Page 110 - Small Animal Internal Medicine, 6th Edition

82 PART I Cardiovascular System Disorders

conduction and increase refractoriness. Another approach is Besides their expense, antiarrhythmic drugs can have serious
IV amiodarone or procainamide. Digoxin is not used in adverse effects, can provoke additional arrhythmias (proar-
VetBooks.ir cases with preexcitation. Although it slows AV conduction, rhythmic effects), and may not be efficacious. Pretreatment
and posttreatment 24- to 48-hour ambulatory ECG record-
it can accelerate conduction in the accessory pathway and
provoke ventricular tachycardia or fibrillation. Procainamide
frequency provide the best indicator of a drug’s efficacy in
and quinidine may prevent AVRT because they lengthen the ings showing at least a 70% to 80% reduction in arrhythmia
refractory period of the accessory pathway. Although high- suppressing an arrhythmia. Intermittent ECG recordings
dose procainamide, with or without a β-blocker or diltiazem, cannot truly differentiate between drug effect (or lack
has prevented recurrent tachycardia in some cases, oral pro- thereof) and the spontaneous, marked variability in arrhyth-
cainamide is no longer available in the United States. Intra- mia frequency that occurs commonly. However, in-hospital
cardiac electrophysiologic mapping and catheter ablation of ECG recordings of 15 seconds to several minutes in duration
accessory pathways have been used successfully to abolish often are used as a pragmatic, if not thorough, attempt to
refractory AVRT in dogs, although this technique is not monitor arrhythmias.
widely available. Several factors influence the decision to use ventricular
Atrial tachycardia caused by a persistent automatic ectopic antiarrhythmic drug therapy. These factors include the
focus can be particularly difficult to suppress. If the antiar- nature of the animal’s underlying disease, the perceived
rhythmic strategies outlined in the preceding paragraphs are severity of the arrhythmia, and evidence of hemodynamic
unsuccessful, the goal of therapy shifts to ventricular rate compromise. Diseases such as DCM, arrhythmogenic right
control. By prolonging AV conduction time and refractori- ventricular cardiomyopathy (ARVC), HCM, and subaortic
ness, fewer atrial impulses are conducted, and ventricular stenosis, among others, frequently are associated with sudden
rate is slowed (and often becomes irregular). Therapy with death from arrhythmias. Therefore ventricular antiarrhyth-
combinations of diltiazem or a β-blocker and digoxin, mic therapy would appear most urgent in animals with these
sotalol, or amiodarone can be effective. The animal with diseases. However, the efficacy of a particular therapy to
persistent automatic atrial tachycardia could be a candidate prolong survival and suppress the arrhythmia is difficult to
for a cardiac ablation procedure, if available. Alternatively, accurately assess. Traditional guidelines for instituting ven-
heart rate control could be achieved by AV node ablation tricular antiarrhythmic therapy have been based on fre-
with permanent pacemaker implantation. quency, prematurity, and variability of the QRS configuration
Vagal maneuver of the arrhythmia. Characteristics thought to imply increased
A vagal maneuver can help the clinician differentiate electrical instability include rapid paroxysmal or sustained
among tachycardias caused by an ectopic automatic focus, ventricular tachycardia, multiform (polymorphic) VPC con-
those dependent on a reentrant circuit involving the AV figuration, or close coupling of VPCs to preceding complexes
node, or excessively rapid sinus node activation. The vagal (R-on-T phenomenon). However, clear evidence that these
maneuver may transiently slow or intermittently block AV guidelines predict greater risk of sudden death in all patients
conduction, exposing abnormal P′ waves, and thus allow an is lacking. It is probably more important to consider the
ectopic atrial focus to be identified. Vagal maneuvers can animal’s underlying heart disease and whether the arrhyth-
terminate reentrant SVTs involving the AV node by inter- mia is causing signs of hypotension or low cardiac output.
rupting the reentrant circuit. The maneuver tends to tempo- Animals that are hemodynamically unstable or have a disease
rarily slow the rate of sinus tachycardia. associated with sudden cardiac death are treated earlier and
A vagal maneuver is performed either by firmly massag- more aggressively.
ing the area over the carotid sinuses (below the mandible in Acute therapy for ventricular tachycardia
the jugular furrows) or by applying firm bilateral ocular pres- Sustained ventricular tachycardia should be treated
sure for 15 to 20 seconds. Although initial attempts often are aggressively because it can lead to marked decrease in arte-
unsuccessful, repeating the vagal maneuver after antiar- rial blood pressure, especially at faster rates. Lidocaine (IV)
rhythmic drug injection may be more effective. Diltiazem, a generally is the first-choice drug for controlling serious ven-
β-blocker, digoxin, and other agents can increase a vagal tricular tachyarrhythmias in dogs. It is effective against
maneuver’s effect. The maneuver can be potentiated further arrhythmias caused by several underlying mechanisms and
in dogs by administering intramuscular (IM) morphine has minimal adverse hemodynamic effects. Because the
sulfate (0.2 mg/kg) or IV edrophonium chloride (but have effects of an IV lidocaine bolus last only about 10 to 15
atropine and an endotracheal tube readily available). minutes, constant-rate infusion (CRI) is warranted if the
drug is effective. Small supplemental IV boluses can be given
Ventricular Tachyarrhythmias in addition to the CRI, if needed, to maintain therapeutic
Occasional VPCs in an otherwise asymptomatic animal are drug concentrations until steady state is achieved. IV infu-
not treated. Moderately frequent single VPCs generally do sion can be continued for several days, if necessary. When
not require antiarrhythmic drug treatment either, if underly- lidocaine is ineffective even at maximal recommended doses,
ing heart function is reasonably normal. However, specific several other strategies can be tried (Fig. 4.3).
guidelines as to whether, when, and how best to treat inter- IV amiodarone, oral sotalol, or oral mexiletine can be
mittent ventricular tachyarrhythmias remain undefined. more effective in some cases. When using IV amiodarone,