Cardiac arrhythmias result from alterations in the orderly sequence of depolarization followed by repolar-ization in the heart. Cardiac arrhythmias may result in alterations in heart rate or rhythm and arise from alterations in impulse generation or conduction. The clinical implications of disordered cardiac activation range from asymptomatic palpitations to lethal arrhythmia.

Pharmacological management of arrhythmias uses drugs that exert effects directly on cardiac cells by inhibiting the function of specific ion channels or by altering the autonomic input into the heart. Recent technological advances have lead to an increase in nondrug strategies, including transcatheter radiofrequency ablation, intraoperative cryoablation, implanted pacemakers, and defibrillation. Physicians caring for patients with arrhythmias therefore must understand and appreciate the benefits and risks provided by each therapeutic modality, what the indication for each is, and how these modalities may interact.

Successful antiarrhythmic drug therapy requires a combination of understanding the pathophysiology of the arrhythmia, identification of a drug that can influence the relevant electrophysiological parameters, and careful titration of the drug's dose to correct the abnormal electrophysiological events giving rise to the arrhythmia. This is accomplished while avoiding the omnipresent risk of side effects such as proarrhythmia.

This chapter first provides a brief overview of the cellular events that underlie the cardiac action potential and lead to the formation and propagation of the normal cardiac impulse. Basic mechanisms of arrhythmias are reviewed, and the pharmacology of specific antiarrhythmic agents is discussed.

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