The drugs used most commonly in veterinary practice to treat ventricular arrhythmias are the Class I drugs (local anaesthetic agents) and the Class II drugs (beta-adrenoceptor antagonists). Site shows the ways in which these drugs interfere with the pathological mechanisms involved in arrhythmogenesis. Since the mechanisms involved in the generation of most ventricular arrhythmias cannot be determined from the surface ECG, the choice of drug remains empirical and trial therapy is essentially the only way by which the efficacy of a particular drug can be assessed.
Lignocaine is a Class 1b anti-arrhythmic agent and seems to have the advantage of showing selective suppressant action on damaged and ischaemic cardiac muscle cells with a less negative resting membrane potential while having little or no effect on the automaticity of atria I and normal ventricular myocardial tissue. In most cases. Therefore, it is the first drug of choice for treating serious ventricular arrhythmias. It is essential to ensure preparations of lignocaine without adrenaline are used. Lignocaine is administered as an intravenous bolus injection (given over 1-2 min) at a dose rate of 2 mg kg-1 in the dog and 0.5-1 mg kg-1 in the cat initially. Further boluses may be given (up to 6 mg kg-1 total dose in the dog) if no response is seen initially. Lignocaine toxicity can result in seizures which may be controlled with diazepam. If the plasma potassium concentration is normal, lignocaine will, in most cases, successfully suppress the arrhythmia or at least reduce the frequency of VPCs. A more sustained effect can be achieved by continuous intravenous infusion of lignocaine at a rate of 30-80 μg kg-1 min-1 in the dog and 10-20 μg kg-1 min-1 in the cat. Orally active Class 1b drugs are available and have been shown to be elfective in longer-term therapy (tocainide at a dose of 10-20 mg kg-1 tid, for example).
If lignocaine is not successful, procainamide (Class 1a agent) would be the next drug to try at a dose rate of 5-15 mg kg-1 intravenously or intramuscularly. In an intensive care setting, procainamide can be given by continuous intravenous infusion at a dose of 25-40 μg kg-1 min-1. Oral procainamide can be administered at 10-20 mg kg-1 every 6 h for longer-term therapy. In some cases, administration of propranolol (0.25—1 mg kg-1 orally or 0.1 mg kg-1 intravenously) with lignocaine or procainamide may provide a synergistic effect. Caution must be exercised when using these agents, particularly by the intravenous route, as they all possess the ability to reduce myocardial contractility. In addition, propranolol will reduce the clearance of lignocaine from the circulation, thus potentiating the toxicity of lignocaine, hence the need to reduce the dose of lignocaine if combined with propranolol.
The goals of drug therapy for ventricular arrhythmias should be an improvement of the animal’s haemodynamic status and a reduction in the frequency of VPCs. If this can be achieved and if the underlying disease can be successfully resolved, the need for drug therapy should also disappear. If the underlying problem is not amenable to treatment, long-term drug therapy may be necessary. There is no evidence that anti-dysrhythmic drugs used under these circumstances will prolong the duration of the animal’s life but the quality of life may improve if the frequency and duration of syneopal attacks are reduced. Unfortunately, it is equally possible that some arrhythmias can be worsened by long-term administration of anti-arrhythmic drugs. The significance and incidence of worsening of arrhythmias by the drugs used to treat them can only be assessed by studies which use continuous ambulatory ECG monitoring. The use of two drugs with different mechanisms of action (such as propranolol and procainamide) may produce a synergistic effect. This may allow a reduction in the dosage of the two agents used, which is beneficial since it should reduce the side effects of the drugs, including their pro-arrhythmogenic potential.