Reentry and The Development of Cardiac Arrhythmias: Author: Section Editor: Deputy Editor

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Reentry and the development of cardiac arrhythmias

Author: Philip J Podrid, MD, FACC
Section Editor: Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC
Deputy Editor: Brian C Downey, MD, FACC
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature rev iew current through: Mar 2020. | This topic last updated: Mar 09, 2020.
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, atrial flutter, atrioventricular (AV) nodal reentry, AV reentry involving a
bypass tract, ventricular tachycardia after myocardial infarction (MI) with the presence of left ventricular
scar, 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.
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 "New onset atrial fibrillation" and "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".)
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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, 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.
● 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
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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.
● 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,
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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 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), 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.
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● 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.
● 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."
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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); 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", section on 'Sudden cardiac arrest and syncope'.)
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
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between the tricuspid annulus and area of the inferior vena caval 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, 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 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
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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), 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 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 is the
same as the preexcited complex during sinus rhythm, although it may be wider as it is maximally
preexcited. 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 [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]. Ischemia, infarction, and the resulting 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) occur spontaneously or
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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. 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 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.
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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 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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26. Narula OS. Sinus node re-entry: a mechanism for supraventricular tachycardia. Circulation 1974;
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50:1114.
27. Wu D, Amat-y-leon F, Denes P, et al. Demonstration of sustained sinus and atrial re-entry as a
mechanism of paroxysmal supraventricular tachycardia. Circulation 1975; 51:234.
28. Moe, GK . On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacol Dyn Ther
1962; 140:183.
29. Allessie MA, Lammers WJEP, Bonke FIM, et al. Experimental evaluation of Moe's multiple wavelet
hypothesis of atrial fibrillation. In: Cardiac Arrhythmias, Zipes DP, Jalife J (Eds), Grune & Stratton,
New York 1985. p.265.
30. Denes P, Wu D, Amat-y-Leon F, et al. The determinants of atrioventricular nodal re-entrance with
premature atrial stimulation in patients with dual A-V nodal pathways. Circulation 1977; 56:253.
31. Denes P, Wu D, Dhingra R, et al. Dual atrioventricular nodal pathways. A common

electrophysiological response. Br Heart J 1975; 37:1069.
32. Denes P, Wu D, Dhingra RC, et al. Demonstration of dual A-V nodal pathways in patients with
paroxysmal supraventricular tachycardia. Circulation 1973; 48:549.
33. Rosen KM, Mehta A, Miller RA. Demonstration of dual atrioventricular nodal pathways in man. Am
J Cardiol 1974; 33:291.
34. Sung RJ, Waxman HL, Saksena S, Juma Z. Sequence of retrograde atrial activation in patients
with dual atrioventricular nodal pathways. Circulation 1981; 64:1059.
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1975; 2:459.
36. Sung RJ, Styperek JL, Myerburg RJ, Castellanos A. Initiation of two distinct forms of
atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man.
Am J Cardiol 1978; 42:404.
37. Gallagher JJ, Sealy WC, Kasell J, Wallace AG. Multiple accessory pathways in patients with the
pre-excitation syndrome. Circulation 1976; 54:571.
38. Wellens HJJ, Brugada P. Value of programmed stimulation of the heart in patients with the Wolff-
Parkinson-White syndrome. In: Tachycardias: Mechanisms, Diagnosis, Treatment, Josephson M
E, Wellens HJJ (Eds), Lea & Febiger, Philadelphia 1984. p.1991.
39. Newman BJ, Donoso E, Friedberg CK. Arrhythmias in the Wolff-Parkinson-White syndrome. Prog
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40. Bardy GH, Packer DL, German LD, Gallagher JJ. Preexcited reciprocating tachycardia in patients
with Wolff-Parkinson-White syndrome: incidence and mechanisms. Circulation 1984; 70:377.
41. Wellens HJJ. Electrophysiologic properties of the accessory pathway in Wolff-Parkinson-White sy

ndrome. In: Conduction System of the Heart: Structure, Function, and Clinical Implication, Wellen
s HJJ, Lie KI, Janse MJ (Eds), Stenfert Krose BV, Leiden 1976. p.567.
42. Josephson ME, Marchlinski FE, Buxton AE, et al. Electrophysiologic basis for sustained ventricula
r tachycardia: The role of reentry. In: Tachycardias: Mechanisms, Diagnosis, Treatment, Josephso
n ME, Wellens HJJ (Eds), & Febiger, Philadelphia 1984. p.305.
43. Costeas C, Peters NS, Waldecker B, et al. Mechanisms causing sustained ventricular
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44. Mandapati R, Asano Y, Baxter WT, et al. Quantification of effects of global ischemia on dynamics
of ventricular fibrillation in isolated rabbit heart. Circulation 1998; 98:1688.
45. Lee JJ, Kamjoo K, Hough D, et al. Reentrant wave fronts in Wiggers' stage II ventricular
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46. Kwan YY, Fan W, Hough D, et al. Effects of procainamide on wave-front dynamics during
ventricular fibrillation in open-chest dogs. Circulation 1998; 97:1828.
47. Akhtar M, Gilbert C, Wolf FG, Schmidt DH. Reentry within the His-Purkinje system. Elucidation of
reentrant circuit using right bundle branch and His bundle recordings. Circulation 1978; 58:295.
48. Wiggers, CJ, Wegria, R . Ventricular fibrillation due to single, localized induction and condenser
shocks applied during the vulnerable phase of ventricular systole. Am J Physiol 1940; 128:500.
Topic 954 Version 14.0
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GRAPHICS
Mechanisms of reentry in cardiac arrhythmias
S c hematic repres entation of pos s ible reentrant c irc uits . T he thic k

blac k arrow repres ents the c irc ulating impuls e; thin blac k lines
repres ent adv anc ing wav efronts in c ompletely refrac tory tis s ue;
s pec k led areas are partially refrac tory tis s ue; white areas are fully
ex c itable tis s ue.
A is the original model of c irc us mov ement around a fix ed obs tac le.
T here is a fully ex c itable gap, and the length and loc ation of the c irc uit
are fix ed.
B repres ents c irc us mov ement around 2 fix ed anatomic obs tac les . A
fully ex c itable gap is pres ent.
C repres ents rapidly c onduc ting bundles forming c los ed loops that
s erv e as preferential c irc uits through whic h the impuls e may trav el.
D is the leading c irc le ty pe of reentry whic h does not require an
anatomic obs tac le. I ns tead, the impuls e propagates around a
func tionally refrac tory c ore and among neighboring fibers that hav e
different elec trophy s iologic properties . S inc e the refrac torines s of the
c ore is v ariable, the c irc uit s ize c hanges but will be the s malles t
pos s ible c irc uit that c an c ontinue to propagate an impuls e. F unc tional
c irc uits tend to be s mall, rapid, and uns table.
E repres ents reentry around a fix ed anatomic obs tac le, but a fully
ex c itable gap is abs ent.
F demons trates an area of s lowed c onduc tion (hatc hed lines ) between
anatomic boundaries , while in
G all areas of s lowed c onduc tion neighbor an anatomic obs tac le.
H repres ents anis otropic reentry. T here are differenc es in the
c onduc tion of a s ingle impuls e in v arious fibers as a res ult of
differenc es in their orientation.
Courtesy of Philip J Podrid, MD, FACC.
Graphic 52134 Version 5.0
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Anisotropic reentry
P anel A is an ac tiv ation map of a s ingle reentrant c irc uit at the

epic ardial border zone of a my oc ardial infarc tion. T he large arrows
repres ent the general ac tiv ation pattern whic h oc c urs around a long
line of bloc k (blue arrow). P arallel is oc hrones 1 3 0 and 1 4 0 whic h are
adjac ent to the bloc k s ugges t that ac tiv ation is oc c urring ac ros s the
bloc k , res ulting in a s maller c irc uit (s haded area) s hown by the s mall
blac k arrow. P anel B is an enlarged repres entation of this s haded area;
the dark blac k rec tangle repres ents an area of bloc k around whic h
there is a reentrant c irc uit (s mall arrows ). R apid ac tiv ation oc c urs
parallel to the long ax is of the fiber orientation (is oc hrones 1 0 - 4 0 and
1 3 0 - 1 5 0 ), while in the trans v ers e direc tion ac tiv ation is s low
(bunc hed is oc hrones 5 0 - 1 2 0 ).
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Mechanism of torsades de pointes
T he top panels A - F are ex amples of epic ardial is oc hrone maps

obtained from the s urfac e of the anterior left v entric ular (L V ) wall and
free wall of the right v entric le (R V ) during an epis ode of quinidine-
induc ed tors ades de pointes . E ac h map c orres ponds to a Q R S
deflec tion of the s urfac e E C G and s imultaneous monophas ic ac tion
potential (M A P ). E arly afterpotentials (E A D s ) res ult in triggered
ac tiv ity (panels A - C ) whic h is followed by a long epis ode of s piral- lik e
reentry (panels D - F ). P anel C s hows the firs t reentrant wav e whic h is
not s tationary, but gradually s hifts upward and to the right. T his is
as s oc iated with a gradual dec reas e in the Q R S c omplex amplitude.
Reprinted with permission from the American College of Cardiology. Journal of the
American College of Cardiology, 1997; 29:831.
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Sites of reentry in supraventricular tachyarrhythmias
R eentry may oc c ur around a fix ed anatomic obs tac le or may be func tional,
dev eloping in the abs enc e of an anatomic obs tac le and res ulting from the
intrins ic heterogeneity of elec trophy s iologic properties of the my oc ardial
tis s ue. R eentrant c irc uits leading to a s uprav entric ular tac hy arrhy thmia may
dev elop in v arious parts of the heart: within and around the s inoatrial node
(s inus node reentry ); within the atrial my oc ardium (atrial tac hy c ardia, atrial
flutter, or atrial fibrillation); within the atriov entric ular (A V ) node due to the
pres enc e of a s low and fas t pathway (atriov entric ular nodal reentrant
tac hy c ardia); or inv olv ing the A V node and an ac c es s ory pathway (A P )
(atriov entric ular reentrant tac hy c ardia).
LAF: left anterior fascicle; LPF: left posterior fascicle.
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Single-lead electrocardiogram (ECG) showing

sinoatrial (SA) nodal reentrant tachycardia
E lec troc ardiogram s howing S A nodal reentrant tac hy c ardia. T he firs t

three beats are normal s inus beats at a rate of about 1 0 7 beats /min;
the fourth beat is an atrial premature beat that is followed by a return
to s inus rhy thm. T he eighth beat (arrow) repres ents the s udden ons et
of S A nodal reentrant tac hy c ardia at a rate of about 1 4 5 beats /min.
S inc e the P wav es are s imilar to the s inus beats , the diagnos is is
s ugges ted only by the abrupt ons et of the tac hy c ardia.
Courtesy of Morton F Arnsdorf, MD.
Normal rhythm strip
N ormal rhy thm s trip in lead I I . T he P R interv al is 0 .1 5 s ec and the

Q R S duration is 0 .0 8 s ec . B oth the P and T wav es are upright.
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Two types of reentry in atrial fibrillation
T he is oc hronal ac tiv ation maps demons trate two ty pes of reentry in

atrial fibrillation. M ap A s hows random reentry with three s imultaneous
wav efronts (blac k arrows ) ac tiv ating mos t of the rec ording area. M ap B
als o s hows three s imultaneous wav efronts , but they are c oming from
different direc tions than thos e in map A . M aps C and D s how two
c ons ec utiv e c y c les of c omplete reentry. T he wav e of ac tiv ation (blac k
arrow) s preads c loc k wis e in a c irc ular fas hion around a line of
unex c ited tis s ue.
Reproduced with permission from Holm M, Johansson R, Brandt J, et al. Eur Heart J
1997; 18:290.
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Single-lead electrocardiogram (ECG) showing atrial fibrillation
L ead V 1 s howing c oars e A F with moderate v entric ular res pons e. T he two
c harac teris tic findings in A F are pres ent: the v ery rapid atrial fibrillatory wav es (f
wav es ), whic h are v ariable in appearanc e; and the irregularly irregular v entric ular
res pons e as the R - R interv al between beats is unpredic table. C oars e A F may
appear s imilar to atrial flutter. H owev er, the v ariable height and duration of the f
wav es differentiate them from atrial flutter (F ) wav es , whic h are identic al in
appearanc e and oc c ur at a c ons tant rate of about 2 5 0 to 3 5 0 beats /min.
AF: atrial fibrillation.
Courtesy of Ary Goldberger, MD.
Normal rhythm strip

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Single-lead electrocardiogram (ECG) showing atrial

fibrillation with minimally apparent atrial activity
F wav es are not apparent in this lead, as the only finding s ugges tiv e of A F is the
irregularly irrregular v entric ular res pons e.
AF: atrial fibrillation.
Courtesy of Morton Arnsdorf, MD.
Normal rhythm strip

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Typical atrioventricular nodal reentrant tachycardia
T he firs t two c omplex es are normal s inus beats with a normal P wav e
followed by a Q R S c omplex . T he third c omplex , an atrial premature beat
(A P B ), has a prolonged P R interv al; it initiates a c ommon or ty pic al
atriov entric ular nodal reentrant tac hy c ardia (A V N R T ) in whic h antegrade
c onduc tion to the v entric le is v ia the s low pathway and retrograde atrial
ac tiv ation is by the fas t pathway. A lthough no dis tinc t P wav e is s een,
the Q R S c omplex has a s mall terminal deflec tion, k nown as a ps eudo r',
whic h is the P wav e s uperimpos ed upon the terminal portion of the Q R S
c omplex .
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Slow-fast form of atrioventricular nodal reentrant

tachycardia (AVNRT)
R epres entation of dual pathway phy s iology inv olv ing the
atriov entric ular (A V ) node and perinodal atrial tis s ue in the c ommon
form of A V N R T.
L eft panel: A normal s inus beat (A 1 ) is c onduc ted through the fas t
pathway (F ) to the final c ommon pathway (fc p) in the A V node and into
the B undle of H is . T he c onduc tion through the s low pathway (S ) runs
into the refrac tory period of the impuls e through the fas t pathway and
is ex tinguis hed.
M iddle panel: A c ritic ally timed atrial premature beat (A 2 ) finds the
fas t pathway refrac tory in the antegrade direc tion but is able to
c onduc t antegrade through the s low pathway, whic h has a s horter
refrac tory period. I f ex c itability in the fas t pathway has rec ov ered by
the time the impuls e reac hes the fc p, there may be retrograde
ac tiv ation of the fas t pathway.
R ight panel: T he retrograde impuls e throws off an ec ho to the atrium
(A * ), and, if the s low pathway has rec ov ered its ex c itability, the
impuls e reenters the s low pathway and produc es v entric ular
depolarization (V * ). I f the mec hanis m pers is ts , a repetitiv e c irc uit is
es tablis hed that c reates a s us tained reentrant tac hy c ardia. T he
s equenc e of antegrade (S ) and retrograde (F ) c onduc tion is c alled the
s low- fas t form of A V N R T.
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Atypical atrioventricular nodal reentrant tachycardia
S hown are three s imultaneous E C G leads (I , I I , and I I I ) during an

unc ommon or aty pic al form of an atriov entric ular nodal reentrant
tac hy c ardia (A V N R T ) in whic h antegrade c onduc tion to the v entric le
is v ia the fas t pathway and retrograde atrial ac tiv ation is by the s low
pathway. A s a res ult of delay ed atrial ac tiv ation, there is a long R P and
s hort P R interv al and a negativ e P wav e in the inferior leads I I and I I I .
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Uncommon fast-slow variant of atrioventricular nodal

reentrant tachycardia (AVNRT)
D iagrammatic repres entation in the c irc uit (left panel) and the ladder
diagram (right panel) of the unc ommon form of A V N R T (fas t- s low v ariant).
A ntegrade c onduc tion is through the fas t (F ) pathway and retrograde
c onduc tion is through the s low (S ) pathway. B ec aus e of s low retrograde
ac tiv ation of the atrium, the P wav e oc c urs after the Q R S c omplex with a
long R P interv al and relativ ely s hort P R interv al before the nex t Q R S
c omplex .
ECG: electrocardiogram.
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12-lead electrocardiogram (ECG) showing orthodromic

atrioventricular reentrant tachycardia (AVRT) in a patient with
an accessory AV pathway
T he 1 2 - lead E C G from a patient with Wolff- P ark ins on- White s hows a regular
tac hy c ardia. H owev er, in c ontras t to the Q R S pattern during s inus rhy thm, the Q R S
c omplex es are narrow, without ev idenc e of a delta wav e or preex c itation; this is
due to the fac t that antegrade v entric ular ac tiv ation oc c urs v ia the normal
atriov entric ular node- H is P urk inje pathway, while retrograde atrial ac tiv ation is v ia
the ac c es s ory pathway. T herefore, this is c alled an orthodromic atriov entric ular
reentrant tac hy c ardia (O A V R T ).
Courtesy of Martin Burke, DO.
ECG in Wolff-Parkinson-White
27 of 36 4/24/2020, 10:56 PM
T he 1 2 - lead E C G s hows the ty pic al features of Wolff- P ark ins on- White; the P R
interv al is s hort (* ) and the Q R S duration prolonged as a res ult of a delta wav e
(arrow), indic ating v entric ular preex c itation.
28 of 36 4/24/2020, 10:56 PM
Orthodromic atrioventricular reentrant tachycardia

(AVRT) in the setting of an accessory AV pathway
T he rhy thm s trip s hows a s inus (S ) beat that has a s hort P R interv al
and a wide Q R S c omplex as a res ult of a delta wav e (d). P anel A s hows
an atrial premature beat (A P B ,* ) that is bloc k ed in the ac c es s ory
pathway (A P ), whic h has a long refrac tory period but is c onduc ted
antegradely through the atriov entric ular node (N ) and the H is - P urk inje
s y s tem, res ulting in a normal P R interv al and a narrow and normal
Q R S c omplex , as s een on the rhy thm s trip. A fter normal my oc ardial
ac tiv ation, the impuls e is c onduc ted retrogradely along the A P,
ac tiv ating the atrium in a retrograde fas hion (panel B ), whic h res ults in
a negativ e P wav e. I f this ac tiv ation s equenc e repeats its elf (panel C ),
an orthodromic atriov entric ular reentrant (or rec iproc ating)
tac hy c ardia (A V R T ) is es tablis hed.
29 of 36 4/24/2020, 10:56 PM
12-lead electrocardiogram (ECG) showing antidromic

atrioventricular reentrant tachycardia (AVRT) in a patient with
an accessory AV pathway
T he 1 2 - lead E C G of a patient with Wolff- P ark ins on- White s hows a regular
tac hy c ardia. T he Q R S c omplex es are widened and are identic al to the Q R S
c omplex es s een in s inus rhy thm; the antegrade c onduc tion to the v entric le is v ia
the ac c es s ory pathway and retrograde c onduc tion is v ia the normal H is -
atriov entric ular node pathway. T his is , therefore, an antidromic atriov entric ular
reentrant tac hy c ardia (A V R T ).
ECG in Wolff-Parkinson-White
T he 1 2 - lead E C G s hows the ty pic al features of Wolff- P ark ins on- White; the P R
30 of 36 4/24/2020, 10:56 PM
interv al is s hort (* ) and the Q R S duration prolonged as a res ult of a delta wav e
(arrow), indic ating v entric ular preex c itation.
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Antidromic atrioventricular reentrant tachycardia

(AVRT) in the setting of an accessory AV pathway
T he rhy thm s trip s hows a s inus (S ) beat that has a s hort P R interv al
and a wide Q R S c omplex as a res ult of a delta wav e (d). P anel A s hows
the ac tiv ation s equenc e with an atrial premature beat (A P B ,* ). T he
impuls e reac hes the atriov entric ular node (N ) before it has repolarized
and henc e is bloc k ed in this s truc ture. H owev er, the ac c es s ory
pathway (A P ), whic h has a s hort refrac tory period, is able to c onduc t
the impuls e antegradely, res ulting in an A P B with a widened Q R S
morphology s imilar to the s inus beat. A s s een in panel B , following
my oc ardial ac tiv ation, the impuls e is c onduc ted retrogradely along the
H is - P urk inje s y s tem and A V node, res ulting in retrograde atrial
ac tiv ation, s een on the rhy thm s trip as an inv erted P wav e. I f this
ac tiv ation s equenc e repeats its elf (panel C ), a wide Q R S c omplex
antidromic atriov entric ular reentrant (or rec iproc ating) tac hy c ardia
(A V R T ) is es tablis hed.
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Single lead electrocardiogram (ECG) showing

monomorphic ventricular tachycardia
T hree or more s uc c es s iv e v entric ular beats are defined as v entric ular

tac hy c ardia (V T ). T his V T is monomorphic s inc e all of the Q R S c omplex es
hav e an identic al appearanc e. A lthough the P wav es are not dis tinc t, they
c an be s een altering the Q R S c omplex and S T-T wav es in an irregular
fas hion, indic ating the abs enc e of a relations hip between the P wav es and
the Q R S c omplex es (ie, A V dis s oc iation is pres ent).
AV: atrioventricular.
Normal rhythm strip

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ECG 12-lead ventricular fibrillation
1 2 - lead E C G s howing c ours e v entric ular fibrillation.
ECG: electrocardiogram.
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Mechanism of bundle branch reentrant ventricular

tachycardia
S c hematic repres entation of the reentrant c irc uit in bundle branc h

reentrant v entric ular tac hy c ardia (B B R V T ) s howing a v entric ular
premature beat that bloc k s in the right bundle branc h (R B B ), c onduc ts
s lowly up the left bundle branc h (L B B ), ac tiv ates the bundle of H is , and
returns antegradely down the R B B . I f the R B B has rec ov ered its
ex c itability from the prec eding beat, the c irc uit is c ompleted, and the
reentrant c irc uit may bec ome repetitiv e.
AV: atrioventricular; PVC: premature ventricular contraction.
35 of 36 4/24/2020, 10:56 PM
Contributor Disclosures
Philip J Podrid, MD, FACC Nothing to disclose Bernard J Gersh, MB, ChB, DPhil, FRCP,
MACC Consultant/Advisory Boards: Bain Institute [CRO for trials involving Edw ards percutaneous valve devices];
Boston Scientific Corporation [Data Safety Monitoring Board (REPRISE study)]; Cardiovascular Research Foundation
[Data Safety Monitoring Board (RELIEVE-HF Trial)]; Duke Clinical Research Institute [Data Safety Monitoring Board
(PIONEER HCM)]; Icahn School of Medicine at Mount Sinai [Data Safety Monitoring Board (ENVISAGE-TAVI study)];
Janssen Scientific Affairs [Executive committee (ORBIT Registries); Chairman (DSMB); Steering Committee & Writing
Committee (REVEAL Trial)]; Kow a Research Institute [Data Safety Monitoring Board (PROMINENT study)]; Medtronic
[REVEAL AF study]; Mount Sinai St Luke's [Chairman (TWILIGHT study)]; MyoKardia [General consulting]; Sirtex Med
Limited [General consulting]; Thrombosis Research Institute [Data Safety Monitoring Board (GARFIELD study)]; Baim
Institute [CRO for trials involving Edw ards Percutaneous Valve Devices]. Brian C Dow ney, MD, FACC Nothing to
disclose
Contributor disclosures are review ed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be provided
to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate
standards of evidence.
Conflict of interest policy
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Reentry and The Development of Cardiac Arrhythmias: Author: Section Editor: Deputy Editor

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Reentry and the development of cardiac arrhythmias

DEFINITION AND CHARACTERISTICS

Reentrant tachycardia (variously named reentrant excitation, reciprocating tachycardia, circus

● Transient or permanent unidirectional block of one pathway must exist as a result of

present at exactly the same time.

CRITERIA FOR DIAGNOSIS

● Activation of the myocardium mapped in one direction around a continuous loop.

entrainment is more likely to occur when the excitable gap is longer.

Functional circuits have the following properties:

● There is usually a short excitable gap associated with functional reentry.

One animal study reported the following additional properties [11]:

CLINICAL ARRHYTHMIAS DUE TO REENTRY

● Different direction of rotation around the same circuit

• Anatomic reentrant tachycardia requires a discrete anatomic obstacle, such as an area of

• Functional reentry depends upon the intrinsic heterogeneity of the electrophysiologic

Use of UpToDate is subject to the Subscription and License Agreement.

1. Mayer AG. Rhythmical pulsation in scyphomedusae. Carnegie Institution of Washington Publicati

2. Mines GR. On dynamic equilibrium in the heart. J Physiol 1913; 46:349.

differences in propagation following modification of the sodium conductance in human atrial

31. Denes P, Wu D, Dhingra R, et al. Dual atrioventricular nodal pathways. A common

41. Wellens HJJ. Electrophysiologic properties of the accessory pathway in Wolff-Parkinson-White sy

Topic 954 Version 14.0

Mechanisms of reentry in cardiac arrhythmias

S c hematic repres entation of pos s ible reentrant c irc uits . T he thic k

Courtesy of Philip J Podrid, MD, FACC.

Graphic 52134 Version 5.0

P anel A is an ac tiv ation map of a s ingle reentrant c irc uit at the

Graphic 54711 Version 1.0

Mechanism of torsades de pointes

T he top panels A - F are ex amples of epic ardial is oc hrone maps

Graphic 56857 Version 3.0

Sites of reentry in supraventricular tachyarrhythmias

LAF: left anterior fascicle; LPF: left posterior fascicle.

Graphic 82249 Version 4.0

Single-lead electrocardiogram (ECG) showing

E lec troc ardiogram s howing S A nodal reentrant tac hy c ardia. T he firs t

Courtesy of Morton F Arnsdorf, MD.

Graphic 76364 Version 5.0

Normal rhythm strip

N ormal rhy thm s trip in lead I I . T he P R interv al is 0 .1 5 s ec and the

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

Two types of reentry in atrial fibrillation

T he is oc hronal ac tiv ation maps demons trate two ty pes of reentry in

Graphic 73931 Version 2.0

Single-lead electrocardiogram (ECG) showing atrial fibrillation

AF: atrial fibrillation.

Courtesy of Ary Goldberger, MD.

Graphic 73958 Version 6.0

Normal rhythm strip

N ormal rhy thm s trip in lead I I . T he P R interv al is 0 .1 5 s ec and the

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0

Single-lead electrocardiogram (ECG) showing atrial

AF: atrial fibrillation.

Courtesy of Morton Arnsdorf, MD.

Graphic 53988 Version 4.0

Normal rhythm strip

N ormal rhy thm s trip in lead I I . T he P R interv al is 0 .1 5 s ec and the

Courtesy of Morton F Arnsdorf, MD.

Graphic 59022 Version 3.0