected into an IV in the patient’s hand, the drug may be metabolized before it reaches the heart!) If the arrhythmia is dependent on the AV node to continue (reentrant loop that includes the AV node), then these maneuvers will terminate the rhythm (AVNRT, AVRT). If the arrhythmia is not dependent on the AV node, these maneuvers will only serve to slow ventricular rate by decreasing the number of impulses conducting through the AV node while the atrial arrhythmia continues. Therefore, in atrial flutter, multifocal atrial tachycardia, and atrial tachycardia, this allows for further evaluation of the atrial signal and identification of the rhythm.

The next step is to complete workup of the patient, which includes laboratory evaluation with CBC, basic metabolic panel (BMP), and TSH. In some instances, atrial arrhythmias (any type) can be due to coronary ischemia or active infarction, and evaluation for coronary artery disease can be pursued in specific populations, particularly those who have chest pain with the tachycardia. Also, underlying processes (lung disease) may lead to these arrhythmias, and in select populations should be investigated. After initial evaluation and identification of the rhythm, the final step is rhythm management, with short- and long-term therapy. If adenosine fails to terminate the rhythm during evaluation, then other agents (beta-blockers, calcium channel blockers) can be used. These are usually very effective in suppression of atrial arrhythmias. Long-term management can be strictly medication-based; however, most forms of non-AV tachycardia are very amenable to catheter-based ablation, with success rates over 95% in the electrophysiology (EP) lab.

Approach To:
Narrow Complex Tachycardia


NARROW COMPLEX TACHYCARDIA (NCT): Fast arrhythmia with heart
rates >100 bpm, and QRS duration <120 ms; almost always caused by atrial or reentrant

SUPRAVENTRICULAR TACHYCARDIA (SVT): Narrow complex tachcycardia, which is most commonly used to describe nonfibrillation/nonflutter atrial arrhythmia. The most common of these is AVNRT.

LONG RP TACHYCARDIA: SVT where the RP interval is longer than the PR interval. Differential includes atrial tachycardia, sinus tachycardia, AVRT, atrial flutter, and atypical AVNRT.

SHORT RP TACHYCARDIA: SVT where the RP interval is shorter than the PR interval. Typically diagnosis is AVNRT.


Supraventricular tachycardias (SVTs), or narrow complex tachycardias (NCTs), are caused by one of two different mechanisms, reentry or increased automaticity. The first of these, reentry, is when there is an abnormal circuit formed within the heart that allows for recurrent cycling of the electrical impulse (Figure 13-2). As a result, there will be sequential activation of the atria and then the ventricles, after which the atria are again activated after the impulse conducts retrograde to the atria. Reentry can occur in a number of places and be caused by a number of factors: scar

AV Nodal Reentrant Tachycardia ECG

Figure 13-2. Reentry explained. Reentry occurs when fast- and slow-conducting tissues are connected
proximally and distally by common tissue. All tissue in the circuit must be able to conduct in antegrade
and retrograde fashion. (A) Normal AV node conduction. An atrial impulse travels down the fast and
slow (checked area) pathways simultaneously . The fast pathway delivers the wave front to the distal
circuit, which becomes refractory and blocks antegrade conduction down the s ow pathway . (B) The
fast pathway becomes transiently refractor (dark blue area). Antegrade conduction continues down
the slow pathway . (C) The wave front from the slow pathway reaches the distal end of the circuit to
find the fast pathway recovered. Retrograde conduction through the fast pathway begins. (D) The
retrograde wave front arrives at the proximal end of the circuit from the fast pathway to find the slow
pathway recovered. Retrograde activation of the atria occurs, and the cycle repeats itself.

tissue from ischemia or surgery, abnormal conductive tissue between the atria and ventricles from birth such as a Wolff-Parkinson-White pathway, anatomic structures for a circuit to form (around tricuspid or mitral valves), or dual pathways within the AV node. When dependent on the AV node as part of the circuit, medications or maneuvers that slow AV conduction can effectively terminate the rhythm.

The second cause of SVT is increased automaticity. Each cardiac cell has its own automaticity, or rate of spontaneous depolarization. Typically, the sinus node has the highest automaticity, and therefore “drives” the rest of the heart at its rate. However, if another tissue outside the sinus node develops increased automaticity, the impulse rate of that tissue will override the sinus node and become the dominant rate of the heart. The onset of initiation is usually abrupt, which is different from normal increased automaticity (sinus tachycardia) in the setting of exercise or stress when the rate slowly rises to meet increased oxygen demand.

Types of Narrow Complex Tachycardia
Sinus tachycardia: Tachycardia originating from the sinus node. On ECG, the P wave will appear as the same morphology as the baseline ECG. Typically has a gradual onset in response to stressors (exercise, pain, anemia, infection, emotional stress, etc). If it is persistent, it is usually due to significant systemic stress, and treatment consists in correcting the underlying abnormality. Rarely, persistent sinus tachycardia in the absence of a stressor may occur, termed inappropriate sinus tachycardia (IST).

Atrial fibrillation: This type will be discussed elsewhere in this book. However, it is described as an absence of identifiable organized atrial rhythm (no identifiable P waves), and usually results in irregularly irregular ventricular rate.

Atrial flutter: Also discussed elsewhere. Typical atrial flutter is due to reentry around the tricuspid valve, and is identified by sawtooth pattern waves on the inferior ECG leads.

AV nodal reentrant tachycardia (AVNRT): Tachycardia caused by reentrant circuit within the AV node, utilizing a “fast” and “slow” pathway. Typical AVNRT conducts down the slow pathway of the node and retrograde up the fast pathway (Figure 13-2). As a result, the atrium is activated immediately after the ventricle, so the P wave may be buried in the QRS complex or may cause a pseudo-R′ in V1 reflecting retrograde atrial activation (short RP interval).

Atypical AVNRT: Conducts down the fast pathway and up the slow pathway. Therefore the atrium is conducted just before, rather than just after, the ventricle. On ECG, there is a long RP interval.

Atrioventricular reciprocating tachycardia (AVRT): An abnormal pathway exists between the ventricles and atria (accessory pathway). Electrical signal travels down the AV node to the His-Purkinje system. The signal then traverses from the ventricle to the atrium through the accessory pathway, which completes the cycle (orthodromic). This can result in either long or short RP interval. Antidromic impulses are conducted down the accessory pathway from atria to ventricles, then in retrograde fashion from ventricles to atria through the AV node. Antidromic conduction results in wide complex tachycardia.

Atrial tachycardia: Tachycardia with P waves before each QRS. This may be attributed to the increased firing rate of some atrial tissue that is not the sinus node (increased automaticity). However, P wave morphology differs from sinus rhythm P wave. RP interval may vary (long versus short) depending on where the abnormal activation is originating.

Multifocal atrial tachycardia (MAT): P waves present before each QRS. However, there are multiple areas where the tachycardia is originating. Therefore, three or more P wave morphologies are noted, and PR intervals may differ, as the distance from each location to the AV node may also vary. This abnormality is typically due to systemic disease, in particular pulmonary pathology (COPD, pulmonary embolism, pneumonia, etc).

Patient Presentation
Patients who present with supraventricular tachycardia typically have palpitations as their presenting symptoms. However, more severe symptoms can be present depending on the rate of the rhythm and comorbidities of the patient. Shortness of breath may be present, and may be due specifically to the tachycardia, or induced by anxiety from their palpitations. Further chest pain can be present, particularly in patients with coronary disease; presence of chest pain, particularly in at-risk populations, should be a signal to evaluate for possible ischemic disease. In some cases, syncope can manifest as well.

The onset of the arrhythmia is usually spontaneous, and patients will describe the abrupt onset of palpitations or feeling their “heart racing” on palpation. Exercise can precipitate the arrhythmia in certain cases. The duration of the arrhythmia can range from only a few seconds to hours or days in the most extreme cases. Patients will describe abrupt termination of the palpitations as well, or describe that with straining or cough (vagal maneuvers) the arrhythmia terminates.

In very rare situations, prolonged time in tachycardia can precipitate heart failure symptoms and reduced LV systolic function (tachycardia-mediated cardiomyopathy). Typically, in this situation, control of rhythm and return to sinus rhythm will allow for recovery of LV function over weeks.

Diagnosis of the particular arrhythmia, as stated before, requires identification of ECG features that are specific to one arrhythmia over another. However, this is limited by considerable overlap between these rhythms, or difficult-to-identify atrial activity due to the fast heart rate. Sometimes use of vagal maneuvers or adenosine while running a continuous ECG is still not able to identify the arrhythmia. In those situations, consultation with a cardiac electrophysiologist, and likely an electrophysoiolgy (EP) study in the lab, will provide the definitive rhythm, as well as possibly curative ablation.

Treatment should be divided into short- and long-term management regimes. In the short (immediate) term, when a patient presents with SVT, arrhythmia termination  should be sought after initial ECG and diagnosis. Adenosine can be used in rapid infusion to try to terminate the rhythm; alternatively, vagal maneuvers can be applied; these methods are used for reentrant arrhythmias. If adenosine is not effective, or if the arrhythmia is due to increased automaticity, then use of IV beta-blockers or IV calcium channel blockers may terminate the rhythm. Long-term management should include use of oral beta-blockers or calcium channel blockers. In patients with severe symptoms, or who have frequent recurrences despite medical therapy, catheter ablation can be pursued, and has a high success rate.

  • See also Case 11 (atrial fibrillation and flutter).


13.1 Which of the following is not considered appropriate long-term therapy for a patient presenting with AVNRT?
A. Metoprolol
B. Diltiazem
C. Adenosine
D. Catheter ablation

13.2 A 45-year-old man presents to the emergency department complaining of palpitations for the past 30 minutes. He has associated chest pain, and initial assessment shows a systolic blood pressure of 80 mmHg. Your first step in the evaluation and management of this patient (after ECG) is
A. Reassurance
B. Activating the catheterization lab for coronary angiography
C. Metoprolol IV push
D. Immediate electrical cardioversion

13.3 A patient presents to your clinic with palpitations and is found to have a regular, narrow complex tachycardia on ECG. You run continuous ECG and perform carotid massage. Which of the following rhythms would be expected to terminate with CSM?
A. Atrial tachycardia
B. AV nodal reentrant tachycardia (AVNRT)
C. Sinus tachycardia
D. Multifocal atrial tachycardia
E. Atrial flutter
F. Atrial fibrillation


13.1 C. Adenosine is only a short-acting therapy and is not used for long-term management.

13.2 D. Immediate electrical cardioversion is needed as this patient has chest pain and hemodynamic instability, possibly indicating coronary ischemia/ infarction due to the myocardial strain from tachycardia.

13.3 B. AVNRT is the only rhythm listed previously that is dependent on the AV node to sustain tachycardia, and therefore should terminate with AV node suppressing actions.

  • NCT should be evaluated with ECG, to identify whether the rhythm is regular or irregular (afib), and whether it is a long RP or short RP tachycardia.
  • Adenosine or vagal maneuvers performed with continuous ECG can help identify the rhythm.
  • AV nodal dependent rhythms will likely terminate, whereas rhythms that do not rely on the AV node to sustain tachycardia will manifest slowing of ventricular rate so that P wave morphology can be better evaluated with fewer QRS complexes.
  • Immediate cardioversion to sinus rhythm (pharmacologic or electrical) is not necessary in stable patients, affording time to perform maneuvers and correctly identify the presenting rhythm. However, hemodynamic instability or alarming symptoms (chest pain) should prompt cardioversion.
  • Multifocal atrial tachycardia (MAT) is usually secondary to noncardiac disease causing systemic stress, particularly pulmonary pathology.

DiMarco JP, Sellers TD, Berne RM, West GA, Belardinelli L. Adenosine: electrophysiologic effects and therapeutic use for terminating paroxysmal supraventricular tachycardia. Circulation. 1983;68: 1254–1263. 

DiMarco JP, Sellers TD, Lerman BB, Greenberg ML, Berne RM, Belardinelli L. Diagnostic and therapeutic use of adenosine in patients with supraventricular tachycardia. J Am Coll Cardiol. 1985;6(2): 417–425. 

Kwaku KF, Josephson ME. Typical AVNRT–an update on mechanisms and therapy. Cardiac Electrophysiol Rev. 2002;6(4):414–421.


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