Page 105 - Small Animal Internal Medicine, 6th Edition

CHAPTER 4
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Cardiac Arrhythmias and

Antiarrhythmic Therapy

GENERAL CONSIDERATIONS disease. Genetic factors and environmental stresses contrib-
ute to this. However, additional triggering (such as a prema-
Cardiac arrhythmias occur for many reasons. Although ture stimulus or abrupt change in heart rate) and/or
some arrhythmias are of no clinical consequence, others modulating factors (such as changes in autonomic tone, cir-
cause serious hemodynamic compromise and sudden death, culating catecholamines, ischemia, or electrolyte distur-
especially in animals with underlying heart disease. It is bances) are thought to be necessary to provoke and sustain
important to make an accurate electrocardiographic diagno- a rhythm disturbance. For example, episodes of anger or
sis, as well as to consider the arrhythmia’s clinical context, aggressive behavior have been linked to increased suscepti-
before deciding whether to use antiarrhythmic therapy. For bility to ischemic arrhythmias and sudden arrhythmic death
example, the risk of death associated with ventricular in both dogs and people. Various stresses that lead to abnor-
tachyarrhythmias is higher in people when myocardial func- mal cardiac remodeling also could play a role in arrhythmia
tion is impaired. Dogs with cardiomyopathy also are known development. Remodeling can involve myocyte hypertrophy,
to have increased risk for sudden death, especially Dober- changes in the structure or function of ion channels, tissue
man Pinschers and Boxers. In addition, an inherited disorder fibrosis, and other changes related to neurohormonal activ-
predisposing to sudden death has been identified in young ity, cytokines, and other signaling systems (see Chapter 3).
German Shepherds. On the other hand, the ventricular pre- Although some of these changes act as positive compensa-
mature activity that occurs commonly after thoracic trauma tory mechanisms in the short term, they can have harmful
or splenectomy in previously healthy animals (see p. 41) and arrhythmogenic long-term effects. It is thought that if
usually is benign and resolves without therapy. such underlying arrhythmogenic modulators could be con-
Occasional ventricular premature complexes (VPCs) trolled or reduced, arrhythmias would be lessened. The
occur without consequence in many animals. However, higher survival in human heart failure patients treated with
arrhythmias that compromise cardiac output and coronary angiotensin-converting enzyme inhibitors (ACEI), spirono-
perfusion promote myocardial ischemia, hypotension, lactone, and some β-blockers supports this concept. There is
reduced cardiac pump function, and sometimes sudden similar evidence for ACEIs in dogs with dilated cardiomy-
death. These arrhythmias tend to be either quite rapid (such opathy (DCM) and reason to suspect that other therapies
as sustained ventricular or supraventricular tachyarrhyth- might be beneficial as well.
mias) or slow (such as advanced atrioventricular [AV] block
with a slow or unstable ventricular escape rhythm). Some- APPROACH TO ARRHYTHMIA
times, however, a lethal arrhythmia such as ventricular MANAGEMENT
fibrillation (VF) occurs without an antecedent sustained Specific antiarrhythmic drug therapy may or may not be
arrhythmia. Sustained tachycardia of either supraventricular warranted in an individual patient (see guidelines later). If
or ventricular origin reduces cardiac output acutely, and antiarrhythmic therapy is pursued, it should be with defined
eventually (within weeks) it leads to myocardial dysfunction goals in mind. For example, usually an immediate goal is to
and congestive heart failure (CHF). restore hemodynamic stability. Although ideal goals might
include conversion to sinus rhythm, correction of underly-
DEVELOPMENT OF ARRHYTHMIAS ing cause, and prevention of further arrhythmia and sudden
Multiple factors underlie cardiac rhythm disturbances. death, suppression of all abnormal beats generally is not
Abnormalities of conduction or automaticity caused by a realistic goal. Successful therapy could mean sufficient
cardiac structural or pathophysiologic remodeling can pre- reduction in frequency (e.g., by ≥70%-80%) or repetitive
dispose to arrhythmias, even in the absence of overt cardiac rate of ectopic beats to eliminate clinical signs. It must be

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