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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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.
Jalife J, Delmar M, Davidenko J, et al. Basic cardiac electrophysiology for the clinician. Armonk: Futura Publishing; 1999.
Lerman BB, Stein KM, Markowitz SM, et al. Ventricular arrhythmias in normal hearts. Cardiol Clin. 2000;18:265–91.
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.
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.
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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
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DOI: https://doi.org/10.1007/978-1-4614-6705-2_15
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