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14 Agents Used in Cardiac
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Arrhythmias

Robert D. Harvey, PhD,
& Augustus O. Grant, MD, PhD *

C ASE STUD Y

A 69-year-old retired teacher presents with a 1-month history ensuing month, she continues to have intermittent palpita-
of palpitations, intermittent shortness of breath, and fatigue. tions and fatigue. Continuous ECG recording over a 48-hour
She has a history of hypertension. An electrocardiogram period documents paroxysms of atrial fibrillation with heart
(ECG) shows atrial fibrillation with a ventricular response of rates of 88–114 bpm. An echocardiogram shows a left ven-
122 beats/min (bpm) and signs of left ventricular hypertrophy. tricular ejection fraction of 38% (normal ≥ 60%) with no
She is anticoagulated with warfarin and started on sustained- localized wall motion abnormality. At this stage, would you
release metoprolol, 50 mg/d. After 7 days, her rhythm reverts initiate treatment with an antiarrhythmic drug to maintain
to normal sinus rhythm spontaneously. However, over the normal sinus rhythm, and if so, what drug would you choose?

Cardiac arrhythmias are a common problem in clinical practice, describes the pharmacology of drugs that suppress arrhythmias
occurring in up to 25% of patients treated with digitalis, 50% of by a direct action on the cardiac cell membrane. Other modes
anesthetized patients, and over 80% of patients with acute myo- of therapy are discussed briefly (see Box: The Nonpharmacologic
cardial infarction. Arrhythmias may require treatment because Therapy of Cardiac Arrhythmias, later in the chapter).
rhythms that are too rapid, too slow, or asynchronous can reduce
cardiac output. Some arrhythmias can precipitate more serious ELECTROPHYSIOLOGY OF NORMAL
or even lethal rhythm disturbances; for example, early premature
ventricular depolarizations can precipitate ventricular fibrilla- CARDIAC RHYTHM
tion. In such patients, antiarrhythmic drugs may be lifesaving.
On the other hand, the hazards of antiarrhythmic drugs—and in The electrical impulse that triggers a normal cardiac contraction orig-
particular the fact that they can precipitate lethal arrhythmias in inates at regular intervals in the sinoatrial (SA) node (Figure 14–1),
some patients—have led to a reevaluation of their relative risks usually at a frequency of 60–100 bpm. This impulse spreads
and benefits. In general, treatment of asymptomatic or minimally rapidly through the atria and enters the atrioventricular (AV)
symptomatic arrhythmias should be avoided for this reason. node, which is normally the only conduction pathway between
Arrhythmias can be treated with the drugs discussed in this the atria and ventricles. Conduction through the AV node is slow,
chapter and with nonpharmacologic therapies such as pacemakers, requiring about 0.15 seconds. (This delay provides time for atrial
cardioversion, catheter ablation, and surgery. This chapter contraction to propel blood into the ventricles.) The impulse then
propagates down the His-Purkinje system and invades all parts
of the ventricles, beginning with the endocardial surface near the
* apex and ending with the epicardial surface at the base of the
The authors thank Joseph R. Hume, PhD, for his contributions to
previous editions. heart. Activation of the entire ventricular myocardium is complete
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