Cardiac arrhythmias may originate from many factors, such as the examples listed below (Table 1).
Table 1. Common sources of cardiac arrhythmias.
This short list of arrhythmias is by no means complete. Identification and correction of the underlying causes of arrhythmias
are key to their long-term, successful management. For instance, in a cat with atrial standstill as a result of hyperkalemia
from urethral obstruction, the arrhythmia is best addressed by correction of the underlying problem, hyperkalemia, as primary
antiarrhythmic therapy is generally unsuccessful when such electrolyte abnormalities are present. Despite this caveat, short-term
control of arrhythmias may be necessary while the underlying condition is identified and controlled, such as treatment of
digoxin-associated arrhythmias until the plasma digoxin concentration drops to non-toxic levels. Some underlying diseases,
such as congestive heart failure (CHF), may not be curable whereas other diseases, such as endocarditis, may require prolonged
therapy before the underlying problem can be controlled. Both short-term and chronic therapy with an antiarrhythmic agent
may be warranted in such situations.
Table 2: Phases of the action potential of the cardiac myocyte.
As in all pharmacological interventions, the goal of therapy should be clearly identified from the outset of treatment. In
the case of antiarrhythmic therapy, the goal may include the treatment of an existing arrhythmia or prophylaxis for anticipated
arrhythmias. The use of antiarrhythmic agents for prophylaxis should be considered carefully, as few antiarrhythmic agents
have been approved for use in veterinary medicine, and these agents may have considerable risk associated with their use.
The successful prophylactic use of beta-blocking antiarrhythmic agents in human medicine has stimulated interest in the prevention
of arrhythmias in veterinary patients with conditions that are also associated with sudden death, such as dilated cardiomyopathy.
For example, it is well-established that the strategic use of antiarrhythmic therapy can prolong survival in humans with myocardial
infarction, where nonselective beta-blocker drugs have been shown in large randomized control clinical trials to decrease
mortality.1 Unfortunately, there are few comparable trials in veterinary species. Scientific support for the use of beta-blockers and
other antiarrhythmics in dogs with ventricular tachyarrhythmias is primarily based upon retrospective survival studies, decrease
in the number of arrhythmic episodes per day, and improved quality of life.
Table 3: Prominent phases of the action potential of the pacemaker cells.
A good clinical understanding of the appropriate use of antiarrhythmic therapy depends on a generally knowledge of the electrophysiology
underlying the generation of the cardiac action potential, as most antiarrhythmic drugs work at the level of the relevant
ion channels. The pacemaker cells of the sinoatrial node are responsible for the generation of the normal sinus rhythm. The
sinus node depolarizes, followed by the atrial depolarization wave, atrioventricular nodal conduction, bundle branch conduction,
and ventricular depolarization. The shape of the action potential differs between the cardiac myocytes and pacemaker cells,
reflecting the prominent role that differences in ion channels play in the function of cardiac tissues (Tables 2 & 3).