Treatment of Cardiac Arrhythmias and Conduction Disturbances

Chapter 16 Treatment of Cardiac Arrhythmias and Conduction Disturbances



Marc S. Kraus, Anna R.M. Gelzer, Sydney Moise



INTRODUCTION TO TREATMENT OF CARDIAC ARRHYTHMIAS


Cardiac arrhythmias are defined as variations of the cardiac rhythm from normal sinus rhythm. Some cardiac arrhythmias are benign and clinically insignificant and require no specific therapy whereas other arrhythmias may cause severe clinical signs such as syncope or degenerate into malignant arrhythmias (i.e., ventricular fibrillation [VF]) leading to cardiac arrest and sudden death. The goal of this section is to discuss treatment strategies for management of arrhythmias.



General Remarks


Antiarrhythmic drugs commonly target two general areas of the heart due to their specific electrophysiologic properties:


• Sinoatrial and Atrioventricular (AV) nodal tissue: Depolarization is calcium channel driven. To treat arrhythmias that originate from the sinoatrial and AV nodal tissue calcium channel blockers (CCB) and beta blockers (BBs) are primarily used. The most commonly prescribed CCB for treatment of arrhythmias is diltiazem (available PO and IV). The beta-1 selective BB atenolol and esmolol (IV only) are the most frequently used antiarrhythmic BB. Digoxin has a vagomimetic effect and can therefore indirectly prolong AV node conduction time. Its antiarrhythmic application is limited to the treatment of atrial fibrillation (AF). For drug dosages consult Table 16-1 and Table 16-2.

• Atrial or ventricular myocardium: Depolarization is sodium channel gated and repolarization is potassium channel dominated. To treat arrhythmias that originate from the atrial and ventricular myocardium, Na channel blockers (NCB), K channel blocker (KCB) or combinations thereof are often used in conjunction with BBs. The NCB used for treatment of arrhythmias in dogs are lidocaine (IV only) and mexiletine and rarely procainamide. The most important KCB is sotalol, which also has BB properties. The authors also use amiodarone, which is predominantly a KCB, but also has potent NCB and some CCB and BB activity. For drug dosages consult Table 16-1 and Table 16-2.


Table 16-1 Agents for Rate Control/Abolishing Arrhythmias in Canine Patients with Supraventricular Arrhythmias

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Table 16-2 Agents for Rate Control/Abolishing Arrhythmias in Canine Patients with Ventricular Arrhythmias

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For optimal long-term management of most arrhythmias, a 24-hour Holter recording should be acquired in addition to the electocardiogram (ECG). Even though a correct diagnosis of an arrhythmia may be obtained by a short in-hospital ECG, in some patients with an intermittent arrhythmia, the 24-hour Holter recording is required to establish a definitive diagnosis.


The decision regarding how and when to treat an arrhythmia should be based on the clinical signs and urgency of intervention. Emergency management using intravenous drugs may be required before a 24-hour Holter recording can be obtained. Both diltiazem and esmolol are available in an IV formulation, allowing emergency treatment of excessively rapid supraventricular arrhythmias (SVAs), Lidocaine is the most important intravenous drug used for life-threatening ventricular arrhythmias.


• The benefits of a 24-hour Holter recording include in-depth assessment of quantity and quality of the arrhythmia(s). The following parameters should be examined: Number of abnormal beats (supraventricular and or ventricular) relative to overall number of beats, duration and rate of runs of abnormal beats; the average hourly and daily heart rate, the amount of time when the heart rate is greater than 120 or lesser than 50 bpm as well as the presence and length of pauses. A diary kept by the client or hospital staff with the sleep/wakefulness activity or observed events such as syncope or excessive anxiety or panting help correlate ECG changes on the Holter with clinical signs. These parameters are vital for a baseline evaluation of a patient’s arrhythmias and needs for antiarrhythmic therapy.

• If treatment is instituted, it is critical to obtain a repeat Holter recording after 1 or 2 weeks to determine if the drugs are efficacious at suppressing the abnormal rhythms, or possibly harmful by being pro-arrhythmic, that is causing ventricular arrhythmias or excessive pauses. This can only be established if a comparison to the pre-drug baseline is performed.

• If a Holter shows that a drug is effective, we recommend monitoring the progression of the arrhythmia by repeat Holter recordings every 6 to 12 months. If an animal experiences recurrent syncope during that time, an immediate repeat Holter is recommended.

• In animals that need to be stabilized immediately (no time for a baseline 24-hour Holter recording prior to intravenous antiarrhythmics), it is still advised to acquire a post-treatment Holter recording to evaluate drug efficacy and possible toxicity once the dog is stabilized and receiving chronic oral antiarrhythmic therapy.


Supraventricular Arrhythmias


SVAs include rhythms that originate in the sinus node, atrial tissue and AV junction. Importantly, SVA must be differentiated from accelerated normal sinus rhythm. Physiologic sinus tachycardia can be caused by many conditions including febrile states, anemia, heart failure, adrenergic medications and anxiety. In these cases, management should foremost be focused on correcting the underlying cause or disease resulting in increased sympathetic tone.


• Because of the mechanism of action of antiarrhythmic drugs, it is useful to assess SVA as either AV node independent (does not need the AV node to sustain the rhythm) or AV node dependent (pathway requires the AV node to sustain the rhythm).

• An SVA is AV node independent, if the ECG contains P waves not conducted to the ventricle without termination of the SVA. Interventions such as vagal maneuvers or drugs that slow AV node conduction can help identify the underlying mechanism:
• If the atrial activation rate is unchanged (PP interval the same) following the intervention, but the ventricular rate slows due to AV block, the SVA is likely AV node independent.

• If the intervention results in abolishment of the SVA and restoration of a normal sinus rhythm (even if it is only transient), the arrhythmia is likely AV node dependent.

• Examples of AV node–independent rhythms include sinus node reentrant tachycardia, AF, AFL, and ectopic atrial tachycardia. These arrhythmias can be challenging to manage, since the antiarrhythmic drugs (NCB, KCB or combinations thereof) are often not very efficacious for suppression of these arrhythmias. If the abnormal rhythm cannot be abolished with drugs, the secondary mode of treatment aims at controlling the ventricular response rate by slowing the AV node conduction with CCBs, BBs or digoxin.

• AV node–dependent SVAs include AV reentrant tachycardia (accessory pathway [AP] mediated) and AV nodal reentrant tachycardia. AV node–dependent arrhythmias can usually be treated with drugs that target the AV node (CCBs and BBs).


Key Point


To help guide treatment of SVAs, they should be characterized as AV node dependent or independent.



ATRIAL FIBRILLATION


• AF is one of the most commonly seen SVAs in veterinary practice. In dogs and cats, AF is usually a chronic arrhythmia associated with advanced stages of chronic AV valve insufficiency or cardiomyopathy. In those patients, the ventricular response rate is often markedly elevated, which contributes to the clinical signs of heart failure. AF can also occur in the absence of overt structural heart disease (lone or primary AF). In these cases, the ventricular response rate can be normal or only mildly elevated.

Key Point


The management of AF largely depends on the average heart rate. A baseline 24-hour Holter recording, acquired in the home environment is ideal to determine the average heart rate of a patient.


• The following flow chart (Figure 16-1) should serve to identify patients in need of treatment for AF and to decide which therapeutic approach might be best in each individual case.

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Figure 16-1 Flow chart describing the approach to treatment of atrial fibrillation (AF) based on the average heart rate (HR) of a patient as determined by a 24-hour Holter recording. AF, Atrial fibrillation; HR, heart rate; bpm, beats per minute; DCM, dilated cardiomyopathy.



Therapy


• AF is an AV node–independent arrhythmia, caused by multiple simultaneous intra-atrial reentrant circuits. Medical conversion of AF to sinus rhythm with drugs is very difficult and rarely achieved in canine patients. In most cases, ventricular rate control via slowing of AV node conduction with diltiazem and or digoxin is the goal (drug dosages are listed in Table 16-1). The veterinary literature also cites atenolol as effective for rate control of AF. The authors do not have much personal experience with atenolol for this purpose. The reluctance to use atenolol for rate control stems in part from the concomitant degree of advanced myocardial failure in many patients with AF. In our experience diltiazem XR is very well tolerated even in dogs with severe systolic myocardial dysfunction.

• Dogs with normal cardiac function or only mild dysfunction and normal to moderately elevated ventricular response rates may be candidates for electric cardioversion of AF to sinus rhythm.

• Medical management varies with the initial average heart rate and overall condition of the dog (Figures 16-2 through 16-4). Treatment can be tailored to the patient based on the approximate average heart rate. The authors prioritize treatment according to three general categories of ventricular response rate: (1) fast (Figure 16-2: average heart rate faster than 180 bpm), (2) moderate (Figure 16-3: average heart rate 130 to 160 bpm) and (3) slow (Figure 16-4: heart rate around 100 bpm). The dosages for the drug listed in Figures 16-2, 16-3 and 16-4 are provided in Table 16-1.

• Treatment of AF in cats is challenging. There is usually significant underlying heart disease present, resulting in markedly enlarged atria and very rapid AF. Medical management for rate control with a target heart rate of 130 to 150 bpm may be achieved using either CCB or BB (for drug dosages for antiarrhythmic drugs in cats see Table 16-3).

• Occasionally, the administration of narcotics has been associated with the induction of AF in large dogs. This is likely caused by the increased vagal tone that occurs with narcotics. Treatment with 2 mg/kg lidocaine IV within 4 hours of onset has been demonstrated to restore sinus rhythm. Vagolytic drugs (atropine) should prevent onset or recurrence of AF in such cases.


Key Point


Digoxin monotherapy does not control the ventricular response rate adequately during times of excitement, stress or exercise. Thus, dogs with AF and moderate to fast heart rates will require combination therapy of digoxin with diltiazem or atenolol.


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Figure 16-2 Management of dogs with AF with a fast heart rate (average heart rate > 180 bpm). HR, Heart rate; bpm; beats per minute; CRI, constant-rate infusion.


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Figure 16-3 Management of dogs with AF with a moderately elevated average heart rate of 130 to 160 bpm. HR, Heart rate; bpm, beats per minute; AF, atrial fibrillation.


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Figure 16-4 Management of dogs with AF with a low average heart rate (≤ 100 bpm). HR, Heart rate; bpm, beats per minute; AF, atrial fibrillation.



Table 16-3 Agents for Rate Control/Abolishing Arrhythmias in Feline Patients with Arrhythmias

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Electric Cardioversion (Rhythm Control)


In a subgroup of canine patients with mild structural heart disease or lone AF, electric cardioversion of AF to sinus rhythm can be achieved. The patients selected for this treatment are well compensated and the goal of cardioversion is to avoid structural or functional remodeling from chronic AF, even if the heart rate is slow. The rate of recurrence of AF after successful cardioversion is high and morbidity associated with repeat transthoracic cardioversions under general anesthesia make this management less practical. Pretreatment with sotalol, amiodarone or angiotensin-converting enzyme inhibitors may improve the chances of cardioversion and lessen the rate of recurrence of AF; however, no studies in veterinary medicine have proven these concepts.



Transthoracic Electrical Cardioversion Procedure


• Procedure requires a brief general anesthesia

• Fast Patch electrodes are recommended instead of hand-held paddles to optimize electrode position for cardioversion.

• Dog is shaved before application of the patch over the heart on both lateral sides of the thorax.

• Dog is positioned in lateral recumbency to optimally “position” heart between the two patch electrodes.

• Defibrillator ECG cables need to record patient’s ECG and synchronize to the R waves. With false synchronization to T waves (occurs if T wave is taller than the R wave) the cardioversion shock can induce VF!

• Using a monophasic defibrillator:
• Start with 4 J/kg; If no cardioversion occurs, increase dose by 50 J and repeat until a maximum of 360 J.

• Using a biphasic defibrillator:
• Start with 1 to 2 J/kg; If no cardioversion occurs, increase dose by 50 J and repeat until a max of 360 J.

• Short, transient runs of ventricular tachycardia (VT) or sinus pauses or AV block are common following electric cardioversion.


ATRIAL FLUTTER


• Atrial flutter (AFL) is relatively uncommon in veterinary patients. Theoretically, AFL could set the stage for development of AF due to the remodeling that occurs with continuous rapid activation of the atrial myocardium. In some patients AFL co-exists with AF on a 24-hour Holter, which might represent a transition phase to chronic AF. AFL is an AV node–independent intra-atrial macro-reentry rhythm. The atrial activation rate (PP interval) is 300 to 600 bpm. AFL is paroxysmal or chronic and can be associated with excessively high ventricular response rates. AV conduction usually changes between 1:1 and 3:1 or 2:1 due to variable degrees of AV block.

• A baseline 24-hour Holter is recommended to determine of the arrhythmia is chronic or paroxysmal. If it is chronic, drug therapy is indicated.

• If it is paroxysmal and infrequent, treatment may be postponed, but a reevaluation by Holter 6 months later should be performed to check for progression from paroxysmal to chronic AFL or presence of concurrent AF.


Drug Therapy


• Ideally, therapy is aimed at suppressing the atrial reentry circuit using sotalol, amiodarone or procainamide; however, abolishing the AFL with drugs is often unsuccessful; propafenone and flecainide are used in humans with AFL, but the authors have had little success in dogs with these drugs. The adequate dose for dogs has not been identified. Rate-control via slowing of the AV node with CCBs or BBs is used effectively in dogs (for drug dosages see Table 16-1). Digoxin monotherapy is ineffective for management of AFL.

• A post-drug 24-hour Holter should be obtained to determine if drugs are effective at suppressing the AFL or producing the desired AV block, thereby slowing the ventricular response adequately. It also allows survey for drug toxicity, manifest as bradycardia or pauses secondary to excessive AV block. Pauses, if they occur only during sleep or rest, are usually of no concern.


ECTOPIC ATRIAL TACHYCARDIA


• Atrial tachycardia (AT) occurs when ectopic foci in the atria develop the ability to fire rapidly on their own. It is an AV node–independent arrhythmia. Ectopic AT is often paroxysmal and may display a gradual onset and offset (warm-up and cool-down period) if the underlying mechanism involves abnormal automaticity. The heart rate can vary from 150 to 300 bpm and can cause anxiety or panting in affected dogs. In cats ectopic AT is rare.

• A baseline 24-hour Holter should be obtained to determine what percentage of time a dog is in AT, and how fast the heart rate is during the AT.


Therapy


• Ideally, suppression of the rapidly firing atrial focus is attempted by using sotalol, amiodarone or procainamide. In people, propafenone is used for treatment of AT, but we have not found these agents efficacious in our patients. In fact, targeting the abnormal rhythm directly with these drugs is often unsuccessful. Thus, as a second choice, therapy for AT should be aimed at slowing AV node conduction with CCBs or BBs to reduce the ventricular response. Digoxin is ineffective for management of AT.

• A post-drug 24-hour Holter should be obtained to determine if drugs are effective at suppressing the AT or producing the desired AV block, thus slowing the ventricular response adequately. The Holter also allows survey for excessive AV block; this may be undesired if it occurs other than during rest or sleep.


Key Point


Although amiodarone is a potent antiarrhythmic drug, its benefits must be balanced against its slow onset to action and adverse effects which include hepatic toxicity, gastrointestinal disturbances and blood dyscrasias in canine patients.



ATRIOVENTRICULAR NODAL REENTRANT TACHYCARDIA


• Atrioventricular nodal reentry tachycardia (AVNRT) is a form of micro-reentry within the AV node that gives rise to rapid, simultaneous activation of the ventricles and atria. AVNRT is AV node dependent, thus AV node slowing medication may terminate the arrhythmia. The prevalence in dogs is likely very low, but definitive diagnosis requires intracardiac mapping studies to prove dual AV node physiology.

• For treatment of AVNRT see the following discussion of treatment of atrioventricular reentrant tachycardia (AVRT).


ATRIOVENTRICULAR REENTRANT TACHYCARDIA


• AVRT is a macro-reentry arrhythmia whose circuit comprises the AV node as well as an AP that can conduct impulses from the atria to the ventricles directly, thereby bypassing the AV node and His- Purkinje system. Response to a vagal maneuver or intravenous drug challenge may be used to confirm its AV node–dependent properties. One-to-one AV association is a requisite of AVRT because the atria and ventricles are both integral parts of the arrhythmia circuit. If AV dissociation occurs spontaneously without termination of the SVA, AV reentrant tachycardia can be excluded.

• AVRT is a paroxysmal, intermittent SVA and 24-hour Holter may be required to make a definitive diagnosis of this SVA, as well as determine its clinical significance. Animals with AVRT may be asymptomatic, or present with syncope, episodic weakness or lethargy.

• In dogs the arrhythmia most commonly follows a pattern of orthodromic conduction through the AV node (from atria down to the ventricles) and retrograde over the AP back up to the atria, implying that the AP is only able to conduct in one direction (concealed conduction). This form is prevalent in Labrador Retrievers and termed orthodromic AV reciprocating tachycardia or orthodromic AV reciprocating tachycardia.

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Aug 15, 2016 | Posted by in SMALL ANIMAL | Comments Off on Treatment of Cardiac Arrhythmias and Conduction Disturbances

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