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Antiarrhythmic therapies

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Abstract

Optimal cardiac function is achieved by a coordinated pattern of cardiac contraction and relaxation that is regulated by electrical activity within the heart. Severe arrhythmias (or the development of an arrhythmia in a patient with already compromised cardiac function) may result in impaired cardiac output, increased filling pressures and increased myocardial work (haemodynamic instability). Less severe arrhythmias may not cause haemodynamic instability; however, some can be a premonitory sign of a more severe arrhythmia or sudden death (electrical instability). The following topics are discussed: Is there a treatable underlying condition?; What are the potential adverse effects of the arrhythmia?; What are the potential effects of antiarrhythmic therapy?; and Therapy for specific arrhythmias.

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Figures

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20.1 Cardiac action potentials.
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20.3 Electrical (DC) cardioversion in a Labrador Retriever with AF. The first four complexes have arrowheads above the QRS complexes, indicating that the device is correctly identifying the R waves. A shock is delivered synchronous with the R wave of the fourth complex. Sinus rhythm ensues, with a ventricular premature complex interpolated between the first and second sinus complex. Note that synchronous mode automatically turns off after the shock is delivered. Lead II shown. Paper speed 25 mm/s; gain 1 cm/mV. (Courtesy of A. Boswood.)
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20.4 Pacemaker pulse generators of various sizes, makes and models. The pulse generator at the top left has two lead connectors (arrowed) to allow dual chamber pacing. The pulse generator on the right is in its sterile package, which includes the key to screw the lead into the lead connector.
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20.5 Pacemaker programmer. A foldable screen and programming magnet are features of all models.
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20.7 Temporary transthoracic pacing in a German Shepherd Dog with third-degree AV block, undergoing general anaesthesia for permanent pacemaker implantation. Pacing electrodes (adhesive pads) are placed on either side of the thoracic wall, over the heart. Cables attached to the pads run to a cardioverter/defibrillator unit .
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20.8 Approach to narrow QRS complex tachycardia in the dog. Use with caution in cases with systolic dysfunction; avoid use in cases with CHF; do not give together. AV = Atrioventricular; SA = Sinoatrial.
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20.9 Vagal manoeuvres. Carotid sinus massage is achieved by applying continuous digital pressure to the region of the carotid sinuses, just caudal to the larynx, to stimulate carotid baroreceptors. Ocular pressure is achieved by applying firm pressure over both globes for approximately 20 seconds.
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20.10 Vagal manoeuvre in atrial tachycardia/flutter: carotid sinus massage in a 2-year-old Bulldog with SVT. Slowing of the ventricular rate after the ninth QRS complex revealed an atrial rate of about 450 beats/minute. By slowing the ventricular rate independently of the atrial rate, an atrial tachycardia was diagnosed. Leads I–III shown. Paper speed 25 mm/s; gain 1 cm/mV.
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20.11 Pharmacological cardioversion of SVT: conversion of an SVT of >300 beats/minute in a 2-year-old Labrador Retriever following two doses of slow intravenous sotalol, each at a dose of 1 mg/kg given 5 minutes apart. Termination of the SVT and conversion to sinus rhythm occurred shortly after the second dose. Previous attempts at conversion with vagal manoeuvres, intravenous diltiazem, esmolol and lidocaine had been ineffective. The dog was subsequently maintained successfully on oral sotalol. An SVT at 350 beats/minute is seen on the top strip. Conversion to sinus rhythm occurs after the eighth complex in the middle strip. Sinus rhythm at 110 beats/minute is maintained on the lower strip. Lead II shown. Paper speed 25 mm/s; gain 0.5 cm/mV.
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20.12 Approach to AF in the dog.
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20.13 Approach to wide QRS complex tachycardia in the dog. Use with caution in cases with systolic dysfunction; avoid use in cases with signs of CHF. Do not give together.
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20.14 Pharmacological cardioversion of ventricular tachycardia: conversion of sustained ventricular tachycardia in a 5-year-old Domestic Shorthaired cat following slow intravenous lidocaine at a dose of 0.5 mg/kg. Ventricular tachycardia at 380 beats/minute is seen on the top strip. Conversion to sinus rhythm occurs two-thirds of the way along the middle strip. Sinus rhythm is maintained on the lower strip. Hypertrophic cardiomyopathy with focal ventricular wall thickening was diagnosed on echocardiography. Oral therapy was continued with sotalol. Lead II shown. Paper speed 25 mm/s; gain 1 cm/mV.
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20.15 Approach to bradyarrhythmias in the dog.

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