Page 117 - Small Animal Internal Medicine, 6th Edition

CHAPTER 4 Cardiac Arrhythmias and Antiarrhythmic Therapy 89

TABLE 4.1
VetBooks.ir Classification and Effects of Antiarrhythmic Drugs MECHANISM AND ECG EFFECTS

DRUG
CLASSIFICATION
+
Class I Decreases fast inward Na current; membrane-stabilizing effects
(decreased conductivity, excitability, and automaticity)
IA Quinidine Moderately decreases conductivity, increases action potential duration;
Procainamide can prolong QRS complex and Q-T interval
IB Lidocaine Little change in conductivity, decreases action potential duration; QRS
Mexiletine complex and Q-T interval unchanged
Phenytoin
IC Flecainide Markedly decreases conductivity without change in action potential
Propafenone duration
Class II Atenolol β-adrenergic blockade—reduces effects of sympathetic stimulation (no
Propranolol direct myocardial effects at clinical doses)
Esmolol
Metoprolol
Carvedilol
Others
Class III Sotalol Selectively prolongs action potential duration and refractory period;
Amiodarone antiadrenergic effects; Q-T interval prolonged
Ibutilide
Dofetilide
Others
Class IV Verapamil Decreases slow inward Ca current (greatest effects on SA and AV
++
Diltiazem nodes)
Others
Other Antiarrhythmic Agents Digoxin Antiarrhythmic action results mainly from indirect autonomic effects
(especially increased vagal tone)
Atropine Anticholinergic agents oppose vagal effects on SA and AV nodes
Glycopyrrolate (glycopyrrolate and other drugs also have this effect)
Others

AV, Atrioventricular; ECG, electrocardiogram; SA, sinoatrial.

Lidocaine However, toxic concentrations of lidocaine can cause
Lidocaine HCl generally is the first-choice IV ventricu- hypotension.
lar antiarrhythmic agent in dogs. It usually is not effective Lidocaine undergoes rapid hepatic metabolism by cyto-
against supraventricular arrhythmias, with the exception chrome P-450 (CYP) enzyme activity; some metabolites
of some recent-onset, vagally induced AF or tachycardias. might contribute to its antiarrhythmic and toxic effects.
At recommended doses, it has little effect on sinus node Lidocaine is not effective orally because of its virtually com-
rate, AV conduction, and refractoriness. Lidocaine sup- plete first-pass hepatic elimination. IV administration,
presses automaticity in normal Purkinje fibers and dis- usually as slow boluses followed by CRI, is most effective.
eased myocardial tissue, slows conduction, and reduces the Antiarrhythmic effects after IV bolus occur within 2 minutes
supernormal period (during which the cell can be reex- and abate within 10 to 20 minutes. CRI without a loading
cited before complete repolarization occurs). It has greater dose produces steady-state concentrations in 4 to 6 hours.
effects on diseased and hypoxic cardiac cells and at faster The half-life is less than 1 hour in the dog. An initial bolus
stimulation rates. The electrophysiologic effects of lido- of 2 mg/kg is used in dogs and can be repeated two to three
caine are influenced by extracellular potassium concentra- times if necessary. Lower doses should be used in cats to
tion. Hypokalemia may render the drug ineffective, and avoid toxicity (loading dose of 0.25-0.5 mg/kg slowly IV).
hyperkalemia intensifies its depressant effects on cardiac The half-life in cats is 1 to 2 hours. Therapeutic plasma con-
membranes. Lidocaine produces little or no depression centrations are thought to range from 1.5 to 6 µg/mL in
of contractility at therapeutic doses when administered dogs. Only lidocaine without epinephrine should be used for
slowly IV. The lidocaine congener mexiletine similarly pro- antiarrhythmic therapy. If IV access is not possible, IM
duces minimal negative inotropic and hypotensive effects. administration could be used but is less effective.