Page 112 - Small Animal Internal Medicine, 6th Edition

84 PART I Cardiovascular System Disorders

or atenolol with procainamide or lidocaine) or a class IA Frequent reevaluation is important for patients on long-
drug with a IB drug (such as procainamide with lidocaine term antiarrhythmic therapy (for any rhythm disturbance).
VetBooks.ir 4. Maximize the dose of the antiarrhythmic drug having the When possible, continuous 24- to 48-hour ambulatory ECG
or mexiletine).
recordings are most accurate for assessing efficacy. Although
greatest effect.
5. Consider the possibility that the drug therapy is exacer- clearly not an ideal strategy, the patient’s owner also can be
shown how to use a stethoscope or palpate the chest wall to
bating the rhythm disturbance (proarrhythmia). Poly- count the number of “skipped” beats per minute at home to
morphic ventricular tachycardia (torsades de pointes) has approximate the frequency of arrhythmic events (either
been associated with quinidine, procainamide, and other single or paroxysms). The decision to continue or discon-
drug toxicities. tinue successful antiarrhythmic therapy also is based on con-
6. MgSO 4 may be effective in animals with ventricular sideration of the clinical situation and any underlying cardiac
tachyarrhythmias associated with digoxin toxicity or with disease.
suspected polymorphous ventricular tachycardia (tors-
ades de pointes). A slowly administered IV bolus of 25 to Atrial Fibrillation
40 mg/kg, diluted in D 5 W, followed by an infusion of the AF most often develops when there is marked atrial enlarge-
same dose over 12 to 24 hours, has been suggested. Given ment. It is a serious arrhythmia, especially when the ven-
that MgSO 4 contains 8.13 mEq magnesium per gram, a tricular response rate is high. Predisposing conditions
similar magnesium dose is provided by calculating 0.15 include DCM, advanced degenerative mitral valve disease,
to 0.3 mEq/kg. congenital malformations that cause atrial enlargement, and
7. If the animal is tolerating the arrhythmia well, continue hypertrophic or restrictive cardiomyopathy in cats. Clinical
supportive care, correct other abnormalities as possible, heart failure is common in these animals. AF is characterized
and continue cardiovascular monitoring alone or with the by an irregular and usually rapid ventricular response rate.
most effective antiarrhythmic drug. When little time is available for ventricular filling, stroke
8. Direct current (DC) cardioversion or ventricular pacing volume is compromised. Furthermore, atrial contraction
may be available at some centers; ECG-synchronized (the “atrial kick”), which is especially important to ventricu-
equipment and anesthesia or sedation are required. High- lar filling at faster heart rates, is lost. In patients with under-
energy, nonsynchronized shock (defibrillation) can be lying cardiac dysfunction, cardiac output tends to decrease
used for rapid polymorphic ventricular tachycardia or considerably when AF develops. Therefore it is important to
flutter degenerating into fibrillation. control the ventricular response rate (i.e., the heart rate) as
soon as possible.
Chronic oral therapy for Long-lasting conversion to sinus rhythm is uncommon in
ventricular tachyarrhythmias the face of marked underlying cardiac disease, even after
The same drug that was most effective during acute successful electrical cardioversion. Therefore treatment in
therapy, or a similar one, often is continued orally when most cases is directed at reducing the ventricular response
longer-term therapy is necessary. Although suppression of rate by slowing AV conduction (Fig. 4.4). A slower heart rate
ventricular ectopy is one aim, reducing the risk of sudden allows more time for ventricular filling and lessens the rela-
arrhythmic death is the main goal for long-term therapy. tive importance of atrial contraction. In-hospital heart rates
Whereas the class IB drugs (lidocaine and mexiletine) appear of fewer than 150 (or <180 in cats) beats/min are desirable.
to raise the fibrillation threshold more than the class IA The patient’s ventricular rate should be documented by ECG
agents (procainamide and quinidine), class III agents appear recording; counting the heart rate by auscultation or palpa-
to have greater antifibrillatory effects than the class I drugs. tion can be highly inaccurate in animals with AF. Resting
Concurrent disease should be treated as thoroughly as possi- heart rate at home, which some owners can monitor, is a
ble. It is likely that animals with arrhythmias associated with better indicator of drug effectiveness. Heart rates of 70 to 110
underlying heart disease also benefit from β-blocker, ACEI, beats/min in dogs and 80 to 140 beats/min in cats are prob-
and other therapies, as do people. However, β-blockers alone ably acceptable.
do not appear effective in suppressing ventricular tachyar- Therapy for atrial fibrillation
rhythmias in Doberman Pinschers with cardiomyopathy. When the heart rate exceeds 180 to 200 beats/min at rest,
Fish oil (omega-3 fatty acid) supplements appear to reduce especially in the setting of heart failure, it is important to
the frequency of VPCs in Boxers with ARVC and possibly expediently reduce the ventricular rate. IV diltiazem acts
in other patients as well. more quickly than oral dosing, but caution must be used
Several strategies are used for long-term oral therapy of especially in patients with DCM because the drug has nega-
patients with ventricular tachyarrhythmias. Presently, the tive inotropic effects. Tiny doses are used if given IV, along
most favored options include sotalol, mexiletine with ateno- with immediate institution of pimobendan therapy (if not
lol, mexiletine with sotalol, or amiodarone. These are likely currently being given). Blood pressure, as well as heart rate,
to provide a greater antifibrillatory effect than class I agents should be monitored. A more conservative approach is to
alone. The potential for serious adverse effects with long- use oral loading dose(s) of diltiazem, although the onset of
term or high-dose use must be considered. effect is more gradual. Diltiazem’s negative inotropic effect is