Introduction:
In veterinary medicine pharmacologic treatment to control or convert arrhythmias is the most common method employed. Drugs
chosen are often limited to clinicians' experience and comfort level and drug availability. Appropriate pharmacologic management
of patients with cardiac rhythm disturbances is often successful but these drugs are not without downsides some of which are
lethal in nature. These problems include (but are not limited to) the narrow toxic to therapeutic ratio of some drugs.
Many of these agents have negative inotropic effects that limit there use in patients with systolic dysfunction; inhibition
of normal sinus function, pro-arrhythmic effects, arrhythmias are or become refractory to appropriate drug therapies. When
pharmacologic therapy fails or is inappropriate for a given case, clinicians should be aware of other options that clients
may avail their animals to.
Arrhythmogenesis and Pharmacologic therapy review:
As a matter of review arrhythmias can be caused by abnormalities of impulse initiation, impulse conduction or both. Conduction
abnormalities commonly result in conduction delays and blocks with resultant bradycardia but can also become an important
contributor to the formation of tachyarrhythmias. Abnormalities of impulse formation can produce both bradyarrhythmias and
tachyarrhythmias. General these mechanisms result in abnormal automaticity (including enhanced or depressed normal automaticity),
triggered activity or reentry phenomena (considered the most common cause).
Disorders of impulse conduction: Conduction abnormalities may lead to bradyarrhythmias secondary to conduction delays or blocks within the specialized conduction
system. Such failures within this system result in sinus node exit block, second or third-degree atrioventricular (AV) block
and bundle branch block. Conduction blocks can occur in myocardial tissues damaged by ischemia, infarction, stretch, or drug
toxicity. High vagal tone can result in slowed SA nodal discharge or block at the AV node. Lack of impulse conduction may
also lead to tachyarrhythmias as conduction through abnormal or diseased cardiac tissue may behave very differently than through normal cardiac tissue
that could result in a condition termed
reentry
. Normally in sinus rhythm the atria and ventricles are activated in a specific and relatively constant pattern where each
impulse dies as the wave-front reaches its limits. If re-entrant activation occurs, the propagating impulse does not die out
in the usual way and persists to re-excite the chambers of the heart in a cyclic pattern after the end of the refractory period.
There are two necessary conditions for classic re-entry to occur; (1) unidirectional conduction block of the impulse, and
(2) slow conduction (relative to refractoriness of the surrounding cardiac cells). Re-entry is thought to be the most common cause of tachyarrhythmias and can exist as functional re-entry or anatomical re-entry.
Disorders of impulse formation encompass enhanced or depressed impulse formation by normal pacemaker cells and abnormal impulse
formation by cells that are normally not automatic in nature. Depression in normal automaticity results in a decrease in the
discharge rate of an automatic site (often from increased vagal tone or diseased automatic cells) is manifested as bradyarrhythmias.
In contrast enhanced automaticity results in tachyarrhythmias. Sinus tachycardia as the best example is caused enhanced output
from the sinus node. Other automatic tissues (subsidiary pacemakers) may be enhanced and usurp control of the heart's rhythm
thus presenting as premature complexes.
Abnormal automaticity thought to be an important cause of atrial and ventricular arrhythmias originating from working myocardial
cells that lack automaticity under normal circumstances. It can develop after damage to the cardiac tissue secondary to ischemia,
stretch, or drug toxicity. Triggered Activity occurs only if the pacemaker has previously been driven by an appropriate action potential or series of action potentials.
Thus in contrast to automatic rhythms, triggered rhythms occur only after an initiating beat that produces depolarizing afterpotentials.
These afterpotentials are classified into two subgroups:
Early Afterdepolarizations (EADs) occur during either phase 2 or phase 3 of the normal action potential. These interrupt
repolarization and the action potential oscillates to a threshold and depolarizes the cell. In general, conditions that prolong
the action potential duration will tend to increase the amplitude of EADs and thus the likelihood of triggering from the plateau
leve and tend to occur in conditions that slow heart rate/conduction significantly and can be abolished by very short action
potential cycles.
