Page 125 - Small Animal Internal Medicine, 6th Edition

CHAPTER 4 Cardiac Arrhythmias and Antiarrhythmic Therapy 97

Verapamil cats. Ivabradine is metabolized by hepatic cytochrome P450
Verapamil HCl is a phenylalkylamine with potent cardiac enzyme pathways. Dosing at 12-hour intervals appears
VetBooks.ir effects, however it is rarely used now in dogs and cats; diltia- appropriate in healthy cats. The drug should be avoided in
patients with sick sinus syndrome.
zem is far preferred. Verapamil causes dose-related slowing
of the sinus rate and AV conduction. Although it can be
effective for supraventricular and atrial tachycardias, it has ANTICHOLINERGIC DRUGS
important negative inotropic and some vasodilatory effects Atropine and Glycopyrrolate
that can cause cardiac decompensation, hypotension, and Anticholinergic drugs increase sinus node rate and AV
even death in animals with underlying myocardial disease. conduction when vagal tone is increased (see Table 4.2).
If used, a low IV dose is given very slowly; this can be Parenteral atropine or glycopyrrolate is indicated for brady-
repeated at 5- (or more) minute intervals if no adverse effects cardia or AV block induced by anesthesia, CNS lesions, and
have occurred and the arrhythmia persists. Blood pressure certain other diseases or toxicities. Atropine is a competi-
should be monitored because of the potential for hypoten- tive muscarinic receptor antagonist. It is used to determine
sion. Verapamil should not be used in animals with heart whether excess vagal tone is responsible for bradyarrhyth-
failure. Toxic effects of verapamil include sinus bradycardia, mias caused by sinus and/or AV nodal dysfunction via the
AV block, hypotension, reduced myocardial contractility, atropine challenge test (or atropine response test). Response
and cardiogenic shock. Verapamil reduces the renal clear- to atropine challenge is most consistent with IV adminis-
ance of digoxin. tration of 0.04 mg/kg. An ECG is recorded within 5 to 10
minutes after atropine injection. If the heart rate has not
Other Calcium Channel Blockers increased by at least 150%, the ECG is repeated 15 to 20
++
Amlodipine besylate is a dihydropyridine Ca -blocker rec- minutes after atropine injection; sometimes, an initial vago-
ommended as the first-line antihypertensive agent in cats. mimetic effect on the AV node lasts longer than 5 minutes.
It is also used in some hypertensive dogs (see Chapter 11), The normal sinus node response is a rate increase to 150
usually with an ACEI. Amlodipine also is used to provide to 160 beats/min (or >135 beats/min). However, a posi-
additional afterload reduction for dogs with chronic refrac- tive atropine response test may not predict oral anticho-
tory heart failure from mitral valve disease (see Table 3.3). linergic therapy efficacy. Atropine has little to no effect on
Amlodipine is not useful as an antiarrhythmic agent. Nife- bradyarrhythmias caused by intrinsic disease of the sinus or
dipine is another potent vasodilator without antiarrhythmic AV node.
effects. Atropine given by any parenteral route can transiently
exacerbate vagally mediated AV block when the atrial rate
SO-CALLED CLASS V DRUGS increases faster than AV conduction can respond. However,
Digoxin IV administration causes the fastest and most consistent
Digoxin is mainly considered a positive inotropic drug onset and resolution of the exacerbated block, as well as the
(see Chapter 3); however, it also is used to slow the ven- most rapid post-bradycardia heart rates, compared with the
tricular response rate (heart rate in animals with AF). IM and SC routes. Unlike atropine, glycopyrrolate does not
Digoxin also can suppress some supraventricular prema- have centrally mediated effects and its effects are longer
ture depolarizations. These effects are mediated by the lasting than those of atropine.
drug’s enhancement of parasympathetic tone, which mainly
affects the SA and AV nodes and atrial tissue, and its direct Oral Anticholinergic Drugs
effects that prolong AV nodal conduction and refractory Some animals that respond to parenteral atropine or glyco-
period. pyrrolate will also respond to an oral anticholinergic agent.
Clinical signs may be relieved in these animals, at least
Ivabradine for a time. Nevertheless, most animals with symptomatic
Ivabradine is a selective sinus node “funny” current (I f ) bradyarrhythmias eventually require permanent pacemaker
inhibitor that causes a dose-related slowing of heart rate. It implantation to effectively control heart rate. Propanthe-
has minimal effect on other ion channels and cardiac line bromide and hyoscyamine sulfate are commonly
mechanical function. Heart rate reduction can reduce myo- used, but other oral anticholinergic agents also are avail-
cardial oxygen requirement and improve coronary perfu- able. Individual dosage is adjusted to effect. Oral absorp-
sion. Ivabradine could prove useful for heart rate control in tion of propantheline is variable; food may decrease drug
cats with cardiomyopathy or animals with heart failure and absorption.
persistent sinus tachycardia despite reasonable control of Vagolytic drugs can aggravate paroxysmal supraventricu-
congestive signs. However, currently there is little clinical lar tachyarrhythmias (as in sick sinus syndrome) and should
veterinary experience with this agent. Ivabradine and its be used only cautiously as chronic therapy in those patients.
major active metabolite appear to reach peak plasma con- Other adverse effects of anticholinergic therapy include
centrations in ~1 hour after oral dosing in dogs and cats, vomiting, dry mouth, constipation, keratoconjunctivitis
with peak negative chronotropic effect in ~3 hours. Plasma sicca, increased intraocular pressure, and drying of respira-
half-life of ivabradine is ~2 hours in dogs and ~3.5 hours in tory secretions.