Skip to main content

Electrophysiology of Cardiac Arrhythmias

  • Chapter
  • First Online:
Essential Cardiology

Abstract

Abnormalities in the initiation and propagation of cardiac impulses result in a variety of arrhythmias. The cardiac action potential consists of five phases that are determined by channels that allow ions to flow passively down their electrochemical gradients, as well as by a series of energy-dependent ion pumps, thereby leading to cardiac contraction.

Sodium, potassium, calcium, and chloride ions are principally responsible for the membrane potential (phase 4). Phase 0 marks the initiation of the action potential. In nodal cells, the pacemaker current, If, initiates each cycle. In “nonpacemaker” tissue, If is absent. In these cells, phase 0 is triggered when the cell membrane is depolarized by adjacent cells. Phase 1 consists of rapid membrane repolarization. This is achieved by inactivation of the inward Na+ current and activation of a transient outward current, Ito. Phase 2, the plateau phase, is characterized by a small change in membrane potential generated by the L-type calcium channel, ICa–L. Rapid repolarization of the cell occurs during phase 3. ICa–L is inactivated in a time-dependent fashion, thus decreasing the flow of cations into the cell, while several outward potassium currents become active. This results in a net outward positive current and a negative transmembrane potential.

The mechanisms of cardiac arrhythmias can be divided into three categories: (1) abnormal or enhanced automaticity, (2) triggered activity, and (3) reentry. This chapter reviews each of these mechanisms, along with the common clinical correlates of each.

This is a preview of subscription content, log in via an institution to check access.

Access this chapter

Chapter
USD 29.95
Price excludes VAT (USA)
  • Available as PDF
  • Read on any device
  • Instant download
  • Own it forever
eBook
USD 169.00
Price excludes VAT (USA)
  • Available as EPUB and PDF
  • Read on any device
  • Instant download
  • Own it forever
Softcover Book
USD 219.99
Price excludes VAT (USA)
  • Compact, lightweight edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info
Hardcover Book
USD 299.99
Price excludes VAT (USA)
  • Durable hardcover edition
  • Dispatched in 3 to 5 business days
  • Free shipping worldwide - see info

Tax calculation will be finalised at checkout

Purchases are for personal use only

Institutional subscriptions

References

  1. Ackerman MJ, Clapham DE. Ion channels—basic science and clinical disease. N Engl J Med. 1997;336:1575–86.

    Article  PubMed  CAS  Google Scholar 

  2. Ackerman MJ, Clapham DE. Normal cardiac electrophysiology. In: Chien K, editor. Molecular basis of cardiovascular disease. Philadelphia: W. B. Saunders; 1999. p. 281–301.

    Google Scholar 

  3. Surawicz B. Normal and abnormal automaticity. In: Rosen MR, Janse MJ, Wit AL, editors. Cardiac electrophysiology: a textbook. Mount Kisco: Futura Publishing; 1990. p. 159–73.

    Google Scholar 

  4. Lerman BB, Stein KM, Markowitz SM. Adenosine-sensitive ventricular tachycardia: a conceptual approach. J Cardiovasc Electrophysiol. 1996;7:559–69.

    Article  PubMed  CAS  Google Scholar 

  5. Markowitz SM, Stein KM, Mittal S, et al. Differential effects of adenosine on focal and macroreentrant atrial tachycardia. J Cardiovasc Electrophysiol. 1999;10:489–502.

    Article  PubMed  CAS  Google Scholar 

  6. DiFrancesco D, Angoni M, Maccaferri G. The pacemaker current in cardiac cells. In: Zipes DP, Jalife J, editors. Cardiac electrophysiology: from cell to bedside. Philadelphia: W. B. Saunders; 1995. p. 96–103.

    Google Scholar 

  7. Lerman BB. Response of nonreentrant catecholamine-mediated ventricular tachycardia to endogenous adenosine and acetylcholine. Evidence for myocardial receptor-mediated effects. Circulation. 1993;87:382–90.

    Article  PubMed  CAS  Google Scholar 

  8. Schwartz PJ, Stramba-Badiale M, Crotti L, et al. Prevalence of the congenital long-QT syndrome. Circulation. 2009;120:1761–7.

    Article  PubMed  Google Scholar 

  9. Jervell A, Lange-Nielsen F. Congenital deaf-mutism, functional heart disease with prolongation of the QT interval, and sudden death. Am Heart J. 1957;54:59–68.

    Article  PubMed  CAS  Google Scholar 

  10. Romano C, Gemme G, Pongiglione R. Aritmie cardiache rare dell’eta’pediatrica. II. Accessi sincopali per fibrillazione ventricolare parossistica. Clin Pediatr (Bologna). 1963;45:656–83.

    CAS  Google Scholar 

  11. Ward OC. A new familial cardiac syndrome in children. J Ir Med Assoc. 1964;54:103–6.

    PubMed  CAS  Google Scholar 

  12. Yang Y, Yang Y, Liang B, et al. Identification of a Kir3.4 mutation in congenital long QT syndrome. Am J Hum Genet. 2010;86:872–80.

    Article  PubMed  CAS  Google Scholar 

  13. Keating MT. The long QT syndrome: a review of recent molecular genetic and physiologic discoveries. Medicine. 1996;75:1–5.

    Article  PubMed  CAS  Google Scholar 

  14. Schwartz PJ, Moss AJ, Vincent GM, et al. Diagnostic criteria for the long QT syndrome. An update. Circulation. 1993;88:782–4.

    Article  PubMed  CAS  Google Scholar 

  15. Ackerman MJ, Priori SG, Willems S, et al. HRS/EHRA expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies. Heart Rhythm. 2011;8:1308–39.

    Article  PubMed  Google Scholar 

  16. Luo CH, Rudy Y. A dynamic model of the cardiac ventricular action potential. II. Afterdepolarizations, triggered activity, and potentiation. Circ Res. 1994;74:1097–113.

    Article  PubMed  CAS  Google Scholar 

  17. Han X, Ferrier GR. Contribution of Na+-Ca2+ exchange to stimulation of transient inward current by isoproterenol in rabbit cardiac Purkinje fibers. Circ Res. 1995;76:664–74.

    Article  PubMed  CAS  Google Scholar 

  18. Lerman BB, Belardinelli L, West GA, et al. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMP-mediated triggered activity. Circulation. 1986;74:270–80.

    Article  PubMed  CAS  Google Scholar 

  19. Lerman BB, Stein K, Engelstein ED, et al. Mechanism of repetitive monomorphic ventricular tachycardia. Circulation. 1995;92:421–9.

    Article  PubMed  CAS  Google Scholar 

  20. Iwai S, Cantillon DJ, Kim RJ, et al. Right and left ventricular outflow tract tachycardias: evidence for a common electrophysiologic mechanism. J Cardiovasc Electrophysiol. 2006;17:1052–8.

    Article  PubMed  Google Scholar 

  21. Lerman BB, Stein KM, Markowitz SM. Mechanisms of idiopathic left ventricular tachycardia. J Cardiovasc Electrophysiol. 1997;8:571–83.

    Article  PubMed  CAS  Google Scholar 

  22. Lerman BB, Stein KM, Markowitz SM, et al. Catecholamine-facilitated reentrant ventricular tachycardia: uncoupling of adenosine’s antiadrenergic effects. J Cardiovasc Electrophysiol. 1999;10:17–26.

    Article  PubMed  CAS  Google Scholar 

  23. Priori SG, Napolitano CN, Tiso N, et al. Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation. 2001;103:196–200.

    Article  PubMed  CAS  Google Scholar 

  24. Laitinen PJ, Brown DM, Piippo K, et al. Mutations of the cardiac ryanodine receptor (RyR2) gene in familial polymorphic ventricular tachycardia. Circulation. 2001;103:485–90.

    Article  PubMed  CAS  Google Scholar 

  25. Laitinen PJ, Swan H, Kontula K. Molecular genetics of exercise-induced polymorphic ventricular tachycardia: identification of three novel cardiac ryanodine receptor mutations and two common calsequestrin 2 amino-acid polymorphisms. Eur J Hum Genet. 2003;11:888–91.

    Article  PubMed  CAS  Google Scholar 

  26. Jalife J, Delmar M, Davidenko J, et al. Basic cardiac electrophysiology for the clinician. Armonk: Futura Publishing; 1999.

    Google Scholar 

  27. Prystowsky EN, Klein GJ. Mechanism of tachycardia. In: Prystowsky E, Klein G, editors. Cardiac arrhythmias: an integrated approach for the clinician. New York: McGraw-Hill; 1994. p. 81–95.

    Google Scholar 

  28. 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;62:811–32.

    Article  PubMed  CAS  Google Scholar 

  29. Lesh MD, Kalman JM. To fumble flutter or tackle “tach”? Toward updated classifiers for atrial tachyarrhythmias. J Cardiovasc Electrophysiol. 1996;7:460–6.

    Article  PubMed  CAS  Google Scholar 

  30. Josephson ME, Kastor JA. Supraventricular tachycardia: mechanisms and management. Ann Intern Med. 1977;87:346–58.

    Article  PubMed  CAS  Google Scholar 

  31. Wu D, Denes P. Mechanisms of paroxysmal supraventricular tachycardia. Arch Intern Med. 1975;135:437–42.

    Article  PubMed  CAS  Google Scholar 

  32. Benditt D, Reyes W, Gornick C, et al. Supraventricular ­tachycardias: recognition and treatment. In: Naccarelli G, editor. Cardiac arrhythmias: a practical approach. Mount Kisco: Futura; 1991. p. 135–76.

    Google Scholar 

  33. DiMarco JP, Sellers TD, Lerman BB, et al. Diagnostic and therapeutic use of adenosine in patients with supraventricular ­tachyarrhythmias. J Am Coll Cardiol. 1985;6:417–25.

    Article  PubMed  CAS  Google Scholar 

  34. Lerman BB, Greenberg M, Overholt ED, et al. Differential electrophysiologic properties of decremental retrograde pathways in long RP’ tachycardia. Circulation. 1987;76:21–31.

    Article  PubMed  CAS  Google Scholar 

  35. Calkins H, Yong P, Miller JM, et al. Catheter ablation of accessory pathways, atrioventricular nodal reentrant tachycardia, and the atrioventricular junction: final results of a prospective, multicenter clinical trial. Circulation. 1999;99:262–70.

    Article  PubMed  CAS  Google Scholar 

  36. Kalbfleisch SJ, Morady F. Catheter ablation of atrioventricular nodal reentrant tachycardia. In: Zipes D, Jalife J, editors. Cardiac electrophysiology: from cell to bedside. Philadelphia: W. B. Saunders; 1995. p. 1477.

    Google Scholar 

  37. Scherlag BJ, El-Sherif N, Hope R, et al. Characterization and ­localization of ventricular arrhythmias resulting from myocardial ischemia and infarction. Circ Res. 1974;35:372–83.

    Article  PubMed  CAS  Google Scholar 

  38. Caceres J, Jazayeri M, McKinnie J, et al. Sustained bundle branch reentry as a mechanism of clinical tachycardia. Circulation. 1989;79:256–70.

    Article  PubMed  CAS  Google Scholar 

  39. Nademanee K, Veerakul G, Chandanamattha P, Chaothawee L, Ariyachaipanich A, Jirasirirojanakorn K, et al. Prevention of ventricular fibrillation episodes in Brugada syndrome by catheter ablation over the anterior right ventricular outflow tract epicardium. Circulation. 2011;123:1270–12709.

    Article  PubMed  Google Scholar 

  40. Brugada P, Brugada J. Right bundle branch block, persistent ST segment elevation and sudden cardiac death: a distinct clinical and electrocardiographic syndrome. J Am Coll Cardiol. 1992;20:1391–6.

    Article  PubMed  CAS  Google Scholar 

  41. Chen Q, Kirsch G, Zhang D, et al. Genetic basis and molecular mechanism for idiopathic ventricular fibrillation. Nature. 1998;392:293–6.

    Article  PubMed  CAS  Google Scholar 

  42. Yan G, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation. 1999;100:1660–6.

    Article  PubMed  CAS  Google Scholar 

Recommended Reading

  • Ackerman MJ, Priori SG, Willems S, et al. HRS/EHRA expert consensus statement on the state of genetic testing for the channelopathies and cardiomyopathies. Heart Rhythm. 2011;8:1308–39.

    Article  PubMed  Google Scholar 

  • Jalife J, Delmar M, Davidenko J, et al. Basic cardiac electrophysiology for the clinician. Armonk: Futura Publishing; 1999.

    Google Scholar 

  • Lerman BB, Stein KM, Markowitz SM, et al. Ventricular arrhythmias in normal hearts. Cardiol Clin. 2000;18:265–91.

    Article  PubMed  CAS  Google Scholar 

  • Priori SG, Napolitano CN, Tiso N, et al. Mutations in the cardiac ryanodine receptor gene (hRyR2) underlie catecholaminergic polymorphic ventricular tachycardia. Circulation. 2001;103:196–200.

    Article  PubMed  CAS  Google Scholar 

  • Yan G, Antzelevitch C. Cellular basis for the Brugada syndrome and other mechanisms of arrhythmogenesis associated with ST-segment elevation. Circulation. 1999;100:1660–6.

    Article  PubMed  CAS  Google Scholar 

Download references

Author information

Authors and Affiliations

Authors

Corresponding author

Correspondence to Bruce B. Lerman MD .

Editor information

Editors and Affiliations

Rights and permissions

Reprints and permissions

Copyright information

© 2013 Springer Science+Business Media New York

About this chapter

Cite this chapter

Iwai, S., Markowitz, S.M., Lerman, B.B. (2013). Electrophysiology of Cardiac Arrhythmias. In: Rosendorff, C. (eds) Essential Cardiology. Springer, New York, NY. https://doi.org/10.1007/978-1-4614-6705-2_15

Download citation

  • DOI: https://doi.org/10.1007/978-1-4614-6705-2_15

  • Published:

  • Publisher Name: Springer, New York, NY

  • Print ISBN: 978-1-4614-6704-5

  • Online ISBN: 978-1-4614-6705-2

  • eBook Packages: MedicineMedicine (R0)

Publish with us

Policies and ethics