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