AV nodal reentrant tachycardia

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] : Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Synonyms and keywords: AVNRT; AV node reentrant tachycardia; AV nodal reentry tachycardia; AV node reentry tachycardia; atrioventricular node reentrant tachycardia; atrioventricular nodal reentry tachycardia; atrioventricular node reentry tachycardia; junctional reciprocating tachycardia; reciprocal or reciprocating AV nodal reentrant tachycardia

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Overview

AV nodal reentrant tachycardia is a type of tachycardia (fast rhythm) of the heart. It is one of several types of supraventricular tachycardia (SVT), and like all SVTs the electrical impulse originates proximal to the bundle of HIS. In the case of AVNRT, the electrical impulse originates in the AV node and the immediately surrounding tissue. AVNRT is the most common cause of supraventricular tachycardia.

Classification

There are several types of AVNRT. The “common form” or “usual” AVNRT utilizes the slow AV nodal pathway as the anterograde limb of the circuit and the fast AV nodal pathway as the retrograde limb. The reentry circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb. This, not surprisingly is referred to as the “uncommon form” of AVNRT. However, there is also a third type of AVNRT that utilizes the slow AV nodal pathway as the anterograde limb and left atrial fibers that approach the AV node from the left side of the inter-atrial septum as the retrograde limb. This is known as atypical, or Slow-Slow AVNRT.

Common AVNRT

In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway (“slow-fast” AVNRT). This accounts for 80%-90% of cases of AVNRT.

Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may not be seen on the surface ECG since they are buried with the QRS complexes. Often the retrograde p-wave is visible, but also in continuity with the QRS complex, appearing as a “pseudo R prime” wave in lead V1 or a “pseudo S” wave in the inferior leads.

Uncommon AVNRT

In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde conduction is via the slow pathway (“fast-slow” AVNRT). Multiple slow pathways can exist so that both anterograde and retrograde conduction are over slow pathways. (“slow-slow” AVNRT).

Because the retrograde conduction is via the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will typically produce an inverted P wave that falls after the QRS complex on the surface ECG.

AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. In the usual form of AVNRT, the conduction from the atrium to the ventricle is down the slow pathway, and the retrograde conduction from the ventricle to the atrium is up the fast pathway.

Pathophysiology

Premature Atrial Complex

The most common trigger for an episode of AVNRT is when an atrial premature complex (APC) approaches the fast pathway, and is blocked due to the longer refractory period of this pathway, and instead conducts down the slow pathway. As the impulse goes down the slow pathway, the fast pathway recovers, and allows the impulse to conduct backward or retrograde toward the atrium. It then re-enters the atrial entrance of the slow pathway and the cycle repeats itself.

Premature Ventricular Complex

The second most common mechanism whereby AVNRT is triggered is via the entry of a premature ventricular complex down either the slow conducting pathway (similar to a premature atrial complex above) or down the rapidly conducting pathway.

Epidemiology and Demographics

AV nodal reentrant tachycardia is the most common regular supraventricular tachycardia and accounts for 60% to 70% of these cases.

Gender

The ratio of female to male involvement is 3:1.

Age

There is no age predilection.

Risk Factors

Underlying structural heart disease is generally absent. Often, there is no precipitant of an episode. Risk factors for precipitation of AVNRT include:

Alcohol
Caffeine
Chocolate
Hyperthyroidism
Hypokalemia
Hypomagnesemia
Myocardial ischemia
Psychological stress
Tea
Theobromine in foods like tea, coffee and chocolate
Theophylline

Natural History, Complications and Prognosis

AVNRT starts and stops abruptly. Patients may develop syncope. The prognosis is good.

Natural History

The rhythm often ceases abruptly and spontaneously. An episode generally last seconds to hours.

Complications

Some patients will develop syncope during episodes of AVRNT. The mechanism of syncope may be due to a reduction of cardiac output and hemodynamic compromise as a result of the short ventricular filling time or alternatively it may be due to transient asystole due to tachycardia-mediated suppression of the sinus node when the rhythm terminates. Those patients who do become symptomatic during episodes of AVNRT (i.e. have syncope) should avoid activities where the occurrence of hemodynamic compromise would endanger their safety or that of others (like driving).
In patients with underlying ischemic heart disease, demand-related myocardial ischemia, angina and even myocardial infarction and/or congestive heart failure can occur.
Tachycardia mediated cardiomyopathy may develop if the AVNRT is chronic and does not terminate.

Prognosis

AVNRT is rarely life threatening and in the absence of underlying structural heart disease, the prognosis is good. Radiofrequency ablation is curative in 95% of cases.

Diagnosis

Symptoms

The following symptoms may be present:

Sudden onset and sudden offset of rapid palpitations is common
Dizziness and rarely syncope, especially at the onset of the episode of tachycardia
Neck “pounding” may occur as a result of the right atrium contracting against a closed atrioventricular valve and Cannon a waves^[1]^[2] and the simultaneous occurrence of the atrial and ventricular contractions.
Chest pain and angina if the patient has ischemic heart disease
Dyspnea
Polyuria can occur after the episode breaks. It has been hypothesized that this is due to the release of atrial natriuretic peptide

Physical Examination

Pulse

The heart rate is typically regular and between 140-280 bpm. In adults the range is 140-250 bpm, but in children the rate can exceed 250 bpm.

Systolic Blood Pressure

Hypotension may be present in some cases.

Neck

Cannon a waves may be present in some cases

Lungs

Rales may be present in some patients with congestive heart failure

Laboratory Findings

Depending upon the patient’s history and demographics, the following laboratory studies should be considered:

Thyroid function tests (TFTs) – an overactive thyroid may increase the risk of AVNRT
Electrolytes – hypokalemia, hypomagnesemia may predispose to AVNRT
Cardiac markers – if there is a concern that myocardial infarction (a heart attack) has occurred either as a cause or as a result of the AVNRT; this is usually only the case if the patient has experienced ischemic chest pain

Electrocardiogram

An electrocardiogram performed during the occurrence of symptoms may confirm the diagnosis of AVNRT.

Slow-Fast AVNRT (Common AVNRT)

This form of AVNRT accounts for 80% to 90% of cases of AVNRT.
The retrograde P wave that is conducted retrograde up the fast pathway is usually burried within the QRS but less frequently may be observed at the end of the QRS complex as a pseudo r’ wave in lead V1 or an S wave in leads II, III or aVF.

Fast-Slow AVNRT (Uncommon AVNRT)

This form of AVNRT Accounts for 10% of cases of AVNRT
In this form of AVNRT, the impulse is first conducted antegrade down the Fast AV nodal pathway and is then conducted retrograde up the Slow AV nodal pathway.
In contrast to Common AVNRT, a retrograde P wave may be observed after the QRS complex before the T wave

Slow-Slow AVNRT (Atypical AVNRT)

This form of AVNRT accounts for 1-5% of cases of AVNRT
In this form of AVNRT, the impulse is first conducted antegrade down the Slow AV nodal pathway and retrograde up the Slow left atrial fibres approaching the AV node.
The p wave may appear just before the QRS complex, and this makes it hard to distinguish the rhythm from sinus tachycardia.

Aberrant Conduction

It is not uncommon for there to be a wide QRS complex due to aberrant conduction due to underlying conduction system disease. This can make it difficult to distinguish AVNRT from VT. The distinguishing features include:

AVNRT is associated with a QRS complex morphology resembles a typical bundle branch block
AVNRT is not associated with AV dissociation where there is variable coupling of the p wave and the QRS complex
AVNRT is associated with Cannon a waves
AVNRT is not associated with capture beats or fusion beats
AVNRT may convert with adenosine or vagal maneuvers

An electrophysiologic study may be needed to confirm AVNRT prior to ablation.

Holter Monitor / Event Recorder

If the patient complains of recurrent palpitations and no arrhythmia is present on the resting EKG, then a Holter Monitor or Cardiac Event Monitor should be considered.

Treatment

An episode of supraventricular tachycardia (SVT) due to AVNRT can be terminated by any action that transiently blocks the AV node. Various methods are possible.

Patient Position

Place the patient in a supine position to improve cerebral perfusion and reduce the odds of syncope. Placing the patient in Trendelenburg position may actually terminate the rhythm.

Vagal maneuvers

Some people with known AVNRT may be able to stop their attack by using various tricks to activate the vagus nerve. This includes carotid sinus massage (pressure on the carotid sinus in the neck), submersion of the face in ice water to trigger the diving reflex, putting the patient in Trendelenburg position or the Valsalva maneuver (increasing the pressure in the chest by attempting to exhale against a closed airway). Vagel maneuvers are contraindicated in the presence of hypotension.

Medication

Medical therapy can be initiated with drugs that slow AV nodal conduction:

First Line Therapy

Adenosine

Adenosine is generally considered first line therapy for AVNRT.

Treatment of AVNRT with adenosine can be complicated by:

The development of shortness of breath due to bronchospasm
In some cases there can be asystole which is transient given the short half life of adenosine
Atrial fibrillation may be induced by adenosine administration
Ventricular fibrillation is rarely induced by adenosine. When it does occur it is due to block of the AV node with rapid antegrade conduction of atrial fibrillation down the bypass tract. It is for this reason that defibrillation equipment be available.
Adenosine should not be used in heart transplant patients
Dipyridamole may potentiate the effect of adenosine
Theophylline may reduce the effectiveness of adenosine

Administration:

Place a large bore (18 gauge and larger) intravenous line
The initial dose is 6 mg and this should be followed a saline flush with elevation of the arm to assure that the drug is infused
If this is not effective, then 12 mg or 18 mg of adenosine can be admininistered

Beta blockers

A short acting beta-blocker such as esmolol (half life of 8 minutes) can be used to terminate an episode of AVNRT. Longer acting beta-blockers such as atenolol, metoprolol, and propranolol can also be used to reduce the risk of recurrent episodes. Atenolol may be preferable among patients with bronchospasm as it selectively blocks beta-1 receptors with little effect on beta- 2 receptors.

Second Line Therapy

Numerous other antiarrhythmic drugs may be effective if the more commonly used medications have not worked; these include flecainide or amiodarone. Both adenosine and beta blockers may cause tightening of the airways, and are therefore used with caution in people who are known to have asthma. Calcium channel blockers should be avoided if there is a wide complex tacycardia and the diagnosis of AVNRT is not clearly established in so far as calcium channel blockers should be avoided in ventricular tachycardia. If the diagnosis of AVNRT is established, then non-dihydropyridine calcium channel blockers (such as verapamil) may be administered to terminate the rhythm if other agents are not effective. Verapamil acts longer than adenosine and acts rapidly. Its administration can be complicated by hypotension, bradycardia and negative inotropic effects.

Cardioversion

In very rare instances, cardioversion (the electrical restoration of a normal heart rhythm) is needed in the treatment of AVNRT. This would normally only happen if all other treatments have been ineffective, or if the fast heart rate is poorly tolerated (e.g. the development of heart failure symptoms, hypotension (low blood pressure) or unconsciousness).

Electrophysiology and Radiofrequency Ablation

After being diagnosed with AVNRT, patients can also undergo an electrophysiology (EP) study to confirm the diagnosis. Catheter ablation of the slow pathway, if successfully carried out, and cures 95% of patients with AVNRT. The risk of complications is quite low. Ablation can be carried out in patients who do not want to take pharmacotherapy, in whom pharmacotherapy fails, or if the patient has side effects from pharmacotherapy.

Prevention

Triggers such as alcohol and caffeine should be avoided.

References

↑ Laurent G, Leong-Poi H, Mangat I, Korley V, Pinter A, Hu X, So PP, Ramadeen A, Dorian P (2009). “Influence of ventriculoatrial timing on hemodynamics and symptoms during supraventricular tachycardia”. Journal of Cardiovascular Electrophysiology. 20 (2): 176–81. doi:10.1111/j.1540-8167.2008.01276.x. PMID 18775049. Retrieved 2012-09-05. Unknown parameter |month= ignored (help)
↑ Gursoy S, Steurer G, Brugada J, et al. Brief report: the hemodynamic mechanism of pounding in the neck in atrioventricular nodal reentrant tachycardia. N Engl J Med. Sep 10 1992;327(11):772-4.

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Historical Perspective

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Overview

In the past, many cases of AVNRT were referred to as paroxysmal atrial tachycardia, or PAT, or PAT with block. With greater understanding of the underlying electrophysiologic mechanism of these arrhythmias, more specific terminology has now been adapted, and these older non-specific terms are now used to refer to supraventricular tachycardia in general rather than AVNRT in specific.

Historical perspective

Report of the first successful surgical ablation of an accessory pathway tracks back to 1958 by Cobb et al in 1968.^[1]
First catheter-based ablation in a human being was done by Scheinman in 1981.^[2]
Much of early knowledge of supraventicular tachycardia was derived from electrocardiogram , but the mechanism insight into these rhythm disturbances is due to Durrer et al^[3], Coumel et al^[4], Wellens^[5],Scherlag et al^[6], Josephson^[7], and Jackman et al^[8] hard work.
Schelrag and collegues developed reliable His bundle ECG recording in late 1960s.

References

↑ Cobb, Frederick R.; Blumenschein, Sarah D.; Sealy, Will C.; Boineau, John P.; Wagner, Galen S.; Wallace, Andrew G. (1968). “Successful Surgical Interruption of the Bundle of Kent in a Patient with Wolff-Parkinson-White Syndrome”. Circulation. 38 (6): 1018–1029. doi:10.1161/01.CIR.38.6.1018. ISSN 0009-7322.
↑ Scheinman MM, Morady F, Hess DS, Gonzalez R (1982). “Catheter-induced ablation of the atrioventricular junction to control refractory supraventricular arrhythmias”. JAMA. 248 (7): 851–5. PMID 7097946.
↑ Durrer, D.; Schoo, L.; Schuilenburg, R. M.; Wellens, H. J. J. (1967). “The Role of Premature Beats in the Initiation and the Termination of Supraventricular Tachycardia in the Wolff-Parkinson-White Syndrome”. Circulation. 36 (5): 644–662. doi:10.1161/01.CIR.36.5.644. ISSN 0009-7322.
↑ Wellens, Hein J.J. (2004). “Cardiac arrhythmias: The quest for a cure”. Journal of the American College of Cardiology. 44 (6): 1155–1163. doi:10.1016/j.jacc.2004.05.080. ISSN 0735-1097.
↑ Wellens, H J; Brugada, P; Stevenson, W G (1985). “Programmed electrical stimulation of the heart in patients with life-threatening ventricular arrhythmias: what is the significance of induced arrhythmias and what is the correct stimulation protocol?”. Circulation. 72 (1): 1–7. doi:10.1161/01.CIR.72.1.1. ISSN 0009-7322.
↑ Scherlag, Benjamin J.; Lau, Sun H.; Helfant, Richard H.; Berkowitz, Walter D.; Stein, Emanuel; Damato, Anthony N. (1969). “Catheter Technique for Recording His Bundle Activity in Man”. Circulation. 39 (1): 13–18. doi:10.1161/01.CIR.39.1.13. ISSN 0009-7322.
↑ Hussien, Khaled; Hammouda, Mohamed; Elakbawy, Hazem; Abdelaziz, Ahmed; Abdelaal, Ahmed; Shehata, Mohamed; AbdelKhalik, EL Shazly; Nagi, Hassan; Mokhtar, Sherif (2009). “Recurrent supraventricular tachycardias prevalence and pathophysiology after RF ablation: A 5-year registry”. Journal of the Saudi Heart Association. 21 (4): 221–228. doi:10.1016/j.jsha.2009.10.005. ISSN 1016-7315.
↑ Jackman, Warren M.; Wang, Xunzhang; Friday, Karen J.; Roman, Carlos A.; Moulton, Kriech P.; Beckman, Karen J.; McClelland, James H.; Twidale, Nicholas; Hazlitt, H. Andrew; Prior, Michael I.; Margolis, P. David; Calame, James D.; Overholt, Edward D.; Lazzara, Ralph (1991). “Catheter Ablation of Accessory Atrioventricular Pathways (Wolff–Parkinson–White Syndrome) by Radiofrequency Current”. New England Journal of Medicine. 324 (23): 1605–1611. doi:10.1056/NEJM199106063242301. ISSN 0028-4793.

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Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Overview

The “common form” or “usual” AVNRT utilizes the slow AV nodal pathway as the anterograde limb of the circuit and the fast AV nodal pathway as the retrograde limb.Uncommon form of AVNRT is reentry circuit reversed in a format that AV nod pathway is anterograde limb and slow AV nodal pathway is the retrograde limb. third type of AVNRT that utilizes the slow AV nodal pathway as the anterograde limb and left atrial fibers that approach the AV node from the left side of the inter-atrial septum as the retrograde limb.

Classification

There are several types of AVNRT. The “common form” or “usual” AVNRT utilizes the slow AV nodal pathway as the anterograde limb of the circuit and the fast AV nodal pathway as the retrograde limb. The reentry circuit can be reversed such that the fast AV nodal pathway is the anterograde limb and the slow AV nodal pathway is the retrograde limb. This, not surprisingly is referred to as the “uncommon form” of AVNRT. However, there is also a third type of AVNRT that utilizes the slow AV nodal pathway as the anterograde limb and left atrial fibers that approach the AV node from the left side of the inter-atrial septum as the retrograde limb. This is known as atypical, or Slow-Slow AVNRT.^[1]^[2]

Common AVNRT

In common AVNRT, the anterograde conduction is via the slow pathway and the retrograde conduction is via the fast pathway (“slow-fast” AVNRT). This accounts for 80%-90% of cases of AVNRT. Because the retrograde conduction is via the fast pathway, stimulation of the atria (which produces the inverted P wave) will occur at the same time as stimulation of the ventricles (which causes the QRS complex). As a result, the inverted P waves may not be seen on the surface ECG since they are buried with the QRS complexes. Often the retrograde p-wave is visible, but also in continuity with the QRS complex, appearing as a “pseudo R prime” wave in lead V1 or a “pseudo S” wave in the inferior leads.

Uncommon AVNRT

In uncommon AVNRT, the anterograde conduction is via the fast pathway and the retrograde conduction is via the slow pathway (“fast-slow” AVNRT). Multiple slow pathways can exist so that both anterograde and retrograde conduction are over slow pathways. (“slow-slow” AVNRT). Because the retrograde conduction is via the slow pathway, stimulation of the atria will be delayed by the slow conduction tissue and will typically produce an inverted P wave that falls after the QRS complex on the surface ECG.

Detailed Chapters on AVNRT Variants

References

↑ Nakagawa, Hiroshi; Jackman, Warren M. (2007). “Catheter Ablation of Paroxysmal Supraventricular Tachycardia”. Circulation. 116 (21): 2465–2478. doi:10.1161/CIRCULATIONAHA.106.655746. ISSN 0009-7322.
↑ Khairy, Paul; Guerra, Peter G.; Rivard, Lena; Tanguay, Jean-François; Landry, Evelyn; Guertin, Marie-Claude; Macle, Laurent; Thibault, Bernard; Tardif, Jean-Claude; Talajic, Mario; Roy, Denis; Dubuc, Marc (2011). “Enlargement of Catheter Ablation Lesions in Infant Hearts With Cryothermal Versus Radiofrequency Energy”. Circulation: Arrhythmia and Electrophysiology. 4 (2): 211–217. doi:10.1161/CIRCEP.110.958082. ISSN 1941-3149.

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Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] ; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Overview

AVNRT occurs when a reentry circuit forms within or just next to the atrioventricular node. The circuit usually involves two anatomical pathways: the fast pathway and the slow pathway, which are both in the right atrium. The slow pathway (which is usually targeted for ablation) is located inferiorly and slightly posterior to the AV node, often following the anterior margin of the coronary sinus. The fast pathway is usually located just superior and posterior to the AV node. These pathways are formed from tissue that behaves very much like the AV node, and some authors regard them as part of the AV node. In the usual form of AVNRT, the conduction from the atrium to the ventricle is down the slow pathway, and the retrograde conduction from the ventricle to the atrium is up the fast pathway.

Pathophysiology

Electrophysiologic Triggers

Premature Atrial Complex

The most common trigger for an episode of AVNRT is when an atrial premature complex (APC) approaches the fast pathway, and is blocked due to the longer refractory period of this pathway, and instead conducts down the slow pathway. As the impulse goes down the slow pathway, the fast pathway recovers, and allows the impulse to conduct backward or retrograde toward the atrium. It then re-enters the atrial entrance of the slow pathway and the cycle repeats itself.^[1]

Premature Ventricular Complex

The second most common mechanism whereby AVNRT is triggered is via the entry of a premature ventricular complex down either the slow conducting pathway (similar to a premature atrial complex above) or down the rapidly conducting pathway.

Genetics

There are certain types of cardiac arrhythmia that are shown to have a genetic basis.
- Wolff-Parkinson-White syndrome has an autosomal dominant inheritance model.^[2]
- familial lone atrial fibrillation which is classified as “channelopathies” and is characterized by autosomal dominant inheritance, corresponding to a locus on chromosome 10.^[3]
However, whether a genetic mechanism also contributes to the development of AVNRT has not been well known, but it is shown that offspring of affected patient is at 3.4% increased risk to develop the disease.

References

↑ Mani, Bhalaghuru Chokkalingam; Pavri, Behzad B. (2014). “Dual Atrioventricular Nodal Pathways Physiology: A Review of Relevant Anatomy, Electrophysiology, and Electrocardiographic Manifestations”. Indian Pacing and Electrophysiology Journal. 14 (1): 12–25. doi:10.1016/S0972-6292(16)30711-2. ISSN 0972-6292.
↑ Vidaillet, Humberto J.; Pressley, Joyce C.; Henke, Elizabeth; Harrell, Frank E.; German, Lawrence D. (1987). “Familial Occurrence of Accessory Atrioventricular Pathways (Preexcitation Syndrome)”. New England Journal of Medicine. 317 (2): 65–69. doi:10.1056/NEJM198707093170201. ISSN 0028-4793.
↑ Brugada, Ramon; Tapscott, Terry; Czernuszewicz, Grazyna Z.; Marian, A.J.; Iglesias, Anna; Mont, Lluis; Brugada, Josep; Girona, Josep; Domingo, Anna; Bachinski, Linda L.; Roberts, Robert (1997). “Identification of a Genetic Locus for Familial Atrial Fibrillation”. New England Journal of Medicine. 336 (13): 905–911. doi:10.1056/NEJM199703273361302. ISSN 0028-4793.

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Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Ayokunle Olubaniyi M.B,B.S [2] Ramyar Ghandriz MD [3]

Overview

AV nodal reentrant tachycardia results from a reentrant circuit in the AV node. The causes include: Lown-Ganong-Levine syndrome, Mahaim fiber tachycardia, mitral valve prolapse, and Wolff-Parkinson-White syndrome. It has also been reported to have a familial etiology.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

AV nodal reentrant tachycardia is usually not life-threatening.

Common Causes

Causes by Organ Systems

Cardiovascular	Lown-Ganong-Levine syndrome^[1], Mahaim fiber tachycardia^[2], mitral valve prolapse, Wolff-Parkinson-White syndrome
Chemical/Poisoning	No underlying causes
Dental	No underlying causes
Dermatologic	No underlying causes
Drug Side Effect	No underlying causes
Ear Nose Throat	No underlying causes
Endocrine	No underlying causes
Environmental	No underlying causes
Gastroenterologic	No underlying causes
Genetic	Familial atrioventricular nodal reentry tachycardia^[3]
Hematologic	No underlying causes
Iatrogenic	No underlying causes
Infectious Disease	No underlying causes
Musculoskeletal/Orthopedic	No underlying causes
Neurologic	No underlying causes
Nutritional/Metabolic	No underlying causes
Obstetric/Gynecologic	No underlying causes
Oncologic	No underlying causes
Ophthalmologic	No underlying causes
Overdose/Toxicity	No underlying causes
Psychiatric	No underlying causes
Pulmonary	No underlying causes
Renal/Electrolyte	No underlying causes
Rheumatology/Immunology/Allergy	No underlying causes
Sexual	No underlying causes
Trauma	No underlying causes
Urologic	No underlying causes
Miscellaneous	No underlying causes

Causes in Alphabetical Order

References

↑ Hunter, Juanita; Tsounias, Emmanouil; Cogan, John; Young, Ming-Lon (2018). “A Case of Lown-Ganong-Levine Syndrome: Due to an Accessory Pathway of James Fibers or Enhanced Atrioventricular Nodal Conduction (EAVNC)?”. American Journal of Case Reports. 19: 309–313. doi:10.12659/AJCR.906767. ISSN 1941-5923.
↑ Sternick EB (2003). “Mahaim fibre tachycardia: recognition and management”. Indian Pacing Electrophysiol J. 3 (2): 47–59. PMC 1513516. PMID 16943957.
↑ ^3.0 ^3.1 Namgung, J.; Kwak, JJ.; Choe, H.; Kwon, SU.; Doh, JH.; Lee, SY.; Lee, WR. (2012). “Familial occurrence of atrioventricular nodal reentrant tachycardia in a mother and her son”. Korean Circ J. 42 (10): 718–21. doi:10.4070/kcj.2012.42.10.718. PMID 23170103. Unknown parameter |month= ignored (help)

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Differentiating AVNRT from other Disorders

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Syed Hassan A. Kazmi BSc, MD [2] Ramyar Ghandriz MD [3]

Overview

AV nodal reentrant tachycardia is diffrentiated mostly by ECG. diseases that may lead to tachycardia and how to differentiate them is discussed below.

Differentiating AV nodal reentrant tachycardia from other Diseases

Supraventricular tachycardias must be differentiated from each other because the management strategies may vary:

AV Nodal Reentry Tachycardia

Rate: In adults the range is 140-250 bpm, but in children the rate can exceed 250 bpm.
Rhythm: Regular
P waves: The p wave is usually superimposed on or buried within the QRS complex
PR interval: The PR interval cannot be calculated as the p wave is generally obscured by the QRS complex. In uncommon AVNRT, the p wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the p wave can appear just before the QRS complex.
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology in the absence of abberant conduction, QRS alternans may be present
Response to Maneuvers: May break with adenosine or vagal maneuvers
Epidemiology and Demographics: Accounts for 60%-70% of all SVTs. 80% to 90% of cases are due to antegrade conduction down a slow pathway and retrograde up a fast pathway.

Atrial Fibrillation

Rate: 110 to 180 bpm
Rhythm: Irregularly irregular
P waves: Absent, fibrillatory waves
PR interval: Absent
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology in the absence of abberant conduction
Response to Maneuvers: Does not break with adenosine or vagal maneuvers
Epidemiology and Demographics: More common in the elderly, following bypass surgery, in mitral valve disease, hyperthyroidism

Atrial Flutter

Rate: 75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) bpm, but 150 is most common
Rhythm: Regular
P waves: Sawtooth pattern of P waves at 250 to 350 beats per minute
PR interval: Varies depending upon the magnitude of the block, but is short
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers: Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm
Epidemiology and Demographics: More common in the elderly, after alcohol

AV Reciprocating Tachycardia

Rate: More rapid than AVNRT
Rhythm:
P waves:
PR interval:
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers: May break with adenosine or vagal maneuvers
Epidemiology and Demographics: More common in males, whereas AVNRT is more common in females, Occurs at a younger age

Junctional Tachycardia

Rate: > 60 beats per minute
Rhythm: Regular
P waves: Usually inverted, may be burried in the QRS complex
PR interval: The p wave is usually buried in the QRS complex
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers: Does not break with adenosine or vagal maneuvers
Epidemiology and Demographics: Common after heart surgery, digoxin toxicity, as an escape rhythm in AV block

Multifocal Atrial Tachycardia

Rate: Atrial rate is > 100 beats per minute (bpm)
Rhythm:
P waves: P waves of varying morphology from at least three different foci, absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude
PR interval: Variable PR intervals, RR intervals, and PP intervals
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers: Does not terminate with adenosine or vagal maneuvers
Epidemiology and Demographics: * High incidence in the elderly and in those with COPD

Sinus Node Reentry Tachycardia

Rate:
Rhythm:
P waves: Upright P waves precede each regular, narrow QRS complex
PR interval:
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers: Although it cannot be distinguished on the surface 12 lead EKG from sinus tachycardia, SA node reentry tachycardia does often terminate with vagal maneuvers unlike sinus tachycardia.
Epidemiology and Demographics:

Sinus tachycardia

Rate: Greater than 100.
Rhythm: Regular.
P waves: Upright, consistent, and normal in morphology (if no atrial disease)
PR interval: Between 0.12–0.20 seconds and shortens with increasing heart rate
QRS complex: Less than 0.12 seconds, consistent, and normal in morphology
Response to Maneuvers:
Epidemiology and Demographics:

Ventricular Tachycardia

Rate:
Rhythm: Generally regular
P waves: Normal morphology, upright, but dissociated from the QRS complex (i.e. “march through” the QRS complex)
PR interval:
QRS complex: Wide and greater than 0.12 seconds
Response to Maneuvers: Does not terminate in response to adenosine or vagal maneuvers
Epidemiology and Demographics:
Risk Factors:: Occurs in the context of myocardial ischemia, myocardial infarction, congestive heart failure, drug toxicity, and inhereted channelopathies

Wolff-Parkinson-White syndrome

Pathophysiology: Anatomically and functionally, the fast and slow pathways of AVNRT should not be confused with the accessory pathways that give rise to Wolff-Parkinson-White syndrome (WPW) syndrome or atrioventricular re-entrant tachycardia (AVRT). In AVNRT, the fast and slow pathways are located within the right atrium in close proximity to or within the AV node and exhibit electrophysiologic properties similar to AV nodal tissue. Accessory pathways that give rise to WPW syndrome and AVRT are located in the atrioventricular valvular rings, they provide a direct connection between the atria and ventricles, and have electrophysiologic properties similar to ventricular myocardium.
Rate:
Rhythm:
P waves: In WPW with orthodromic conduction due to a bypass tract, the p wave generally follows the QRS complex, whereas in AVNRT, the p wave is generally buried in the QRS complex.
PR interval:
QRS complex: In WPW there is a delta wave and evidence of ventricular preexcitation if there is conduction to the ventrilce via antegrade conduction down an accessory pathway. It should be noted, however, that in some patients with WPW, a delta wave and pre-excitation may not be present because bypass tracts do not conduct antegrade.
Response to Maneuvers: May break in response to procainamide, adenosine, vagal maneuvers
Epidemiology and Demographics:
Risk Factors: None, an inhereted disorder


Arrhythmia	Rhythm	Rate	P wave	PR Interval	QRS Complex	Response to Maneuvers	Epidemiology	Co-existing Conditions
Atrioventricular nodal reentry tachycardia (AVNRT)^[1]^[2]^[3]^[4]	Regular	140-280 bpm	Slow-Fast AVNRT: Pseudo-S wave in leads II, III, and AVF Pseudo-R’ in lead V1. Fast-Slow AVNRT P waves between the QRS and T waves (QRS-P-T complexes) Slow-Slow AVNRT Late P waves after a QRS Often appears as atrial tachycardia. Inverted, superimposed on or buried within the QRS complex (pseudo R prime in V1/pseudo S wave in inferior leads)	Absent (P wave can appear after the QRS complex and before the T wave, and in atypical AVNRT, the P wave can appear just before the QRS complex)	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction QRS alternans may be present	May break with adenosine or vagal maneuvers	60%-70% of all supraventricular tachycardias	Structural heart disease Atrial tachyarrhythmias
Atrial Fibrillation (AFib)^[5]^[6]	Irregularly irregular	On a 10-second 12-lead EKG strip, multiply number of QRS complexes by 6	Absent Fibrillatory waves	Absent	Less than 0.12 seconds, consistent, and normal in morphology in the absence of aberrant conduction	Does not break with adenosine or vagal maneuvers	2.7–6.1 million people in the United States have AFib 2% of people younger than age 65 have AFib, while about 9% of people aged 65 years or older have AFib	Elderly Following bypass surgery Mitral valve disease Hyperthyroidism Diabetes Heart failure Ischemic heart disease Chronic kidney disease Heavy alcohol use Left chamber enlargement
Atrial Flutter^[7]	Regular or Irregular	75 (4:1 block), 100 (3:1 block) and 150 (2:1 block) beats per minute (bpm), but 150 is more common	Sawtooth pattern of P waves at 250 to 350 bpm Biphasic deflection in V1	Varies depending upon the magnitude of the block, but is short	Less than 0.12 seconds, consistent, and normal in morphology	Conduction may vary in response to drugs and maneuvers dropping the rate from 150 to 100 or to 75 bpm	Incidence: 88 per 100,000 individuals	Elderly Alcohol
Multifocal Atrial Tachycardia^[8]^[9]	Irregular	Atrial rate is > 100 beats per minute	Varying morphology from at least three different foci Absence of one dominant atrial pacemaker, can be mistaken for atrial fibrillation if the P waves are of low amplitude	Variable PR intervals, RR intervals, and PP intervals	Less than 0.12 seconds, consistent, and normal in morphology	Does not terminate with adenosine or vagal maneuvers	0.05% to 0.32% of electrocardiograms in general hospital admissions	Elderly Chronic obstructive pulmonary disease (COPD)
Paroxysmal Supraventricular Tachycardia	Regular	150 and 240 bpm	Absent Hidden in QRS	Absent	Narrow complexes (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex	Prevalence: 0.023 per 100,000	Alcohol Caffeine Nicotine Psychological stress Wolff-Parkinson-White syndrome
Premature Atrial Contractrions (PAC)^[10]^[11]	Regular except when disturbed by premature beat(s)	80-120 bpm	Upright	> 0.12 second May be shorter than that in normal sinus rhythm (NSR) if the origin of PAC is located closer to the AV node Ashman’s Phenomenon: PAC displaying a right bundle branch block pattern	Usually narrow (< 0.12 s)	Breaks with vagal maneuvers, adenosine, diving reflex, oculocardiac reflex		Infants Cardiomyopathy Myocarditis Elderly Coronary artery disease Stroke Increased atrial natriuretic peptide (ANP) Hypercholesterolemia
Wolff-Parkinson-White Syndrome^[12]^[13]	Regular	Atrial rate is nearly 300 bpm and ventricular rate is at 150 bpm	With orthodromic conduction due to a bypass tract, the P wave generally follows the QRS complex, whereas in AVNRT, the P wave is generally buried in the QRS complex.	Less than 0.12 seconds	A delta wave and evidence of ventricular pre-excitation if there is conduction to the ventricle via ante-grade conduction down an accessory pathway A delta wave and pre-excitation may not be present because bypass tracts do not conduct ante-grade.	May break in response to procainamide, adenosine, vagal maneuvers	Worldwide prevalence of WPW syndrome is 100 – 300 per 100,000	Ebstein’s anomaly Mitral valve prolapse: This cardiac disorder, if present, is associated with left-sided accessory pathways. Hypertrophic cardiomyopathy: This disorder is associated with familial/inherited form of WPW syndrome. Hypokalemic periodic paralysis Pompe disease Tuberous sclerosis
Ventricular Fibrillation (VF)^[14]^[15]^[16]	Irregular	150 to 500 bpm	Absent	Absent	Absent (R on T phenomenon in the setting of ischemia)	Does not break in response to procainamide, adenosine, vagal maneuvers	3-12% cases of acute myocardial infarction (AMI) Out of 356,500 out of hospital cardiac arrests, 23% have VF as initial rhythm	Myocardial ischemia / infarction Cardiomyopathy Channelopathies e.g. Long QT (acquired / congenital) Electrolyte abnormalities (hypokalemia/hyperkalemia, hypomagnesemia) Aortic stenosis Aortic dissection Myocarditis Cardiac tamponade Blunt trauma (Commotio Cordis) Sepsis Hypothermia Pneumothorax Seizures Stroke
Ventricular Tachycardia^[17]^[18]	Regular	> 100 bpm (150-200 bpm common)	Absent	Absent Initial R wave in V1, initial r > 40 ms in V1/V2, notched S in V1, initial R in aVR, lead II R wave peak time ≥50 ms, no RS in V1-V6, and atrioventricular dissociation	Wide complex, QRS duration > 120 milliseconds	Does not break in response to procainamide, adenosine, vagal maneuvers	5-10% of patients presenting with AMI	Coronary artery disease Aortic stenosis Cardiomyopathy Electrolyte imbalances (e.g., hypokalemia, hypomagnesemia) Inherited channelopathies (e.g., long-QT syndrome) Catecholaminergic polymorphic ventricular tachycardia Arrhythmogenic right ventricular dysplasia Myocardial infarction Torsades de pointes is a form of polymorphic VT that is often associated with a prolonged QT interval

References

↑ Katritsis DG, Josephson ME (August 2016). “Classification, Electrophysiological Features and Therapy of Atrioventricular Nodal Reentrant Tachycardia”. Arrhythm Electrophysiol Rev. 5 (2): 130–5. doi:10.15420/AER.2016.18.2. PMC 5013176. PMID 27617092.
↑ Letsas KP, Weber R, Siklody CH, Mihas CC, Stockinger J, Blum T, Kalusche D, Arentz T (April 2010). “Electrocardiographic differentiation of common type atrioventricular nodal reentrant tachycardia from atrioventricular reciprocating tachycardia via a concealed accessory pathway”. Acta Cardiol. 65 (2): 171–6. doi:10.2143/AC.65.2.2047050. PMID 20458824.
↑ “Atrioventricular Nodal Reentry Tachycardia (AVNRT) – StatPearls – NCBI Bookshelf”.
↑ Schernthaner C, Danmayr F, Strohmer B (2014). “Coexistence of atrioventricular nodal reentrant tachycardia with other forms of arrhythmias”. Med Princ Pract. 23 (6): 543–50. doi:10.1159/000365418. PMC 5586929. PMID 25196716.
↑ Lankveld TA, Zeemering S, Crijns HJ, Schotten U (July 2014). “The ECG as a tool to determine atrial fibrillation complexity”. Heart. 100 (14): 1077–84. doi:10.1136/heartjnl-2013-305149. PMID 24837984.
↑ Harris K, Edwards D, Mant J (2012). “How can we best detect atrial fibrillation?”. J R Coll Physicians Edinb. 42 Suppl 18: 5–22. doi:10.4997/JRCPE.2012.S02. PMID 22518390.
↑ Cosío FG (June 2017). “Atrial Flutter, Typical and Atypical: A Review”. Arrhythm Electrophysiol Rev. 6 (2): 55–62. doi:10.15420/aer.2017.5.2. PMC 5522718. PMID 28835836.
↑ Scher DL, Arsura EL (September 1989). “Multifocal atrial tachycardia: mechanisms, clinical correlates, and treatment”. Am. Heart J. 118 (3): 574–80. doi:10.1016/0002-8703(89)90275-5. PMID 2570520.
↑ Goodacre S, Irons R (March 2002). “ABC of clinical electrocardiography: Atrial arrhythmias”. BMJ. 324 (7337): 594–7. doi:10.1136/bmj.324.7337.594. PMC 1122515. PMID 11884328.
↑ Lin CY, Lin YJ, Chen YY, Chang SL, Lo LW, Chao TF, Chung FP, Hu YF, Chong E, Cheng HM, Tuan TC, Liao JN, Chiou CW, Huang JL, Chen SA (August 2015). “Prognostic Significance of Premature Atrial Complexes Burden in Prediction of Long-Term Outcome”. J Am Heart Assoc. 4 (9): e002192. doi:10.1161/JAHA.115.002192. PMC 4599506. PMID 26316525.
↑ Strasburger JF, Cheulkar B, Wichman HJ (December 2007). “Perinatal arrhythmias: diagnosis and management”. Clin Perinatol. 34 (4): 627–52, vii–viii. doi:10.1016/j.clp.2007.10.002. PMC 3310372. PMID 18063110.
↑ Rao AL, Salerno JC, Asif IM, Drezner JA (July 2014). “Evaluation and management of wolff-Parkinson-white in athletes”. Sports Health. 6 (4): 326–32. doi:10.1177/1941738113509059. PMC 4065555. PMID 24982705.
↑ Rosner MH, Brady WJ, Kefer MP, Martin ML (November 1999). “Electrocardiography in the patient with the Wolff-Parkinson-White syndrome: diagnostic and initial therapeutic issues”. Am J Emerg Med. 17 (7): 705–14. doi:10.1016/s0735-6757(99)90167-5. PMID 10597097.
↑ Glinge C, Sattler S, Jabbari R, Tfelt-Hansen J (September 2016). “Epidemiology and genetics of ventricular fibrillation during acute myocardial infarction”. J Geriatr Cardiol. 13 (9): 789–797. doi:10.11909/j.issn.1671-5411.2016.09.006. PMC 5122505. PMID 27899944.
↑ Samie FH, Jalife J (May 2001). “Mechanisms underlying ventricular tachycardia and its transition to ventricular fibrillation in the structurally normal heart”. Cardiovasc. Res. 50 (2): 242–50. doi:10.1016/s0008-6363(00)00289-3. PMID 11334828.
↑ Adabag AS, Luepker RV, Roger VL, Gersh BJ (April 2010). “Sudden cardiac death: epidemiology and risk factors”. Nat Rev Cardiol. 7 (4): 216–25. doi:10.1038/nrcardio.2010.3. PMC 5014372. PMID 20142817.
↑ Koplan BA, Stevenson WG (March 2009). “Ventricular tachycardia and sudden cardiac death”. Mayo Clin. Proc. 84 (3): 289–97. doi:10.1016/S0025-6196(11)61149-X. PMC 2664600. PMID 19252119.
↑ Levis JT (2011). “ECG Diagnosis: Monomorphic Ventricular Tachycardia”. Perm J. 15 (1): 65. doi:10.7812/tpp/10-130. PMC 3048638. PMID 21505622.

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Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Ramyar Ghandriz MD [2]

Overview

AVNRT is more dominant in lower age and is more related to female gender.

Epidemiology and Demographics

Incidence

The incidence of AVNRT is approximately 89,000 in US annually.^[1]

Prevalence

The prevalence of AVNRT is approximately 570,000 per US population

Age

Mean age of symptom onset is 32 ± 18 years.^[2]

Race

There is no racial predilection to AVNRT.

Gender

AVNRT affects women more than men.^[3]

Region

The prevalence of AVNRT globally is similar to the united states.
There is insufficient evidence suggesting a region being more vulnerable to disease.

References

↑ name=”Electrophysiology : the basics”>Steinberg, Jonathan (2017). Electrophysiology : the basics. Philadelphia: Wolters Kluwer Heath. ISBN 9781496340016.
↑ Quattrocelli, Amanda; Lang, Janet; Davis, Andrew; Pflaumer, Andreas (2018). “Age makes a difference: Symptoms in pediatric supraventricular tachycardia”. Journal of Arrhythmia. 34 (5): 565–571. doi:10.1002/joa3.12103. ISSN 1880-4276.
↑ Ghani, A.; Maas, A. H. E. M.; Delnoy, P. P. H. M.; Ramdat Misier, A. R.; Ottervanger, J. P.; Elvan, A. (2010). “Sex-Based Differences in Cardiac Arrhythmias, ICD Utilisation and Cardiac Resynchronisation Therapy”. Netherlands Heart Journal. 19 (1): 35–40. doi:10.1007/s12471-010-0050-8. ISSN 1568-5888.

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Risk Factors

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ramyar Ghandriz MD [2]

Overview

Underlying structural heart disease is generally absent. Often, there is no precipitant of an episode. Risk factors for precipitation of AVNRT include Alcohol, Anemia,Anxiety and Caffeine.

Risk Factors

Common risk factors in the development of [disease name] include Alcohol,Anemia,Anxiety and Caffeine.

Common Risk Factors

Common risk factors in the development of AVNRT may be occupational, environmental, genetic, and viral.
Common risk factors in the development of AVNRT include:
- Alcohol^[1]
- Anemia^[2]
- Anxiety^[3]
- Caffeine
- Chocolate^[4]
- Fever
- Hyperthyroidism^[5]
- Hypokalemia
- Hypomagnesemia
- Hypoxia
- Myocardial ischemia
- Menstruation
- Psychological stress
- Stimulants
- Tea
- Theobromine in foods like tea, coffee and chocolate
- Theophylline

References

↑ Mandyam, Mala C.; Vedantham, Vasanth; Scheinman, Melvin M.; Tseng, Zian H.; Badhwar, Nitish; Lee, Byron K.; Lee, Randall J.; Gerstenfeld, Edward P.; Olgin, Jeffrey E.; Marcus, Gregory M. (2012). “Alcohol and Vagal Tone as Triggers for Paroxysmal Atrial Fibrillation”. The American Journal of Cardiology. 110 (3): 364–368. doi:10.1016/j.amjcard.2012.03.033. ISSN 0002-9149.
↑ Zeljković, Ivan; Đula, Kristijan; Babacanli, Alen; Kruljac, Ivan; Mustapić, Vito; Brkljačić, Diana Delić; Bulj, Nikola; Radeljić, Vjekoslav; Manola, Šime; Pavlović, Nikola (2019). “High prevalence of hyperlipidaemia in patients with AV re-entry tachycardia and AV nodal re-entry tachycardia”. Scientific Reports. 9 (1). doi:10.1038/s41598-019-47940-9. ISSN 2045-2322.
↑ Papiashvili G, Tabagari-Bregvadze N, Brugada J (2018). “INFLUENCE OF CATHETER ABLATION OF PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA ON PATIENTS’ ANXIETY”. Georgian Med News (Issue): 58–60. PMID 29578424.
↑ Wood, Kathryn A.; Wiener, Carolyn L.; Kayser-Jones, Jeanie (2016). “Supraventricular Tachycardia and the Struggle to be Believed”. European Journal of Cardiovascular Nursing. 6 (4): 293–302. doi:10.1016/j.ejcnurse.2007.02.006. ISSN 1474-5151.
↑ Meti, Nicholas; Mongeon, François-Pierre; Guerra, Peter G.; O’Meara, Eileen; Khairy, Paul (2016). “Incessant atrioventricular nodal reentrant tachycardia with tachycardia-induced cardiomyopathy, biventricular thrombosis, and pulmonary emboli”. HeartRhythm Case Reports. 2 (2): 142–145. doi:10.1016/j.hrcr.2015.11.012. ISSN 2214-0271.

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Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Ramyar Ghandriz MD [2]

Overview

AVNRT starts and stops abruptly. Patients may develop syncope. The prognosis is good.

Natural History, Complications and Prognosis

Natural History

The rhythm often ceases abruptly and spontaneously. An episode generally last seconds to hours.

Complications

Some patients will develop syncope during episodes of AVRNT. ^[1]The mechanism of syncope may be due to a reduction of cardiac output and hemodynamic compromise as a result of the short ventricular filling time or alternatively it may be due to transient asystole due to tachycardia-mediated suppression of the sinus node when the rhythm terminates.^[2] Those patients who do become symptomatic during episodes of AVNRT (i.e. have syncope) should avoid activities where the occurrence of hemodynamic compromise would endanger their safety or that of others (like driving).
In patients with underlying ischemic heart disease, demand-related myocardial ischemia, angina and even myocardial infarction and/or congestive heart failure can occur.
Tachycardia mediated cardiomyopathy may develop if the AVNRT is chronic and does not terminate.

Prognosis

AVNRT is rarely life threatening and in the absence of underlying structural heart disease, the prognosis is good. Radiofrequency ablation is curative in 95% of cases.^[3]

References

↑ Leitch, J W; Klein, G J; Yee, R; Leather, R A; Kim, Y H (1992). “Syncope associated with supraventricular tachycardia. An expression of tachycardia rate or vasomotor response?”. Circulation. 85 (3): 1064–1071. doi:10.1161/01.CIR.85.3.1064. ISSN 0009-7322.
↑ Moya, A.; Sutton, R.; Ammirati, F.; Blanc, J.-J.; Brignole, M.; Dahm, J. B.; Deharo, J.-C.; Gajek, J.; Gjesdal, K.; Krahn, A.; Massin, M.; Pepi, M.; Pezawas, T.; Granell, R. R.; Sarasin, F.; Ungar, A.; van Dijk, J. G.; Walma, E. P.; Wieling, W.; Abe, H.; Benditt, D. G.; Decker, W. W.; Grubb, B. P.; Kaufmann, H.; Morillo, C.; Olshansky, B.; Parry, S. W.; Sheldon, R.; Shen, W. K.; Vahanian, A.; Auricchio, A.; Bax, J.; Ceconi, C.; Dean, V.; Filippatos, G.; Funck-Brentano, C.; Hobbs, R.; Kearney, P.; McDonagh, T.; McGregor, K.; Popescu, B. A.; Reiner, Z.; Sechtem, U.; Sirnes, P. A.; Tendera, M.; Vardas, P.; Widimsky, P.; Auricchio, A.; Acarturk, E.; Andreotti, F.; Asteggiano, R.; Bauersfeld, U.; Bellou, A.; Benetos, A.; Brandt, J.; Chung, M. K.; Cortelli, P.; Da Costa, A.; Extramiana, F.; Ferro, J.; Gorenek, B.; Hedman, A.; Hirsch, R.; Kaliska, G.; Kenny, R. A.; Kjeldsen, K. P.; Lampert, R.; Molgard, H.; Paju, R.; Puodziukynas, A.; Raviele, A.; Roman, P.; Scherer, M.; Schondorf, R.; Sicari, R.; Vanbrabant, P.; Wolpert, C.; Zamorano, J. L. (2009). “Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC)”. European Heart Journal. 30 (21): 2631–2671. doi:10.1093/eurheartj/ehp298. ISSN 0195-668X.
↑ O’Hara, Gilles E.; Philippon, François; Champagne, Jean; Blier, Louis; Molin, Franck; Côté, Jean-Marc; Nault, Isabelle; Sarrazin, Jean-François; Gilbert, Marcel (2007). “Catheter ablation for cardiac arrhythmias: A 14-year experience with 5330 consecutive patients at the Quebec Heart Institute, Laval Hospital”. Canadian Journal of Cardiology. 23: 67B–70B. doi:10.1016/S0828-282X(07)71013-9. ISSN 0828-282X.

Template:WH Template:WS CME Category::Cardiology

Diagnosis

Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram

Treatment

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