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2013 | OriginalPaper | Hoofdstuk

15. Electrophysiology of Cardiac Arrhythmias

Auteurs : Sei Iwai, MD, Steven M. Markowitz, MD, Bruce B. Lerman, MD

Gepubliceerd in: Essential Cardiology

Uitgeverij: Springer New York

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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.
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Metagegevens
Titel
Electrophysiology of Cardiac Arrhythmias
Auteurs
Sei Iwai, MD
Steven M. Markowitz, MD
Bruce B. Lerman, MD
Copyright
2013
Uitgeverij
Springer New York
DOI
https://doi.org/10.1007/978-1-4614-6705-2_15