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Reentrant Arrhythmias

Editor: Vasimahmed Lala Updated: 7/30/2023 2:05:23 AM


Tachyarrhythmias are produced by one of the three mechanisms; reentry, enhanced automaticity, or triggered activity.[1] Reentry is the most common mechanism of arrhythmia, and it is responsible for the majority of supraventricular as well as ventricular tachycardias.[2] Reentrant arrhythmias are distinct electrophysiology maladies of the heart caused by the presence of circuits in the normal myocardium. Reentrant arrhythmias occur when a cardiac impulse fails to stop and re-excites the tissues that have recovered from the refractory period. The impulse travels in a circus around a physiologic or anatomic obstacle, forming a reentry circuit in the myocardium.[3] 

The common reentrant arrhythmias include atrial fibrillation, atrial flutter, atrioventricular nodal reentrant tachycardia, atrioventricular reciprocating tachycardia, other pathway-mediated tachycardia, and ventricular tachycardia. In atrial fibrillation, multiple reentry circuits are found in the left atrium and pulmonary veins, while typical atrial flutter is characterized by a macro reentry circuit in the right atrium.[4][5] Atrioventricular nodal reentry tachycardia (AVNRT) is the most common reentrant supraventricular tachycardia and utilizes the atrioventricular (AV) node as its reentry circuit.[6][7] The atrioventricular reciprocating tachycardia and other pathway-mediated tachycardia involve the atrioventricular node, accessory pathway, and/or the surrounding atrial and ventricular myocardium.[8] The reentry circuit in ventricular tachycardia is complex and formed by the scar in the myocardium. Some ventricular arrhythmias may involve bundle branches as a part of the reentry circuit.[9]

The clinical symptoms and signs of different reentry arrhythmias are variable, and the clinical course and outcomes depend on the cardiac status. Atrioventricular nodal reentrant tachycardia is the most benign reentrant arrhythmia, while scar-related ventricular tachycardia is a life-threatening tachyarrhythmia.[10] Atrial fibrillation and atrial flutter are associated with thromboembolic complications, while pathway-mediated tachycardia has a risk of sudden cardiac death.[11][12] The recent advancements in electrophysiologic mapping techniques have improved the understanding of reentrant arrhythmias, while ablation has emerged as an effective treatment option for most of these arrhythmias.[13][14] Understanding the pathophysiology and basic mechanism of reentrant arrhythmias is essential before devising a patient management plan. This chapter will discuss the etiology, epidemiology, and pathophysiology of reentrant tachycardia and review the management of patients with reentrant arrhythmias.


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Reentry arrhythmias can manifest in a multitude of ways depending on the specific variation of the abnormal rhythm. If the origin involves the atrioventricular (AV) node, the arrhythmia purely occurs due to an anatomic abnormality in the AV node associated with the different conduction pathways in the node itself.[15] The AV node has a slow and fast pathway, which, when operating correctly, does not allow for the re-excitation of the node.[15] Atrioventricular reciprocating tachycardia and other accessory pathway-mediated tachycardias are caused by the congenital accessory connections between the atria and ventricles or the connections between the different parts of the cardiac conduction system.[16][17] The accessory pathways are more common in the presence of congenital cardiac conditions, including Ebstein anomaly and transposition of the great arteries (TGA).[18] Genetic origins for non-AV nodal circuits are commonly seen in younger patients with reentrant arrhythmias. Glycogen-storage diseases, adenosine monophosphate-activated protein kinase mutations, and lysosomal membrane protein mutations have been associated with the formation of the reentrant circuits.[19][20]

Atrial fibrillation is the most common sustained cardiac arrhythmia, and multiple cardiac and non-cardiac causes and triggers of atrial fibrillation have been reported in the literature. The most common cardiac triggers of atrial fibrillation include mitral valve diseases, heart failure, myocardial infarction/ischemia, intracardiac shunts, and hypertension. Advanced age is one of the major causes of atrial fibrillation in people with structurally normal hearts.[21] All the conditions result in electrical remodeling of the left atrium, which sustains atrial fibrillation.[22] Multiple genetic mutations have been identified, which lead to atrial fibrosis and the development of atrial fibrillation.[23][24]

The reentry ventricular arrhythmias are caused by structural heart diseases and scars in the myocardium. Ischemic cardiomyopathy is the main etiology of reentrant ventricular tachycardia, followed by non-ischemic, dilated cardiomyopathy.[25] The bundle branch reentrant ventricular tachycardia is a rare ventricular tachycardia characterized by a reentry circuit involving both bundle branches. Bundle branch reentrant arrhythmia is usually seen in patients with cardiomyopathies and structural heart diseases having significant conduction system disease, although patients with structurally normal hearts have been described in the literature.[26][27]


Arrhythmias with pre-excitation origins are estimated to occur in 1 to 3 per 1000 people in the United States, and 60% to 70% of patients discovered to have evidence of pre-excitation, generally detected on routine electrocardiograms, have no other heart disease.[28][29] WPW has an incidence of 15 cases per 10,000 patients. WPW is more prevalent in males than in females. The most common location of the accessory pathway in WPW is the left free wall (53%).[30] Other locations where the accessory pathway is seen include the posteroseptal wall (36%), the right free wall (8%), and the anteroseptal wall (3%).[31]

AVNRT is the most common paroxysmal supraventricular tachycardia. Approximately 89,000 new cases of SVT are discovered each year, with roughly half a million people in the United States currently living with SVTs. AVNRT is more common in females, and this difference is due to the female hormones and autonomic tone.[32]

The global burden of atrial fibrillation has increased exponentially over the last five decades due to population aging.[33] In the United States, around six million people have atrial fibrillation, and it is projected to reach 16 million in 2050.[34] In Europe, the prevalence of atrial fibrillation in a population older than 55 years is estimated to reach 14 million in 2060, while more than 70 million Asian population is projected to have atrial fibrillation at the end of 2050.[35][36] Atrial flutter is less common than atrial fibrillation and is usually associated with structural heart diseases. Its incidence is around 200,000 new cases per year in the United States.[37] Scar-related ventricular tachycardia is the most common reentrant ventricular tachycardia. Sustained ventricular tachycardia is a major cause of sudden cardiac death, and the annual incidence of sudden cardiac death in the United States is around 70 per 100,000 in the general population.[38]


The pathophysiology of reentrant tachycardia depends on the origin and location of the reentrant circuit. A similarity that all reentrant arrhythmias possess is the formation of a circuit that allows for constant re-excitation of the myocardium. This constant re-excitation of the myocardium can manifest in dangerous arrhythmias, syncope, or even sudden death. Reentry has a characteristic mechanism by which tachyarrhythmias are started and sustained. Reentries can be divided into three main types; circus-type reentry, reflection, and phase II reentry.[39]

Circus Type Reentry

This is the basic model of reentry, characterized by circus movement of an impulse around an anatomic or functional obstacle. The ring model of reentry was described by Mayers at the start of the 20th century. In 1913, G.R.Mines proposed the three basic requirements of a circus-type reentry, which included; 1) a unidirectional block, 2) circus movement that allows the excitatory wave to progress along a distinct pathway, return to its origin and recirculate again, and 3) Any interruption in the circuit should result in termination of the reentry.[40] This type of reentry could only happen when the impulse is slow enough in the alternate pathway to allow the tissues proximal to the site of the unidirectional block to recover from the refractory period. Thus, the slow and short propagation wavefront is required to provide that excitatory gap for successful reentry. Circus-type reentry can also occur in the absence of an anatomic obstacle. Multiple models and theories have been proposed for circus-type reentry around a functional obstacle.[41][42]


Reflection is an example of reentry without circus movement. The basic concept of reflection first came after studying the electrical characteristics of potassium-depolarized Purkinje fibers in the 1970s.[43] Reflection is characterized by the to-and-fro (electrotonically-mediated) transmission of the impulse across the inexcitable segment of a myocardium or a cardiac conduction system. The reflection type reentry has been demonstrated in laboratories in the isolated atrial and ventricular myocardium as well as Purkinje fibers.[44][45]

Phase II Reentry 

It is the third mechanism of reentry, does not depend on circus movement, and has been found to have a focal origin in the ventricular myocardium. Phase 2 reentry occurs due to heterogeneity in the action potential in epicardial and endocardial myocytes.[46] It is characterized by the propagation of the dome of the action potential from epicardium to other sites where it does not exist (those sites have recovered). This movement of the action potential dome re-excites the local myocardium and generates extrasystole. These closely coupled extrasystoles precipitate ventricular arrhythmias. Phase II reentry is the primary mechanism of ventricular arrhythmias in Brugada syndrome.[47]

Typical atrioventricular nodal reentrant tachycardia (AVNRT) is a prototype of reentrant arrhythmias. It is characterized by two atrioventricular nodal pathways having different refractory periods (slow and fast pathways). When a premature atrial impulse comes, an antegrade impulse propagates via the slow pathway (the fast pathway is refractory). When the impulse reaches the lower end of the slow pathway, the fast pathway has already recovered, so the retrograde impulse goes via the fast pathway. When this alternate movement of the cardiac impulse continues, it starts a reentrant tachycardia.[48]

History and Physical

Patients with supraventricular reentrant arrhythmias have a multitude of presentations. The common presentations of these arrhythmias include palpitations, shortness of breath, or chest pain; however, the patients may remain asymptomatic until a complication is developed, e.g., atrial fibrillation. If asymptomatic, the diagnosis is likely found on a routine electrocardiogram (ECG) or a rhythm strip while being worked up for another complaint. Other symptoms commonly seen in these patients are nervousness, anxiety, neck pounding, lightheadedness, and even syncopal episodes.[49] Syncope is a rare presentation in supraventricular tachycardia, but it should not be ignored, especially in patients with Wolf-Parkinson-White (WPW) syndrome.

Ventricular reentrant arrhythmias are potentially life-threatening, and the patients may present with palpitations, chest pain, shortness of breath, syncope, or even cardiac arrest.[50] Patients with ventricular tachycardia are generally older than those with supraventricular tachycardia, and shortness of breath, chest pain, and dizziness are more common presentations than palpitations in these patients.[51]

An accurate past medical and surgical history is paramount when working up a patient with suspected reentrant arrhythmia. Since these arrhythmias can be iatrogenic, any cardiac surgery would be an important history to gather from the patient. One should also derive information on medications, illicit drug use, and past medical history that need to be obtained to consider other differentials.[52]

In symptomatic patients, the first thing that needs to be evaluated is the patient’s hemodynamic stability. A proper physical exam is required to work up possible differentials and rule out triggering conditions that would elicit another condition mimicking signs of this arrhythmia. Many patients who truly have a reentrant supraventricular arrhythmia will have a completely normal exam.[53] While patients with reentrant ventricular arrhythmia may have signs of underlying structural heart disease as well as heart failure.


The diagnosis of reentrant supraventricular tachycardia s usually made in the emergency department based on electrocardiographic features; however, certain points in history may indicate the possible diagnosis. The first step in evaluation for a patient with a reentrant arrhythmia is to obtain a 12-lead electrocardiogram (ECG) during tachycardia (if possible) and compare it with an ECG in sinus rhythm.[54] The pattern and morphology of the P waves and QRS complexes can tell an experienced reader where the arrhythmia originates and where the reentrant circuit is. In the absence of a tachycardia ECG, the  12-lead ECG in sinus rhythm may give clues to the possible mechanism of tachycardia, e.g., the delta wave found in WPW syndrome suggests atrioventricular reciprocating tachycardia is the likely diagnosis. The delta wave is the slurring of the initial QRS complex, which occurs due to the ventricles' pre-excitation from the accessory pathway.[55] 

An ambulatory ECG monitoring may be considered in symptomatic patients when resting ECG is normal, and there is no electrocardiographic evidence of arrhythmia. The contemporary guidelines recommend echocardiograms in patients with atrial fibrillation and atrial flutter to assess the underlying cardiac structure and function. Thyroid function tests and other targeted investigations are also recommended in selected patients.[31]

The diagnosis of reentrant ventricular tachycardia is made on a 12-lead ECG. A 12-lead ECG in sinus rhythm should be compared with ECG during tachycardia. A 12-lead ECG sinus rhythm should be evaluated for myocardial ischemia or infarction. For patients with exercise-related symptoms, an exercise ECG is recommended to document exercise-induced ventricular arrhythmias. For symptomatic patients with undocumented ventricular arrhythmia, an ambulatory ECG is recommended to assess the correlation of symptoms with arrhythmia. While those patients with infrequent symptoms, implantable cardiac monitors may help in the diagnosis. [56] All patients presenting with ventricular arrhythmias should have an echocardiogram to assess cardiac structure and function, while cardiac magnetic resonance imaging is recommended in a selected group of patients to diagnose the underlying cause of ventricular arrhythmias. Cardiac magnetic resonance imaging also provides information about the prognosis of patients with reentrant ventricular tachycardia.[57] An invasive electrophysiology study is no longer recommended to diagnose reentrant ventricular arrhythmias; however, it can be used for risk stratification of patients who do not meet the criteria of primary prevention implantable cardioverter defibrillator.[58]

Treatment / Management

There are various modes of management for a patient with a reentrant arrhythmia. Assessment of the patient's hemodynamic status is the first step of management, which determines the mode of treatment. For all patients with hemodynamically unstable reentrant tachycardia, electrical cardioversion is the first choice of management, irrespective of the origin of the arrhythmia. Advanced cardiac life support should be initiated immediately if the patient presents with cardiac arrest.[59] 

Vagal maneuvers are recommended as the first choice treatment for hemodynamically stable patients with reentrant supraventricular tachycardia (SVTs). The recommended vagal maneuvers are the Valsalva maneuver and carotid artery massage. The Valsalva maneuver is performed by instructing the patient to forcefully exhale against a closed glottis. An alternate technique is performed by exhaling against a closed glottis followed by a passive leg raise at a 45-degree angle.[60] The carotid sinus massage is performed by applying pressure to the carotid sinus, which is located inferior to the angle of the mandible at the level of the thyroid cartilage. Intravenous adenosine is recommended as an acute treatment when SVT does not respond to vagal maneuvers. Non-dihydropyridine calcium channel-blocking drugs and beta blockers can be used to manage SVT when adenosine does not work.[54](A1)

Adenosine is a good treatment option in a patient where the AV node is the origin of arrhythmia; however, it can be catastrophic in a patient with a circuit formed by an accessory pathway. If adenosine is given to a patient with Wolff-Parkinson-White syndrome, the AV node will be blocked by the medications. However, the accessory pathway will remain uninhibited, which can lead to ventricular fibrillation and possible cardiac arrest.[61][62] In conclusion, adenosine is a great treatment modality for patients with AVNRT, but clinicians should be cautious in its use with patients who have WPW, making imperative the need for accurate diagnostic measures prior to treatment.(B3)

After initial management, all patients with AVNRT and AVRT should be referred to an electrophysiologist for catheter ablation. Catheter ablation for AVNRT/AVRT is a very safe procedure in the contemporary era, and it has a very high success and very low recurrence. In AVNRT, the cure rate is above 95%, with complications below 1%. In WPW, the success rate is above 90%, with a complication rate of less than 5%.[63][64]

The acute treatment of hemodynamically stable patients with a reentrant ventricular arrhythmia includes intravenous procainamide, amiodarone, or sotalol, while electrical cardioversion is recommended for hemodynamically unstable patients. Beta-blockers and long-term antiarrhythmic drugs can be considered in patients with recurrent arrhythmias.[56] All patients with reentrant ventricular arrhythmias should be evaluated for the indications of implantable cardioverter-defibrillator (ICD). If patients fulfill the criteria for primary or secondary prevention ICD, they should have an ICD implanted as soon as possible.[56][65](A1)

Differential Diagnosis

Differential diagnoses for reentrant arrhythmias include other tachyarrhythmias. Most reentrant circuits are located above the ventricles; consequently, other supraventricular tachycardias can be confused with reentrant arrhythmias. A 12-lead EKG should be obtained during the tachycardia as well as in sinus rhythm to differentiate these arrhythmias from one another.[66][67]

Differentials include:

  • Sinus tachycardia
  • Atrial tachycardia
  • Ectopic junctional tachycardia
  • Torsades de pointes
  • Accelerated atrioventricular rhythm
  • Idiopathic ventricular tachycardia


The prognosis of reentrant arrhythmias depends on the origin of the arrhythmia. Atrial fibrillation and atrial flutter are associated with a long-term risk of thromboembolism (stroke), even in the absence of other structural heart defects. Low-risk patients have less than one percent annual risk of stroke, while the high-risk group of patients has as high as 7 to 10% annual risk of stroke if not anticoagulated properly.[68] 

Atrioventricular nodal reentrant tachycardia has an excellent prognosis, and 9=more than 95% of people remain free of arrhythmias after successful ablation and modification of the slow atrioventricular nodal pathway.[69] Wolf-Parkinson-White syndrome has a less than 0ne percent lifetime risk of sudden cardiac death without treatment; however, radiofrequency ablation eliminates the risk of sudden cardiac death, and it has a high success and low recurrence rate.[70]

Reentrant ventricular arrhythmias are usually found in patients with cardiomyopathy and do not have a good prognosis. Ventricular arrhythmias in patients with cardiomyopathy lead to decompensated heart failure, recurrent hospitalization, impairs quality of life due to hospitalization and repeat implantable cardioverter-defibrillator shock and even result in sudden cardiac death,[71] Ablation of ventricular tachycardia (VT) has been reported to reduce the recurrence of VT and ICD shocks, it doe not improves survival of these patients.[72][73]


Complications in reentrant arrhythmias vary depending on the origin and anatomic location of the arrhythmia. As with any uncontrolled heart rate, reentrant arrhythmias can lead to cardiac remodeling, hemodynamic compromise, and, eventually, heart failure.[74]If the reentrant circuit is formed due to an accessory pathway, such as in Wolff-Parkinson-White syndrome, the patient can have rapid conduction of atrial fibrillation, which may result in ventricular fibrillation and even sudden cardiac death.[12] Although atrioventricular nodal reentrant tachycardia is a benign condition, it may lead to syncope, angina, and heart failure, especially in older individuals.[75]

Atrial fibrillation and atrial flutter are associated with a risk of thromboembolic complications and heart failure.[76][77] While the reentrant ventricular arrhythmias are associated with decompensated heart failure, repeat hospitalization, and recurrent ICD shocks. Repeat hospitalization due to ICD shock and decompensated heart failure impairs the quality of life and reduces the survival of these patients.[78][76]

Many complications can occur from cardiac ablation. The most common complication is bleeding from the site of insertion. Mechanical trauma to the heart valves, vessels, and chambers may lead to pericardial effusion and even cardiac tamponade. A rare but worrisome complication is the iatrogenic creation of another arrhythmia, which potentially could make the patient unstable. The ablation of AVNRT and AVRT may result in an atrioventricular block, and the patient may require a pacemaker.[79]

Deterrence and Patient Education

Patients should be taught that reentrant arrhythmias are caused by a problem with the heart’s conduction mechanism, which coordinates the beating of the heart. They should be informed of the mechanism of the disease, i.e., that the problem occurs when a circuit is formed, causing the conduction system to re-excite itself continuously. Typical symptoms include anxiety, lightheadedness, palpitations, and losing consciousness. Patients need to be taught to watch for worrisome symptoms such as more than a brief time period of headaches, palpitations, and presyncope symptoms. They should be advised to seek medical attention promptly, especially those with prior myocardial infarction,  treated with ablation, and those with recurrent symptoms.

Enhancing Healthcare Team Outcomes

An interprofessional team approach with good communication and established roles is crucial for optimal patient care in a patient with an unstable arrhythmia. This interprofessional team includes clinicians, nursing staff, and pharmacists. Depending on the type of reentrant arrhythmia and the management approach chosen, various interprofessional team members will contribute from their specialty (e.g., pharmacists if medication is chosen, nurses will also participate in medical management, or if surgery or ablation is the choice, nursing will assist throughout the process, including post-procedural monitoring. Open communication channels are essential to optimal outcomes.

Healthcare professionals trained and oriented to the hospital’s specific policies are essential for any rapid response or code blue situation. One study at a Vancouver General Hospital showed that nurses felt the team performed better after training and with assigned team roles. Prior to training, many nurses noted that it was unclear who the team leader was and who had which roles. Establishing proper roles for healthcare professionals on an interprofessional team is extremely important in unstable patients with advanced conditions such as reentrant arrhythmias.[80]



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