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Cardiac arrhythmias reduce cardiac output and commonly occur in the presence of preexisting heart disease. They are the most common cause of death in patients who have had a myocardial infarction, and over 80% of patients with an acute myocardial infarction have arrhythmias. Cardiac arrhythmias also occur in up to 25% of patients treated with digitalis and in 50% of anesthetized patients. Patients with electrolyte imbalances also demonstrate arrhythmias, and diuretics are significant sources of such imbalances. Arrhythmias may require treatment because of rhythms that are too rapid, too slow, or asynchronous. Some arrhythmias may precipitate more serious or even lethal rhythm disturbances. For example, premature ventricular contractions (PVCs) can precipitate ventricular fibrillation, which is fatal unless corrected promptly. In such patients, antiarrhythmic drugs may be lifesaving. In contrast, pharmacologic treatment of asymptomatic or minimally symptomatic arrhythmias is avoided until clinically necessary because of the ability of many of these drugs themselves to induce lethal arrhythmias. In this chapter, we will review the conduction sequence and electrophysiology of normal cardiac rhythm, highlight the mechanisms of arrhythmias, and discuss the antiarrhythmic drugs used in their treatment.

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The most widely used classification of antiarrhythmic drugs recognizes four classes (Figure 10–1) and is based on their mechanisms of action. These mechanisms are blockade of sodium channels (class I), blockade of cardiac β receptors (class II), blockade of potassium channels (class III), and blockade of calcium channels (class IV). A fifth group of miscellaneous antiarrhythmic drugs with no single mechanism of action is also recognized.

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Figure 10–1.
Graphic Jump Location

Classes of drugs used in the treatment of cardiac arrhythmias. They comprise four major classes and an additional miscellaneous group.

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Cardiac Electrical Conduction Pathway

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The electrical impulse that triggers a normal cardiac contraction originates at regular intervals in the sinoatrial (SA) pacemaker node (Figure 10–2), usually at a frequency of 60 to 100 beats per minute. This impulse spreads rapidly through the atria and enters the atrioventricular node (AV), which is normally the only conduction pathway between the atria and ventricles. Conduction through the AV node is slow, requiring about 0.15 second. This delay provides time for atrial contraction to propel blood into the ventricles. The impulse then propagates over the His-Purkinje system and invades all parts of the ventricles. Ventricular activation is complete in less than 0.1 second; therefore, contraction of all of the ventricular muscle is synchronous and hemodynamically effective. A comparison of this cardiac electrical activity to the electrocardiogram is presented in Figure 10–2. Arrhythmias consist of cardiac depolarizations that deviate from the above description in one or more aspects; that is, there is an abnormality in the site of origin of the impulse, its rate or regularity, or its conduction.

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