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Electrophysiology of Cardiac Arrhythmias

Chapter

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.

Keywords

Structural Heart Disease Right Ventricular Outflow Tract Accessory Pathway Slow Pathway Reentrant Tachycardia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Recommended Reading

  1. 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.PubMedCrossRefGoogle Scholar
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Copyright information

© Springer Science+Business Media New York 2013

Authors and Affiliations

  • Sei Iwai
    • 1
  • Steven M. Markowitz
    • 2
  • Bruce B. Lerman
    • 2
  1. 1.Division of Cardiology, Department of MedicineWestchester Medical CenterValhallaUSA
  2. 2.Division of Cardiology, Department of MedicineCornell University Medical Center, New York Presbyterian HospitalNew YorkUSA

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