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An arrhythmia can be broadly defined as any significant deviation from normal cardiac rhythm.1 Various problems in the origination and conduction of electrical activity in the heart can lead to distinct types of arrhythmias. If untreated, disturbances in normal cardiac rhythm result in impaired cardiac pumping ability, and certain arrhythmias are associated with cerebrovascular accidents, cardiac failure, and other sequelae that can be fatal.2,3 Fortunately, a variety of drugs are available to help establish and maintain normal cardiac rhythm.

This chapter presents the primary antiarrhythmic drugs and therapeutic rationale for their use. As indicated throughout this chapter, antiarrhythmic drugs are associated with many side effects, including an increased chance of arrhythmias (pro-arrhythmic effect). Hence, the overall use of these drugs has declined somewhat in recent years, due largely to the development of nonpharmacological interventions such as implantable defibrillator devices and surgical interventions that offer a more permanent solution to rhythm disturbances.4 Nonetheless, antiarrhythmic drugs remain a primary option for many patients with arrhythmias or as an adjunct to maintain normal rhythm after cardiac surgery.

Therapists will encounter patients taking arrhythmic agents in all practice settings. These drugs may offer the opportunity to engage in more strenuous exercise and functional activities by stabilizing heart rate. However, these drugs can produce abnormal heart rate and blood pressure responses in certain patients, and you may be in an ideal position to identify these untoward responses before they produce severe adverse reactions. Consequently, you should have some knowledge of the clinical use of these drugs.

To understand how antiarrhythmic drugs exert their effects, the chapter begins with a review on the origin and spread of electrical activity throughout the heart (cardiac electrophysiology). This is followed by a presentation of the basic mechanisms responsible for producing disturbances in cardiac rhythm and the common types of arrhythmias seen clinically. Finally, antiarrhythmic drugs are presented according to their mechanism of action and clinical use.


Cardiac Action Potentials

The action potential recorded from a cardiac Purkinje fiber is shown in Figure 23-1. At rest, the interior of the cell is negative relative to the cell’s exterior. As in other excitable tissues (neurons, skeletal muscle), an action potential occurs when the cell interior suddenly becomes positive (depolarizes), primarily because of sodium ion influx. The cell interior then returns to a negative potential (repolarizes), primarily because of the efflux of potassium ions. The cardiac action potential has several features that distinguish it from action potentials recorded in other nerves and muscles.5,6 The cardiac action potential is typically divided into several phases. The ionic movement that occurs in each phase is outlined here.

Figure 23-1

The cardiac action potential recorded from a Purkinje cell. The effective refractory period is the time during which the cell cannot be ...

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