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. Use of UpToDate is subject to the Terms of Use. REFERENCES 1. Mayer AG. Rhythmical pulsation in scyphomedusae. Carnegie Institution of Washington Pub lication No. 47, 1906. 2. Mines GR. On dynamic equilibrium in the heart. J Physiol 1913; 46:349. 3. Lewis T. The Mechanism and Graphic Registration of the Heart Beat, & Sons, London 1925. 4. Allessie MA, Bonke FI, Schopman FJ. Circus movement in rabbit atrial muscle as a mechanism of trachycardia. Circ Res 1973; 33:54. 5. Allessie MA, Bonke FI, Schopman FJ. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. II. The role of nonuniform recovery of excitability in the https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 12/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate occurrence of unidirectional block, as studied with multiple microelectrodes. Circ Res 1976; 39:168. 6. Allessie MA, Bonke FI, Schopman FJ. Circus movement in rabbit atrial muscle as a mechanism of tachycardia. III. The "leading circle" concept: a new model of circus movement in cardiac tissue without the involvement of an anatomical obstacle. Circ Res 1977; 41:9. 7. Hoffman BF. Circus movement in the AV ring. In: Cardiac Electrophysiology: A Textbook, Ros en MR, Janse MJ, Wi AL (Eds), Futura, Mt Kisco, NY 1990. p.573. 8. Waldo AL, MacLean WA, Karp RB, et al. Entrainment and interruption of atrial flutter with atrial pacing: studies in man following open heart surgery. Circulation 1977; 56:737. 9. Frame LH, Page RL, Hoffman BF. Atrial reentry around an anatomic barrier with a partially refractory excitable gap. A canine model of atrial flutter. Circ Res 1986; 58:495. 10. Gough WB, Mehra R, Restivo M, et al. Reentrant ventricular arrhythmias in the late myocardial infarction period in the dog. 13. Correlation of activation and refractory maps. Circ Res 1985; 57:432. 11. Kamjoo K, Uchida T, Ikeda T, et al. Importance of location and timing of electrical stimuli in terminating sustained functional reentry in isolated swine ventricular tissues: evidence in support of a small reentrant circuit. Circulation 1997; 96:2048. 12. Spach MS, Miller WT 3rd, Geselowitz DB, et al. The discontinuous nature of propagation in normal canine cardiac muscle. Evidence for recurrent discontinuities of intracellular resistance that affect the membrane currents. Circ Res 1981; 48:39. 13. Spach MS, Dolber PC, Heidlage JF. Influence of the passive anisotropic properties on directional differences in propagation following modification of the sodium conductance in human atrial muscle. A model of reentry based on anisotropic discontinuous propagation. Circ Res 1988; 62:811. 14. Brugada J, Boersma L, Kirchhof CJ, et al. Reentrant excitation around a fixed obstacle in uniform anisotropic ventricular myocardium. Circulation 1991; 84:1296. 15. Spach MS, Dolber PC, Heidlage JF. Interaction of inhomogeneities of repolarization with anisotropic propagation in dog atria. A mechanism for both preventing and initiating reentry. Circ Res 1989; 65:1612. 16. Allessie MA, Schalij MJ, Kirchhof CJ, et al. Experimental electrophysiology and arrhythmogenicity. Anisotropy and ventricular tachycardia. Eur Heart J 1989; 10 Suppl E:2. 17. Allessie MA, Schalij MJ, Kirchhof CJ, et al. Electrophysiology of spiral waves in two dimensions: the role of anisotropy. Ann N Y Acad Sci 1990; 591:247. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 13/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate 18. El-Sherif N, Smith RA, Evans K. Canine ventricular arrhythmias in the late myocardial infarction period. 8. Epicardial mapping of reentrant circuits. Circ Res 1981; 49:255. 19. Davidenko JM, Kent PF, Chialvo DR, et al. Sustained vortex-like waves in normal isolated ventricular muscle. Proc Natl Acad Sci U S A 1990; 87:8785. 20. Pertsov AM, Davidenko JM, Salomonsz R, et al. Spiral waves of excitation underlie reentrant activity in isolated cardiac muscle. Circ Res 1993; 72:631. 21. Davidenko JM, Pertsov AV, Salomonsz R, et al. Stationary and drifting spiral waves of excitation in isolated cardiac muscle. Nature 1992; 355:349. 22. Athill CA, Ikeda T, Kim YH, et al. Transmembrane potential properties at the core of functional reentrant wave fronts in isolated canine right atria. Circulation 1998; 98:1556. 23. Garfinkle A, Qu Z. Nonlinear dynamics of excitation and propagation in cardiac muscle. In: C ardiac Electrophysiology: From Cell to Bedside, Zipes DP, Jalife J (Eds), WB Saunders, Philadel phia 1999. p.515. 24. Davidenko JM. Spiral wave activity: a possible common mechanism for polymorphic and monomorphic ventricular tachycardias. J Cardiovasc Electrophysiol 1993; 4:730. 25. Wathen MS, Klein GJ, Yee R, Natale A. Classification and terminology of supraventricular tachycardia. Diagnosis and management of the atrial tachycardias. Cardiol Clin 1993; 11:109. 26. Narula OS. Sinus node re-entry: a mechanism for supraventricular tachycardia. Circulation 1974; 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 wav elet 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. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 14/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate 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. 35. Wu D, Denes P, Dhingra R, et al. New manifestations of dual A-V nodal pathways. Eur J Cardiol 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 W olff-Parkinson-White syndrome. In: Tachycardias: Mechanisms, Diagnosis, Treatment, Josep hson ME, Wellens HJJ (Eds), Lea & Febiger, Philadelphia 1984. p.1991. 39. Newman BJ, Donoso E, Friedberg CK. Arrhythmias in the Wolff-Parkinson-White syndrome. Prog Cardiovasc Dis 1966; 9:147. 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-Whit e syndrome. In: Conduction System of the Heart: Structure, Function, and Clinical Implicatio n, Wellens 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 ventri cular tachycardia: The role of reentry. In: Tachycardias: Mechanisms, Diagnosis, Treatment, J osephson ME, Wellens HJJ (Eds), & Febiger, Philadelphia 1984. p.305. 43. Costeas C, Peters NS, Waldecker B, et al. Mechanisms causing sustained ventricular tachycardia with multiple QRS morphologies: results of mapping studies in the infarcted canine heart. Circulation 1997; 96:3721. 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 fibrillation. Characteristics and mechanisms of termination and spontaneous regeneration. Circ Res 1996; 78:660. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 15/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate 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 22.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 16/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate GRAPHICS Mechanisms of reentry in cardiac arrhythmias Schematic representation of possible reentrant circuits. The thick black arrow represents the circulating impulse; thin black lines represent advancing wavefronts in completely refractory tissue; speckled areas are partially refractory tissue; white areas are fully excitable tissue. A is the original model of circus movement around a fixed obstacle. There is a fully excitable gap, and the length and location of the circuit are fixed. B represents circus movement around 2 fixed anatomic obstacles. A fully excitable gap is present. C represents rapidly conducting bundles forming closed loops that serve as preferential circuits through which the impulse may travel. D is the leading circle type of reentry which does not require an anatomic obstacle. Instead, the impulse propagates around a functionally refractory core and among neighboring fibers that have different electrophysiologic properties. Since the refractoriness of the core is variable, the circuit size changes but will be the smallest possible circuit that can continue to propagate an impulse. Functional circuits tend to be small, rapid, and unstable. E represents reentry around a fixed anatomic obstacle, but a fully excitable gap is absent. F demonstrates an area of slowed conduction (hatched lines) between anatomic boundaries, while in G all areas of slowed conduction neighbor an anatomic obstacle. H represents anisotropic reentry. There are differences in the conduction of a single impulse in various fibers as a result of differences in their orientation. https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 17/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Courtesy of Philip J Podrid, MD, FACC. Graphic 52134 Version 5.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 18/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Anisotropic reentry Panel A is an activation map of a single reentrant circuit at the epicardial border zone of a myocardial infarction. The large arrows represent the general activation pattern which occurs around a long line of block (blue arrow). Parallel isochrones 130 and 140 which are adjacent to the block suggest that activation is occurring across the block, resulting in a smaller circuit (shaded area) shown by the small black arrow. Panel B is an enlarged representation of this shaded area; the dark black rectangle represents an area of block around which there is a reentrant circuit (small arrows). Rapid activation occurs parallel to the long axis of the fiber orientation (isochrones 10-40 and 130-150), while in the transverse direction activation is slow (bunched isochrones 50-120). Graphic 54711 Version 2.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 19/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Mechanism of torsades de pointes The top panels A-F are examples of epicardial isochrone maps obtained from the surface of the anterior left ventricular (LV) wall and free wall of the right ventricle (RV) during an episode of quinidine-induced torsades de pointes. Each map corresponds to a QRS deflection of the surface ECG and simultaneous monophasic action potential (MAP). Early afterpotentials (EADs) result in triggered activity (panels A-C) which is followed by a long episode of spiral-like reentry (panels D-F). Panel C shows the first reentrant wave which is not stationary, but gradually shifts upward and to the right. This is associated with a gradual decrease in the QRS complex amplitude. Reprinted with permission from the American College of Cardiology. Journal of the American College of Cardiology, 1997; 29:831. Graphic 56857 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 20/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Sites of reentry in supraventricular tachyarrhythmias Reentry may occur around a fixed anatomic obstacle or may be functional, developing in the absence of an anatomic obstacle and resulting from the intrinsic heterogeneity of electrophysiologic properties of the myocardial tissue. Reentrant circuits leading to a supraventricular tachyarrhythmia may develop in various parts of the heart: within and around the sinoatrial node (sinus node reentry); within the atrial myocardium (atrial tachycardia, atrial flutter, or atrial fibrillation); within the atrioventricular (AV) node due to the presence of a slow and fast pathway (atrioventricular nodal reentrant tachycardia); or involving the AV node and an accessory pathway (AP) (atrioventricular reentrant tachycardia). LAF: left anterior fascicle; LPF: left posterior fascicle. Graphic 82249 Version 4.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 21/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Single-lead electrocardiogram (ECG) showing sinoatrial (SA) nodal reentrant tachycardia Electrocardiogram showing SA nodal reentrant tachycardia. The first three beats are normal sinus beats at a rate of about 107 beats/min; the fourth beat is an atrial premature beat that is followed by a return to sinus rhythm. The eighth beat (arrow) represents the sudden onset of SA nodal reentrant tachycardia at a rate of about 145 beats/min. Since the P waves are similar to the sinus beats, the diagnosis is suggested only by the abrupt onset of the tachycardia. Courtesy of Morton F Arnsdorf, MD. Graphic 76364 Version 5.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 22/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Two types of reentry in atrial fibrillation The isochronal activation maps demonstrate two types of reentry in atrial fibrillation. Map A shows random reentry with three simultaneous wavefronts (black arrows) activating most of the recording area. Map B also shows three simultaneous wavefronts, but they are coming from different directions than those in map A. Maps C and D show two consecutive cycles of complete reentry. The wave of activation (black arrow) spreads clockwise in a circular fashion around a line of unexcited tissue. Reproduced with permission from Holm M, Johansson R, Brandt J, et al. Eur Heart J 1997; 18:290. Graphic 73931 Version 2.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 23/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Single-lead electrocardiogram (ECG) showing atrial fibrillation Lead V1 showing coarse AF with moderate ventricular response. The two characteristic findings in AF are present: the very rapid atrial fibrillatory waves (f waves), which are variable in appearance; and the irregularly irregular ventricular response as the R-R interval between beats is unpredictable. Coarse AF may appear similar to atrial flutter. However, the variable height and duration of the f waves differentiate them from atrial flutter (F) waves, which are identical in appearance and occur at a constant rate of about 250 to 350 beats/min. AF: atrial fibrillation. Courtesy of Ary Goldberger, MD. Graphic 73958 Version 6.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 24/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Single-lead electrocardiogram (ECG) showing atrial fibrillation with minimally apparent atrial activity F waves are not apparent in this lead, as the only finding suggestive of AF is the irregularly irrregular ventricular response. AF: atrial fibrillation. Courtesy of Morton Arnsdorf, MD. Graphic 53988 Version 4.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 25/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Typical atrioventricular nodal reentrant tachycardia The first two complexes are normal sinus beats with a normal P wave followed by a QRS complex. The third complex, an atrial premature beat (APB), has a prolonged PR interval; it initiates a common or typical atrioventricular nodal reentrant tachycardia (AVNRT) in which antegrade conduction to the ventricle is via the slow pathway and retrograde atrial activation is by the fast pathway. Although no distinct P wave is seen, the QRS complex has a small terminal deflection, known as a pseudo r', which is the P wave superimposed upon the terminal portion of the QRS complex. Graphic 54290 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 26/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Slow-fast form of atrioventricular nodal reentrant tachycardia (AVNRT) Representation of dual pathway physiology involving the atrioventricular (AV) node and perinodal atrial tissue in the common form of AVNRT. Left panel: A normal sinus beat (A ) is conducted through the fast pathway (F) to the final common pathway (fcp) in the AV node and into the Bundle of His. The conduction through the slow pathway (S) runs into the refractory period of the impulse through the fast pathway and is extinguished. 1 Middle panel: A critically timed atrial premature beat (A ) finds the fast pathway refractory in the antegrade direction but is able to conduct antegrade through the slow pathway, which has a shorter refractory period. If excitability in the fast pathway has recovered by 2 the time the impulse reaches the fcp, there may be retrograde activation of the fast pathway. Right panel: The retrograde impulse throws off an echo to the atrium (A*), and, if the slow pathway has recovered its excitability, the impulse reenters the slow pathway and produces ventricular depolarization (V*). If the mechanism persists, a repetitive circuit is established that creates a sustained reentrant tachycardia. The sequence of antegrade (S) and retrograde (F) conduction is called the slow-fast form of AVNRT. Graphic 79760 Version 6.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 27/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Atypical atrioventricular nodal reentrant tachycardia Shown are three simultaneous ECG leads (I, II, and III) during an uncommon or atypical form of an atrioventricular nodal reentrant tachycardia (AVNRT) in which antegrade conduction to the ventricle is via the fast pathway and retrograde atrial activation is by the slow pathway. As a result of delayed atrial activation, there is a long RP and short PR interval and a negative P wave in the inferior leads II and III. Graphic 66828 Version 2.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 28/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Uncommon fast-slow variant of atrioventricular nodal reentrant tachycardia (AVNRT) Diagrammatic representation in the circuit (left panel) and the ladder diagram (right panel) of the uncommon form of AVNRT (fast-slow variant). Antegrade conduction is through the fast (F) pathway and retrograde conduction is through the slow (S) pathway. Because of slow retrograde activation of the atrium, the P wave occurs after the QRS complex with a long RP interval and relatively short PR interval before the next QRS complex. ECG: electrocardiogram. Graphic 56806 Version 4.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 29/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate 12-lead electrocardiogram (ECG) showing orthodromic atrioventricular reentrant tachycardia (AVRT) in a patient with an accessory AV pathway The 12-lead ECG from a patient with Wolff-Parkinson-White shows a regular tachycardia. However, in contrast to the QRS pattern during sinus rhythm, the QRS complexes are narrow, without evidence of a delta wave or pre-excitation; this is due to the fact that antegrade ventricular activation occurs via the normal atrioventricular node-His Purkinje pathway, while retrograde atrial activation is via the accessory pathway. Therefore, this is called an orthodromic atrioventricular reentrant tachycardia (OAVRT). Courtesy of Martin Burke, DO. Graphic 68804 Version 5.0 ECG in Wolff-Parkinson-White https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 30/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate The 12-lead ECG shows the typical features of Wolff-Parkinson-White; the PR interval is short (*) and the QRS duration prolonged as a result of a delta wave (arrow), indicating ventricular preexcitation. Courtesy of Martin Burke, DO. Graphic 67181 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 31/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Orthodromic atrioventricular reentrant tachycardia (AVRT) in the setting of an accessory AV pathway The rhythm strip shows a sinus (S) beat that has a short PR interval and a wide QRS complex as a result of a delta wave (d). Panel A shows an atrial premature beat (APB,*) that is blocked in the accessory pathway (AP), which has a long refractory period but is conducted antegradely through the atrioventricular node (N) and the His-Purkinje system, resulting in a normal PR interval and a narrow and normal QRS complex, as seen on the rhythm strip. After normal myocardial activation, the impulse is conducted retrogradely along the AP, activating the atrium in a retrograde fashion (panel B), which results in a negative P wave. If this activation sequence repeats itself (panel C), an orthodromic atrioventricular reentrant (or reciprocating) tachycardia (AVRT) is established. Graphic 71302 Version 7.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 32/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate 12-lead electrocardiogram (ECG) showing antidromic atrioventricular reentrant tachycardia (AVRT) in a patient with an accessory AV pathway The 12-lead ECG of a patient with Wolff-Parkinson-White shows a regular tachycardia. The QRS complexes are widened and are identical to the QRS complexes seen in sinus rhythm; the antegrade conduction to the ventricle is via the accessory pathway and retrograde conduction is via the normal His- atrioventricular node pathway. This is, therefore, an antidromic atrioventricular reentrant tachycardia (AVRT). Courtesy of Martin Burke, DO. Graphic 54484 Version 20.0 ECG in Wolff-Parkinson-White https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 33/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate The 12-lead ECG shows the typical features of Wolff-Parkinson-White; the PR interval is short (*) and the QRS duration prolonged as a result of a delta wave (arrow), indicating ventricular preexcitation. Courtesy of Martin Burke, DO. Graphic 67181 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 34/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Antidromic atrioventricular reentrant tachycardia (AVRT) in the setting of an accessory AV pathway The rhythm strip shows a sinus (S) beat that has a short PR interval and a wide QRS complex as a result of a delta wave (d). Panel A shows the activation sequence with an atrial premature beat (APB,*). The impulse reaches the atrioventricular node (N) before it has repolarized and hence is blocked in this structure. However, the accessory pathway (AP), which has a short refractory period, is able to conduct the impulse antegradely, resulting in an APB with a widened QRS morphology similar to the sinus beat. As seen in panel B, following myocardial activation, the impulse is conducted retrogradely along the His-Purkinje system and AV node, resulting in retrograde atrial activation, seen on the rhythm strip as an inverted P wave. If this activation sequence repeats itself (panel C), a wide QRS complex antidromic atrioventricular reentrant (or reciprocating) tachycardia (AVRT) is established. Graphic 50433 Version 4.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 35/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Single lead electrocardiogram (ECG) showing monomorphic ventricular tachycardia Three or more successive ventricular beats are defined as ventricular tachycardia (VT). This VT is monomorphic since all of the QRS complexes have an identical appearance. Although the P waves are not distinct, they can be seen altering the QRS complex and ST-T waves in an irregular fashion, indicating the absence of a relationship between the P waves and the QRS complexes (ie, AV dissociation is present). AV: atrioventricular. Graphic 63176 Version 7.0 Normal rhythm strip Normal rhythm strip in lead II. The PR interval is 0.15 sec and the QRS duration is 0.08 sec. Both the P and T waves are upright. Courtesy of Morton F Arnsdorf, MD. Graphic 59022 Version 3.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 36/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate ECG 12-lead ventricular fibrillation 12-lead ECG showing course ventricular fibrillation. ECG: electrocardiogram. Graphic 118944 Version 1.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 37/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Mechanism of bundle branch reentrant ventricular tachycardia Schematic representation of the reentrant circuit in bundle branch reentrant ventricular tachycardia (BBRVT) showing a ventricular premature beat that blocks in the right bundle branch (RBB), conducts slowly up the left bundle branch (LBB), activates the bundle of His, and returns antegradely down the RBB. If the RBB has recovered its excitability from the preceding beat, the circuit is completed, and the reentrant circuit may become repetitive. AV: atrioventricular; PVC: premature ventricular contraction. Graphic 75164 Version 5.0 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 38/39 7/5/23, 10:47 AM Reentry and the development of cardiac arrhythmias - UpToDate Contributor Disclosures Philip J Podrid, MD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Bernard J Gersh, MB, ChB, DPhil, FRCP, MACC Consultant/Advisory Boards: Bain Institute [CRO for trials involving Edwards percutaneous valve devices]; Cardiovascular Research Foundation [Data safety monitoring board (RELIEVE-HF Trial)]; Caristo Diagnostics Limited [Imaging and inflammation/atherosclerosis]; Philips Image Guided Therapy Corporation [Imaging]; Sirtex Med Limited [General consulting]; Thrombosis Research Institute [Data safety monitoring board (GARFIELD study)]. All of the relevant financial relationships listed have been mitigated. Susan B Yeon, MD, JD, FACC No relevant financial relationship(s) with ineligible companies to disclose. Contributor disclosures are reviewed 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 https://www.uptodate.com/contents/reentry-and-the-development-of-cardiac-arrhythmias/print 39/39