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The term dysrhythmia encompasses an array of abnormal cardiac rhythms that range in clinical significance from merely annoying to instantly life threatening. Antidysrhythmics include all xenobiotics that are used to treat any of these various dysrhythmias. The importance of dysrhythmia management in the modern practice of medicine cannot be overstated because dysrhythmias are among the most common causes of preventable sudden cardiac death.30,53 Despite an incomplete understanding of the underlying mechanisms of dysrhythmia formation, an abundance of antidysrhythmics have been developed, each attempting to alter specific electrophysiologic components of the cardiac impulse generating or conducting system. In addition to the predictable, mechanism-based adverse effect of each xenobiotic, unique and often unanticipated effects also occur.96 Experience with overdose of many of these xenobiotics is limited, and management is generally based on the underlying pharmacologic principles, existing case reports, and the experimental literature.


For a long time, antidysrhythmics were considered among the most rational of the available cardiac medications. This well-earned reputation was related to their high efficacy at reducing the incidence of malignant dysrhythmias. Similarly, they are effective at controlling nuisance rhythm disorders. However, this approach changed dramatically after publication of the Cardiac Arrhythmia Suppression Trials (CAST and CAST II)1,3,29 and, more recently, with the rise of mechanical interventions, such as ablation therapy and implantable defibrillators. CAST assessed the ability of three antidysrhythmics to suppress asymptomatic ventricular dysrhythmias known to be harbingers of sudden death. The original CAST study was discontinued in 1989 before completion, when encainide and flecainide not only failed to prevent sudden death but actually increased overall mortality. The CAST II trial noted similar problems with moricizine.1 It has since become clear that the enhanced mortality associated with many antidysrhythmics is a result of their dysrhythmogenic effects and that virtually all xenobiotics of this group carry such a risk.95 More recently, it has been demonstrated that for patients with atrial fibrillation, there is no benefit to rhythm conversion compared with controlling the ventricular response rate.99


This chapter focuses on the xenobiotics that serve primarily as antidysrhythmics that, with the exception of lidocaine, have few other medicinal indications. Chapters 22 and 23 provide a more detailed description of the electrophysiology of dysrhythmias and a discussion of their genesis. In addition, the toxicities from calcium channel blockers and β-adrenergic antagonists, which have indications in addition to dysrhythmia control, are discussed separately in Chapters 60 and 61.


Antidysrhythmics modify impulse generation and conduction by interacting with various membrane sodium, potassium, and calcium ion channels. Generally, antidysrhythmics affect electrophysiologic effects either through alteration of the channel pore or, more commonly, by modification of its gating mechanism (Fig. 63–1).56 Unfortunately, given their exceedingly complex mechanisms of action, the descriptive terms used to explain their molecular actions are not always completely accurate. For example, the description of an antidysrhythmic as a specific "channel blocker," although representative of the ...

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