7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Official reprint from UpToDate www.uptodate.com 2023 UpToDate, Inc. and/or its affiliates. All Rights Reserved. Reentry and the development of cardiac arrhythmias : Philip J Podrid, MD, FACC : Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC : Susan B Yeon, MD, JD, FACC All topics are updated as new evidence becomes available and our peer review process is complete. Literature review current through: Jun 2023. This topic last updated: Feb 03, 2023. INTRODUCTION Cardiac arrhythmias are generally produced by one of three mechanisms: enhanced automaticity, triggered activity, or reentry. Reentry, due to a circuit within the myocardium, occurs when a propagating impulse fails to die out after normal activation of the heart and persists as a result of continuous activity around the circuit to re-excite the heart after the refractory period has ended; it is the electrophysiologic mechanism responsible for the majority of clinically important arrhythmias. Included among these arrhythmias are atrial fibrillation (where there are multiple small circuits in the left and right atria), atrial flutter (where there is a single circuit in the right atrium), atrioventricular (AV) nodal reentry (where the circuit is in the AV node as a result of dual AV nodal pathways), AV reentry (which involves a bypass tract and the normal AV node His-Purkinje system), ventricular tachycardia (with a circuit in the ventricular myocardium after myocardial infarction [MI] with the presence of left ventricular scar or in the presence of a cardiomyopathy due to fibrosis or infiltration), and ventricular fibrillation. The first demonstration of reentry in its simplest form (ie, the ring model) probably occurred in 1906 following the application of a stimulus to tissue from a jellyfish which initiated rhythmic contraction [1]. However, reentry was first conceived as a mechanism for arrhythmias in 1913 when it was recognized that reentrant tachycardias arise from circular electrical pathways, often initiated by a blocked impulse [2]. It was subsequently realized that reentry tachycardias may also be due to other mechanisms, including functional or leading circle circuits and abnormal electrical circuits caused by diseased myocardium. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 1/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate The definition and characteristics of the different reentry circuits responsible for the most clinically significant arrhythmias are presented here, along with the electrophysiologic properties of these arrhythmias. The clinical presentation and management of the individual arrhythmias are discussed separately. (See "Overview of atrial flutter" and "Atrioventricular nodal reentrant tachycardia" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway" and "Sustained monomorphic ventricular tachycardia in patients with structural heart disease: Treatment and prognosis" and "Atrial fibrillation: Overview and management of new-onset atrial fibrillation".) DEFINITION AND CHARACTERISTICS Reentrant tachycardia (variously named reentrant excitation, reciprocating tachycardia, circus movement, and reciprocal or echo beats) is defined as a continuous repetitive propagation of an excitatory wave traveling in a circular path (reentrant circuit), returning to its site of origin to reactivate that site [1]. The one event crucial to the development of a reentrant tachycardia is the failure of a group of fibers to activate during a depolarization wave. The initiation of a reentrant arrhythmia also requires the presence of myocardial tissue with the following electrophysiologic properties ( figure 1) [3-6]: Adjacent tissue or pathways must have different electrophysiologic properties (conduction and refractoriness) and be joined proximally and distally, forming a circuit. These circuits may be fixed or stationary or may move within the myocardial substrate (as occurs with spiral waves). Each involved pathway of the circuit must be capable of conducting an impulse in an antegrade and retrograde direction. Transient or permanent unidirectional block of one pathway must exist as a result of heterogeneity of electrophysiologic properties of the myocardium. This event usually results when one electrical pathway has either a prolonged refractory period or a prolonged repolarization time, producing a wave which only travels down the remaining pathway. Conduction velocity in the normal unblocked pathway must be slow enough relative to the refractoriness of the blocked pathway to allow recovery of the previously blocked pathway. The impulse can then be conducted through the previously blocked but recovered pathway in a retrograde direction. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 2/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Retrograde conduction in this previously blocked pathway must be slow enough to allow the normal pathway to recover, and again be capable of being excited. A sustained reentrant arrhythmia will occur if these conditions are present and maintained. In general, the onset and offset of the arrhythmia are abrupt. In contrast, when enhanced automaticity is the mechanism for the arrhythmia, there are often warm-up and cool-down phases (gradual increase and gradual decrease in the rate of the arrhythmia). Patients who develop reentrant arrhythmias usually have an anatomic or electrical (functional) abnormality, which could be caused by an accessory pathway, by an abnormal separation of adjacent fibers that may form two limbs of a reentrant circuit, or by juxtaposed fibers that possess different electrophysiologic characteristics, often resulting from abnormalities of the myocardium and Purkinje fibers as the result of a disease process. Susceptible patients with appropriate underlying abnormalities usually do not suffer from incessant tachycardia because the different electrophysiologic mechanisms required for the initiation and maintenance of a reentrant tachycardia are infrequently present at exactly the same time. However, changes in heart rate or autonomic tone, ischemia, electrolyte or pH abnormalities, or the occurrence of a premature beat (which results in transient changes in the electrophysiologic properties of the myocardium) may be sufficient to initiate a reentrant tachycardia. In fact, premature depolarizations frequently initiate these tachyarrhythmias when there are appropriate electrophysiologic conditions (ie, slow conduction and unidirectional block). They are associated with more rapid depolarization (as they are early or premature) that may block in one pathway (ie, unidirectional block), conduct through the second pathway, retrogradely enter the first pathway, and then reenter the second pathway. CRITERIA FOR DIAGNOSIS The initial criteria for the diagnosis of reentry proposed in the early 20th century are still valid, but are often difficult to prove [1]. As a result, the following twelve conditions in the electrophysiology laboratory were proposed to either prove or to identify the existence of a reentrant tachycardia [7]: Activation of the myocardium mapped in one direction around a continuous loop. Correlation of continuous electrical activity occurring when the tachycardia develops. Correlation of unidirectional block with initiation of reentry. Initiation and termination by premature stimulation. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 3/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Dependence of initiation of the arrhythmia on the site of pacing. Inverse relationship between the coupling interval of the initiating premature beat and the interval to the first tachycardia beat. Resetting of the tachycardia by a premature beat with an inverse relationship between the coupling interval of the premature beat and the cycle length of the first or return beat of the tachycardia. Fusion between a premature beat and the tachycardia beat followed by resetting. Transient entrainment (with external overdrive pacing, the ability to enter the reentrant circuit and "capture" the circuit, resulting in a tachycardia at the pacing rate and having fused or paced complexes). Abrupt termination by premature stimulation or the termination of entrainment. Dependence of initiation on a critical slowing of conduction in the circuit. Similarity with experimental models in which reentry is proven and is the only mechanism of tachycardia. The segment of the reentrant circuit that is, at any given time, no longer refractory and is capable of being excited is called the excitable gap [6,8]. Slowing of impulse conduction or shortening of refractoriness will increase the excitable gap. The longer the excitable gap, the more likely it is for an extrastimulus to enter the reentrant circuit and initiate or terminate a reentrant arrhythmia. In addition, entrainment is more likely to occur when the excitable gap is longer. TYPES OF REENTRY Reentry tachycardias have been divided into two different forms based upon the type of anatomic substrate used for the development of the arrhythmia: anatomic or functional. The original ring model requires the presence of an anatomic obstruction (due to a structural abnormality). There are also several models of functional reentry (due to electrophysiologic abnormalities) including the leading circle, anisotropic conduction, figure of eight, and spiral wave ( figure 1 and figure 2). Anatomic reentry Anatomic reentrant tachycardia most closely resembles the original description of reentry arrhythmia because it requires an anatomic obstacle, such as an area of fibrosis [1]. This discrete anatomic block creates a surrounding circular pathway, resulting in a https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 4/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate fixed length and location of the reentrant circuit. A tachycardia is initiated when a depolarization wave splits into two limbs after going around this obstacle, creating a circus movement [9,10]. Tachycardia rates are determined both by the wavelength (defined as conduction velocity and refractory period) and the length of the circuit or the pathlength. Examples of anatomic reentry are supraventricular tachycardia associated with an accessory pathway (preexcitation syndromes) called atrioventricular reentrant tachycardia (AVRT), AV nodal reentrant tachycardia (AVNRT; associated with dual AV nodal pathways), typical atrial flutter originating in the right atrium due to an area of fibrosis in the lower portion of the atrium (termed isthmus), atrial fibrillation resulting from multiple reentrant circuits in the atria, ventricular tachycardia (VT) originating within the His-Purkinje system (bundle branch tachycardia), and VT originating at the terminal portion of the His-Purkinje system or around an area of infarcted tissue (scar mediated). There is often a long excitable gap associated with anatomic reentry. Functional reentry Functional reentry depends upon the intrinsic heterogeneity of the electrophysiologic properties of cardiac muscle (ie, dispersion of excitability or refractoriness) as well as anisotropic differences in intercellular resistances. There is no anatomic obstacle present. Examples of functional reentry include atypical atrial flutter, some cases of atrial fibrillation (AF), and VT in a structurally normal heart. Functional circuits have the following properties: They tend to be small, rapidly conducting, and unstable in that the waves they generate may fragment, establishing other areas of reentry. Circuit times and hence tachycardia rates are significantly dependent upon the refractory period of the involved tissue. The location and size of these tachycardias vary due to the absence of an anatomic block. There is usually a short excitable gap associated with functional reentry. One animal study reported the following additional properties [11]: A thin layer of activation near the core or central region of the circuit is responsible for the maintenance of reentry; the remaining portion of the tissue is activated passively by the outward propagation of wavefronts away from the core. Access to the tissue near the core is essential for termination of reentry by a point stimulation. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 5/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate To terminate reentry with a stimulus applied away from the core, the stimulus must occur at certain critical coupling intervals and the line connecting the stimulus and the core must be roughly parallel to the fiber orientation. Leading circle concept In this model, functional reentry involves the propagation of an impulse around a functionally determined region of unexcitable tissue or a refractory core and among neighboring fibers with different electrophysiologic properties [4-6]. The excitation wave then travels in the smallest possible circuit with the head of the impulse having just enough strength to excite relatively refractory tissue ahead of it. Thus, the "head of the circulating wavefront is continuously biting its tail of refractoriness" ( figure 1) [6]. There is a small excitable gap in this setting. The circulating wave activates peripheral tissue but also gives rise to wavelets that collide at the center, rendering it refractory. Anisotropic reentry Anisotropic reentry is determined by the orientation of myocardial fibers and the manner in which these fibers and muscle bundles are connected to each other [12,13]. In general, the electrical resistances between cells is dependent upon fiber orientation (ie, cell- to-cell communication is more rapid between cell that are parallel to each other), while communication is slower when cells are transverse to each other [14,15]. Anisotropic reentry occurs in myocardium composed of tissue with structural features different from those of adjacent tissue, resulting in variations in conduction velocities and repolarization properties (referred to as anisotropic myocardium) ( figure 2) [16]. As an example, an impulse propagating parallel to the long axis of the myocardial tissue will typically travel three to five times faster than the same impulse traveling in the transverse direction. Therefore, anatomic anisotropy can cause heterogeneity of electrophysiologic properties which can result in blocked impulses and slowed conduction, thereby setting the stage for reentry [17]. Figure of eight reentry This model of reentry involves two counter rotating circuits around a center that is anatomically damaged, but is common to both circuits [18]. The reentrant beat produces a wavefront that circulates in both directions around a long line of functional conduction block and rejoins on the distal side of the block. This results in two concomitant circuits, forming a "figure of eight." Spiral wave (rotor) activity In this model of reentry, there are concentric circular waves that result in reverberators or rotating vortices of electrical activity [19-21]. Spiral waves, which typically describe reentry in two dimensions, can be initiated in an inhomogeneous, excitable medium whenever there is disruption of the wavefront. Spiral waves rotate around an organizing center or core, which includes cells with a transmembrane potential that has a reduced amplitude, duration and rate of depolarization (ie, slow upstroke velocity of phase 0); https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 6/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate these cells are potentially excitable, but remain unexcited [22]. Anisotropy and anatomic obstacles can modify the characteristics and spatiotemporal behavior of the spiral. In addition, the spiral waves may give rise to daughter spirals which can result in disorganized electrical activity; this may be the mechanism for ventricular fibrillation [23]. Spirals may be stationary (the possible mechanism for monomorphic VT), or may continuously drift or migrate away from their origin (possibly the mechanism for polymorphic VT or AF), or may be anchored, initially drifting and then becoming stationary by anchoring to a small obstacle ( waveform 1) [24]. Phase two reentry Phase 2 reentry is a phenomenon largely related to Brugada syndrome and is discussed separately. (See "Brugada syndrome: Epidemiology and pathogenesis", section on 'Ventricular arrhythmias and phase 2 reentry' and "Brugada syndrome: Clinical presentation, diagnosis, and evaluation".) CLINICAL ARRHYTHMIAS DUE TO REENTRY Reentry can cause many clinically significant arrhythmias including sinus node reentry, atrial flutter, atrial fibrillation (AF), AV nodal reentry (AVNRT), AV reentry using an accessory bypass tract (AVRT), and ventricular tachyarrhythmias ( figure 3). Sinus node reentry SA nodal reentrant tachycardia is due to a reentrant circuit that is in the area of the sinus node and involves this structure and the sinoatrial junction. Thus, electrophysiologic studies reveal atrial activation and conduction that is identical to sinus rhythm, with the earliest recorded atrial activation in the reentrant tachycardia being located near the sinus node [25]. As with any reentrant arrhythmia, SA nodal reentrant tachycardia is usually initiated by a premature atrial stimulus, but also rarely by a ventricular premature stimulus [26,27]. It is clinically and electrocardiographically difficult to distinguish this arrhythmia from sinus tachycardia. Both have identical P waves at a rate that is usually less than 150 beats/min. The abrupt onset and termination of the reentrant arrhythmia are the only clinical distinctions from sinus tachycardia, which results from enhanced sympathetic tone and has an onset and termination that are gradual and not abrupt ( waveform 2). (See "Sinoatrial nodal reentrant tachycardia (SANRT)".) Atrial flutter The reentrant circuit resulting in atrial flutter is typically localized within the right atrium. It results from a circuit that is due to an area of fibrosis and slow conduction (isthmus) that is located between the tricuspid annulus and area of the inferior vena caval https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 7/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate insertion. Details regarding the electrocardiographic and electrophysiologic features of atrial flutter are discussed separately. (See "Electrocardiographic and electrophysiologic features of atrial flutter".) Atrial fibrillation AF is currently felt to be caused by multiple leading circle reentrant impulses (ie, the multiple wavelet theory) ( figure 4) [28,29]. Coarse AF, which is usually seen when the AF is more recent in onset, is thought to be caused by a relatively small number of large sized waves, while fine fibrillation (when usually indicated AF that has been present for a longer period of time) is caused by many small, fragmented waves ( waveform 3A-B). It has been estimated that a minimum of six circuits is needed to sustain AF [29]. (See "The electrocardiogram in atrial fibrillation".) AV nodal reentry AVNRT, one of the most frequent paroxysmal supraventricular tachycardias, is caused by a reentrant circuit located within the AV node. It is the result of dual AV nodal pathways (which are linked proximally and distally within the AV node), both of which conduct in an antegrade and retrograde direction [30-35]. The slow or alpha pathway typically has a slower conduction velocity and shorter refractory period (faster recovery) than the faster conducting beta pathway, which has a faster conduction velocity but a longer refractory period. These two pathways are linked proximally and distally within the AV junction. AVNRTs have been divided into two types based upon their mechanism of conduction [36]. (See "Atrioventricular nodal reentrant tachycardia".) The common type, comprising approximately 90 percent of all AVNRTs, is usually initiated by a premature atrial complex (also referred to a premature atrial beat, premature supraventricular complex, or premature supraventricular beat) that reaches the AV node when the fast pathway is still refractory and hence travels down the slow pathway to activate the ventricles in an antegrade fashion. If the impulse reaches the distal end of the circuit when the fast pathway has recovered, it enters the fast pathway and is conducted in a retrograde direction to activate the atrial in a retrograde direction and simultaneously with ventricular activation. If the slow pathway has recovered by the time the impulse reaches the proximally portion of the circuit, the impulse may also reenter the slow pathway. If this situation repeats, an AV nodal reentrant tachycardia results. As ventricular activation is via the slow pathway and retrograde atrial activation is via the fast pathway, this is termed "slow-fast" ( figure 5 and figure 6). The uncommon type of AVNRT uses the fast pathway in an antegrade manner and the slow pathway in the retrograde manner (fast-slow) ( figure 7 and figure 8). This may be initiated by a premature ventricular complex/contraction (PVC; also referred to a premature https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 8/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate ventricular beats or premature ventricular depolarizations) that is blocked in the fast pathway and hence travels up to the atrial via the slow pathway and then down to the ventricles via the fast pathway (fast-slow). Atrioventricular reentry using an accessory bypass tract The presence of an accessory bypass tract, which has electrophysiologic properties that are different from those of the normal AV node-His Purkinje system and resemble the properties of Purkinje fibers, favors the development of reentrant tachycardia by providing two limbs of a possible reentrant circuit: one limb is the AV node and His-Purkinje system; and the other is the bypass tract which directly connects an atrium and a ventricle, bypassing the AV node [37,38]. The circuit, known as a macroreentrant circuit, is formed by a proximal connection via the atria and a distal connection within the ventricular myocardium. Accessory bypass tracts can be found along the perimeter of both the mitral and tricuspid valves or within the ventricular myocardium (bundle of Kent, which links the atrium directly to the ventricular myocardium), may connect the atrium directly to the distal AV node or His Purkinje system (bundle of James), and may also connect the AV node to either the right bundle or the ventricle, termed nodofascicular and nodoventricular tracts, respectively. (See "Anatomy, pathophysiology, and localization of accessory pathways in the preexcitation syndrome".) Accessory bypass tracts may conduct reentrant impulses either in a retrograde or antegrade direction. Orthodromic AVRT is defined by conduction of the depolarization impulse to the ventricles down the AV node and His-Purkinje system in an antegrade manner and its return via the accessory tract in a retrograde manner ( waveform 4 and figure 9). The QRS complex is narrow (although it may have a typical right or left bundle branch block pattern if there is rate- related aberration) as ventricular activation is via the normal conduction pathway. Antidromic AVRT is characterized by the reverse sequence in which the depolarization wave travels down the bypass tract in an antegrade direction to activate the ventricular myocardium and returns to the atria via the His-Purkinje system and AV node ( waveform 5 and figure 10). In this situation, the QRS complex is maximally preexcited and has a wide and strange morphology as a result of direct myocardial activation via the accessory pathway. The complex has the same morphology in every lead as the preexcited complex during sinus rhythm, although it may be wider as it is maximally preexcited. Since it is wide, with a strange morphology, it may look like VT. Orthodromic AVRT is most common, occurring in approximately 90 percent of symptomatic patients with accessory bypass tracts [39]; antidromic AVRT accounts for the remaining 10 percent [40]. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".) The conduction characteristics of bypass tracts can vary significantly not only among patients, but also between retrograde and antegrade directions within the same tract in a given patient https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 9/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate [41]. As an example, a single bypass tract may be involved in both orthodromic and antidromic AVRTs. Ventricular tachycardia and fibrillation Ventricular tachycardia (VT; monomorphic) and ventricular fibrillation (VF), the two most lethal arrhythmias, are both caused by reentry ( waveform 6 and waveform 7) [42]. Pathologic changes associated with ischemic heart disease (infarction resulting in fibrosis) or cardiomyopathy (myocardial infiltration and/or fibrosis) most often produce the cardiac substrate necessary for reentrant ventricular arrhythmias: areas of unidirectional block and sufficiently slow conduction. The reentrant circuits are small, involving the distal Purkinje fibers within normal and abnormal myocardial tissue, and this has been termed "microreentry." Monomorphic VT can be initiated by appropriately timed premature ventricular impulses or by burst pacing and can be terminated by cardioversion, overdrive pacing, or antiarrhythmic drugs. VF can be initiated by appropriately timed premature ventricular impulses but can be terminated only with defibrillation. Although sustained VTs with different QRS morphologies (polymorphic VT without QT prolongation of the sinus complex) occur spontaneously (most commonly due to active ischemia) or during electrophysiologic study after a myocardial infarction, they most commonly arise from reentrant circuits located in the region of the infarction [43]. Factors responsible for different exit routes from circuits in the same region, leading to multiple morphologies include: Different direction of rotation around the same circuit Small differences in the reentrant circuit Reentrant circuits with different sizes and shapes Differences in the refractoriness of the ventricular myocardium and hence its ability to conduct the impulse While sustained VT generally involves one reentrant circuit, or perhaps a single spiral, VF results from multiple circuits simultaneously activating the ventricular myocardium. In an animal model, the most likely underlying mechanism was rotating spiral waves [44]. With the development of global ischemia during VF, the rate of VF decreases due to an increase in the rotation period of the spiral waves that results from an increase in the core area. It has frequently been observed that VF is often preceded by a variable period of VT (monomorphic or polymorphic). The transition from a sustained organized VT to disorganized VF probably involves the breakup of a single propagating wave or spiral into multiple daughter wavelets or spirals, a result of heterogeneity of myocardial electrophysiologic properties (functional block) or anatomic obstacles. This is identical to the process seen with AF. These wavelets rarely reenter themselves but can re-excite portions of the myocardium recently https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 10/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate activated by another wavefront, a process called random reentry. As a result, there are multiple wavefronts of activation that may collide with each other, extinguishing themselves or creating new wavelets or spiral and wavefronts, thereby perpetuating the arrhythmia [45,46]. Spontaneous wave breaks without apparent collision may also occur during VF; in an experimental model, procainamide can reduce the incidence of these events, decreasing the number of wavelets [46]. Spontaneously occurring reentrant arrhythmias are infrequent in a healthy ventricle, because the substrate for reentry is lacking. However, these tachyarrhythmias can occur in a normal heart in the right clinical setting. As an example, bundle branch reentry can be initiated by an early coupled premature impulse; VT may then develop based upon the difference in the refractory periods either between the two bundles or between one of the bundles and ventricular muscle ( figure 11) [47]. (See "Bundle branch reentrant ventricular tachycardia".) VF can also be induced in a healthy heart if a properly timed, strong stimulus is applied to the ventricle. The critical moment occurs immediately after the refractory period, generally at the downstroke of the T wave just after its peak, a period of time termed the vulnerable period, when a heterogeneous state of excitability and refractoriness exists [48]. A strong stimulus applied during the vulnerable period is postulated to set up a number of functional reentrant circuits. The amount of energy that provokes VF is termed the VF threshold. The VF threshold in a normal, nonischemic heart is high, while the VF threshold is low in the presence of active ischemia. In this situation, a premature ventricular complex or a pacing stimulus occurring at the downstroke of the T wave (R on T phenomenon) may have sufficient energy to provoke VF. SUMMARY Cardiac arrhythmias are generally produced by one of three mechanisms: enhanced automaticity, triggered activity, or reentry. Reentry, which occurs when a propagating impulse fails to die out after normal activation of the heart and persists to re-excite the heart after the refractory period has ended, is the electrophysiologic mechanism responsible for the majority of clinically important arrhythmias. (See 'Introduction' above.) While the one event which is crucial to the development of a reentrant tachycardia is the failure of a group of fibers to activate during a depolarization wave, the initiation of a reentrant arrhythmia also requires various electrophysiologic properties (eg, ability to conduct antegrade and retrograde, presence of unidirectional block, etc) to be present concurrently within the myocardial tissue making up the circuit. Changes in heart rate or autonomic tone, ischemia, electrolyte or pH abnormalities, or the occurrence of a https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 11/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate premature beat (which results in transient changes in the electrophysiologic properties of the myocardium) may be sufficient to initiate a reentrant tachycardia. (See 'Definition and characteristics' above.) Twelve conditions which may be seen during invasive electrophysiology study in the electrophysiology laboratory have been proposed to either prove or to identify the existence of a reentrant tachycardia. (See 'Criteria for diagnosis' above.) Reentry tachycardias have been divided into two different forms based upon the type of anatomic substrate used for the development of the arrhythmia: anatomic or functional. Anatomic reentrant tachycardia requires a discrete anatomic obstacle, such as an area of fibrosis, resulting in a fixed length and location of the reentrant circuit. Examples of anatomic reentry are supraventricular tachycardia associated with an accessory pathway (preexcitation syndromes), AV nodal reentrant tachycardia, atrial flutter, ventricular tachycardia originating within the His-Purkinje system (bundle branch tachycardia), and ventricular tachycardia originating at the terminal portion of the His- Purkinje system or around an area of infarcted tissue. (See 'Anatomic reentry' above.) Functional reentry depends upon the intrinsic heterogeneity of the electrophysiologic properties of cardiac muscle (ie, dispersion of excitability or refractoriness) as well as anisotropic differences in intercellular resistances. There is no anatomic obstacle present. Examples of functional reentry include type II (atypical) atrial flutter and atrial tachycardia. 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