Diagnosis & Assessment of Supraventricular and Ventricular Rhythm & Conduction Disturbances
ACVIM 2008
John D. Bonagura, DVM, DACVIM (Cardiology, Internal Medicine-SA)
Columbus, OH, USA

Introduction

The cardiac impulse forming and conduction system includes the sinoatrial node, bi-atrial electrical chamber, specialized inter-nodal pathways, atrioventricular node, His-Purkinje system (including His bundle, bundle branches, and Purkinje cells), and the bi-ventricular chamber. Sequential activation of these structures generates the electrocardiogram. The P-QRS-T complexes vary among species (shorter and smaller in cats) and across the various limb and precordial leads. Cardiac arrhythmias are disorders of heart rate, rhythm, or conduction.

One can arbitrarily classify clinical associations for arrhythmias into five general categories. 1) Arrhythmias may represent primary electrical disturbances of the heart, often due to macroscopic or microscopic structural cardiac disease or related to channelopathies. Some examples (among dozens) are sick sinus syndrome in miniature schnauzers, primary atrial standstill in English Springer spaniels, atrial premature complexes in dogs with right atrial hemangiosarcoma, lone atrial fibrillation (AF) in Irish wolfhounds, chronic atrial fibrillation associated with dilated cardiomyopathy, atrioventricular block in older Cocker spaniels, inherited ventricular ectopy in German shepherd dogs, and ventricular ectopy in Boxers and English bulldogs. 2) Metabolic and endocrine diseases often are associated with arrhythmias: the problem may be reversible if the underlying condition is treated. Examples include sinus bradycardia with hypothyroidism, sinus tachycardia with hyperthyroidism, atrial premature complexes with hypokalemia, atrial standstill with hyperkalemia/Addison's disease/urinary obstruction, and ventricular ectopy related to hypomagnesemia and hypokalemia. 3) The autonomic nervous system can initiate or aggravate arrhythmias. Examples include sinus bradycardia from elevated CNS pressure, sinus tachycardia caused by heightened sympathetic activity (from stress, hyperthyroidism, fever, anemia, infection, or pain), and triggered atrial and ventricular premature complexes from excess sympathomimetic stimulation of the heart. Sympathetic activity relates in a complex manner to cellular calcium transients, repolarization, and pacemaker activities. 4) Drugs and toxins can affect the electrical activity of the heart. Examples include sinus bradycardia from overdose of a beta-blocker or digoxin, junctional and ventricular ectopy from digitalis intoxication, sinus tachycardia from methylxanthine toxicity, conduction disturbances from chronic doxorubicin administration, and sinus bradycardia related to many sedatives and anesthetics. 5) Finally, some clinical disorders are consistently associated with the development of cardiac arrhythmias. These "usual suspects" are learned from experience or by consulting a reference textbook. For example, ventricular ectopy is often observed in the setting of chest or abdominal trauma, hypotension, hypoxia, gastric dilatation, splenic disease, and systemic inflammation.

Electrophysiologic mechanisms are well studied in laboratory settings. Certainly, the mechanism of some arrhythmias, such as atrioventricular nodal dependent, re-entrant, supraventricular tachycardia can be discerned from the ECG and responses to treatment. However, in most instances the electrical disorder underlying a specific arrhythmia is unknown from the surface electrocardiogram and speculative at best. Accordingly, consideration of the underlying mechanism of an arrhythmia is not likely to influence the choice of therapy.

Arrhythmias (dysrhythmias) can be classified based on ECG analysis based on the heart rate (normal, bradyarrhythmias, tachyarrhythmias); anatomic origin of the rhythm disturbance (SA, atrial, atrioventricular, or ventricular); or electrophysiologic mechanism when evident. Keys to recognizing cardiac arrhythmias include an analysis of rate, regularity, patterns, P-QRS relationship, waveform morphology, and conduction intervals. In terms of a methodological approach to rhythm diagnosis, it is recommended that one begin as follows:

1) Identify the patient, lead(s), paper speed, calibration signals, and artifacts; 2) Decide if the rate is slow, normal, or fast for the species; 3) Identify regularity or lack thereof and search for repetitive patterns in irregular rhythms; 4) Identify P and QRS complexes and the relationship between these waveforms; 5) Scrutinize the morphology and consistency of the P-waves and the QRS complexes; 6) Consider the conduction intervals across the atria (P-wave duration), atrioventricular conduction system (P-R interval), ventricles (QRS duration), and overall repolarization time (Q-T interval); 7) Identify the frontal axis as normal, left, or right; 8) Evaluate the QRS morphology for conduction disturbances, obvious bundle branch or fascicular blocks, and for cardiomegaly pattern(s); 9) Assess the ST-T for repolarization abnormalities; and 10) interpret the ECG with consideration of the entire clinical and laboratory picture.

Sinus Rhythms

The normal rhythm begins in the SA node and generates positive P-waves in leads II and aVF. P-wave morphology may vary cyclically with heart rate in sinus arrhythmia of dogs. While heart rate is generally more regular in cats under examination, ambulatory monitoring often shows substantial HR variability1. Assuming conduction is normal, the PR interval will be within normal limits for that species and breed, and the QRS complex of normal width and morphology. The normal QRS complex also is positive in leads II and aVF and is relatively compact (or "narrow") because rapid conduction across the bundle branches and Purkinje system spreads the impulse quickly through the myocardium.

The sinus node can discharge regularly at normal rates of about ~60 to 180 in dogs and ~160 to 240 in cats (normal sinus rhythm), irregularly due to vagal influences (sinus arrhythmia), slowly (sinus bradycardia), rapidly (sinus tachycardia), or not at all (sinoatrial block or sinus arrest). Average heart rate per day in dogs based on Holter ECG is about 65 to 75/minute with rates as low as 30/minute and higher than 200/minute commonly observed in healthy dogs. Normal sinus rhythm refers to a regular sinus discharge rate in which the P-to-P intervals vary by <10%. Sinus arrhythmia is also "normal" physiologically, but it is not regular, making the term "normal sinus arrhythmia" somewhat peculiar. A failure of sinus node discharge leads to a transient absence of P-waves and the ensuing rhythm is called sinoatrial block, sinus pause, or sinus arrest. SA block is diagnosed when the pause is a multiple of a normal P to P interval or when a prominent pause is always preceded by progressively shorter P to P intervals (Wenckebach periods). In most cases of sinus arrest, the heart is rescued by normally-subsidiary pacemaker cells found in the atrial tissues, atrioventricular nodal region, or ventricles. These rescue depolarizations generate escape complexes or an escape rhythm. When continual, the rhythm may be called an idionodal (from the atrioventricular junction) or idioventricular rhythm ("idio" = self). Escape rhythms are very slow in dogs but can be surprisingly rapid, over 100/minute, in cats.

Sinus rhythm disturbances are often related to altered vagal or sympathetic tone, and any patient with sinus bradycardia or sinus tachycardia should first be evaluated with this in mind. Drugs, temperature, and endocrine status also can affect sinus discharge rate. Marked (pronounced) respiratory sinus arrhythmia can be observed in dogs and in cats with respiratory diseases, including a pattern of coupled beating called atrial bigeminy. At times, it can be difficult to distinguish the short cycles of marked sinus arrhythmia from atrial premature complexes. Another potential mechanism for coupled sinus beats (with P-waves of similar morphology) is sinus node reentry wherein the first sinus impulse reenters another portion of the SA node, conducts slowly, and finally exits again to re-stimulate the atria.

Management of sinus node disturbances in most situations relates to treatment of the underlying condition, though occasionally inappropriate or excessive sinus tachycardia (hyperthyroidism, methylxanthine toxicity, cocaine ingestion) is be treated with a beta-blocker. Sinus tachycardia can approach 300/minute in dogs under maximal sympathetic stimulation and even higher rates in cats, creating a diagnostic dilemma relative to ectopic atrial or reentrant supraventricular tachycardias. Typically, sinus tachycardia conducts 1:1 (P: QRS).

Chronic, progressive, sinus node dysfunction related to degenerative disease is common in older dogs, particularly miniature schnauzers, cocker spaniels, and West Highland white terriers2. Common rhythm disturbances include sinus bradycardia, inappropriate heart rate responses to exercise, and sinus arrest with or without escapes. Failure to develop suitable escape activity may result in collapse or syncope (creating the sick sinus syndrome). Sometimes sinus node disease is uncovered most inconveniently during induction of general anesthesia. If escapes are suppressed by the anesthetics, asystole may occur. Advanced sick sinus syndrome can include atrioventricular block, insufficient escape activity, inappropriate sinus tachycardia, periods of ectopic atrial tachycardia followed by sinus arrest (tachycardia-bradycardia syndrome), and inappropriate pacemaker response to vagolytic drugs (ectopic atrial or junctional rhythms).

While atropine, glycopyrrolate, and sympathomimetics may increase the rate of sinus or subsidiary pacemakers, in emergent or anesthetic situations, the drugs may be ineffective. Clearly, the best long-term therapy is permanent transvenous pacing as discussed below for atrioventricular block. Pacing, even in a simple VVI (demand) mode, carries an excellent long-term prognosis when the system is implanted by a skilled operator and the pacing system and patient are monitored by individuals experienced in pacemaker evaluation and programming. The typical system is implanted in the right ventricle via the jugular vein under fluoroscopic guidance. The generator is positioned under superficial muscle in the dorsal--lateral cervical region. Programming is critical for optimal performance of the system. We typically use a VVIR mode--a rate response mode that changes with activity programmed at rates of ~66 to 140/minute. Dual chamber pacing (DDD) also can be used with a single or two leads.

Atrial Rhythms

Atrial rhythm disturbances are very common rhythm disturbances. These also can also be among the most difficult problems in terms of both ECG diagnosis and management options3, 4. The atrial arrhythmias include premature atrial complexes, atrial tachycardia, atrial flutter, atrial fibrillation, and atrial standstill. Many cases of reentrant supraventricular tachycardia use the atria a part of the circuit. Atrial arrhythmias can be transient, recurrent, or permanent. In most cases, recurrent or permanent arrhythmias are due to structural heart diseases such as chronic valvular disease or cardiomyopathy. Some giant canine breeds develop chronic atrial arrhythmias without evidence of structural heart disease, including "lone atrial fibrillation" often observed in Irish wolfhounds and in some Great Danes. In many cases, following these patients will demonstrate the arrhythmia as the predecessor of a more progressive cardiomyopathic process.

Atrial tissues are normally "driven" by the sinus node. When impulses arise independently within the atrial tissues, but outside of the SA node, the resultant P-waves are called atrial ectopics. Since these are usually early relative to the dominant P-wave to P-wave cycle, the resultant complexes are called atrial premature complexes (or premature atrial complexes). If a series of APC's occurs, the rhythm is called atrial tachycardia. This may be sustained or nonsustained (paroxysmal). In each case, P-waves will be present, but they are typically occurring at a faster rate than the normal sinus rate. Furthermore, the ectopic P-waves are generally different from those found during sinus rhythm in that lead. Atrial premature complexes can be benign, when related to surges of sympathetic activity, but when chronic likely indicate atrial stretch, disease, neoplasia, or fibrosis. Infrequently multifocal atrial tachycardia is diagnosed (ectopic atrial rhythms of varying rate and P-wave morphology).

When the atrial tissues develop abnormal re-entrant electrical activity, the resultant rhythms are called either atrial flutter (circuit movement, generally around the right atrium) or atrial fibrillation (caused by either disordered re-entry in the atria or fibrillatory conduction of a rapidly discharging atrial or pulmonary venous electrical focus). With atrial flutter, the current travels across the atrium rapidly and circuitously, producing hundreds of saw-toothed waves each minute. The flutter rate can change subtly or markedly with alterations of vagal tone or following drug administration. If there is fibrillatory conduction of impulses across the atrial myocardium, the current becomes fragmented into numerous small wavelets. No P-waves will be evident when there is no organized activity; instead, there may be fine undulations of the baseline. The QRS complexes in atrial arrhythmias occur whenever an atrial impulse crosses the atrioventricular node and enters the ventricle.

The ventricular rate response in supraventricular tachyarrhythmias such as atrial tachycardia or flutter is determined by atrioventricular nodal conduction and may be regular or irregular. In high sympathetic states, atrioventricular conduction can be very rapid. For example in atrial fibrillation in the setting of congestive heart failure (CHF), ventricular rate is often 250/minute in dogs and often approaches or exceeds 300/minute in cats. Some organized supraventricular tachycardias can lead to ventricular responses of almost 400 per minute! In 2:1 atrioventricular conduction of atrial tachycardia or flutter, the rate may suddenly double if the conduction changes to 1:1 (P' : QRS). Even with atrial tachycardia or flutter with 2:1 atrioventricular conduction the atrial activity may be hidden unless a transient block in atrioventricular conduction can be identified. Conversely, atrioventricular conduction in atrial fibrillation is always variable, creating irregular R-R intervals, although rapidly conducted atrial fibrillation (as in cats) may appear regular on first glance.

A common diagnostic problem is sorting out a regular, non-sinus, supraventricular tachycardia with a normal (narrow) QRS complex. Numerous leads, including chest leads should be scrutinized for P-waves. The P-R or the R-P should be measured. Subtle electrical alternans is a commonly observed finding regardless of mechanism. Thus, one should not be surprised to see alternans in atrial flutter, ectopic atrial tachycardia, or re-entrant supraventricular tachycardia using the atrioventricular node. This finding may help to separate these rhythms from a "fast" sinus tachycardia where alternans is less common. Less often the QRS complexes change dramatically every other beat, constituting a differential diagnosis for so-called bi-directional ventricular tachycardia. Supraventricular tachyarrhythmias also can be conducted with bundle branch block, and the resultant QRS complexes can be readily confused with a ventricular tachycardia.

Drug trials also can be informative, and one of the most common strategies to reveal the rhythm involves blocking the atrioventricular node. Initially a vagal maneuver can be tried. If the patient is hypotensive (systolic ABP <90 mm Hg), a bolus of crystalloid or colloid can be given followed by drugs. While adenosine is the drug of choice in people for acutely blocking the atrioventricular node, in dogs and cats diltiazem works better and is well tolerated except in patients with severe congestive heart failure. Up-titrating the total dosage in increments of 0.05 to 0.1 mg/kg IV every 5-10 minutes with ABP monitoring will usually break the rhythm (if reentrant supraventricular tachycardia) or expose the atrial ectopic activity or flutter waves. An alternative drug is the rapidly hydrolyzed beta-blocker, esmolol (50 to 200 micrograms/kg/minute), which in my experience is more useful for cats. For acute atrial arrhythmias, it is also worthwhile to try lidocaine (2-6 mg/kg IV for dogs). Dofetilide and related compounds have also been used infrequently in an attempt to convert atrial fibrillation. While traditionally used for ventricular arrhythmias, lidocaine does occasionally convert a sustained atrial arrhythmia to sinus rhythm5.

Drug management of atrial arrhythmias also can be confusing. While traditional treatment plans such as digoxin and beta-blockers (see later) are still in common use, recurrent atrial premature complexes or atrial tachycardia are often treated with drugs more commonly used to suppress ventricular ectopic rhythms in dogs, including sotalol and "low-dose" amiodarone. These drugs suppress ectopy and impair conduction down the atrioventricular node. When efforts to suppress ectopics fail, heart rate control should be gained. Atrioventricular nodal blockade will reduce the number of impulses entering the ventricle and represents the alternative path for controlling ventricular heart rate. Digoxin, diltiazem, and beta-blockers can reduce ventricular response rate. When atrial tachyarrhythmias are associated with congestive heart failure, digoxin is chosen first. Otherwise, diltiazem and a beta-blocker are usually more effective for heart rate control, and sometimes will result in conversion to normal sinus rhythm.

Increasingly there is interest in synchronized DC cardioversion of atrial flutter/fibrillation, particularly in dogs with lone atrial fibrillation6. The success rate with new cardioversion/defibrillators is quite high (>80%), especially when using units that deliver a biphasic waveform. Usual initial settings are 1 to 2 joules per kg body weight. Patches or paddles are placed on either side of the clipped thorax (larger the better) and the system is synchronized to the R-wave rhythm prior to charging and shocking. The procedure is painful and short-lasting general anesthesia is required. Amiodarone or sotalol are often prescribed after cardioversion to sustain sinus rhythm. These drugs should be continued for at least three months if possible. Some recommend indefinite therapy to prevent reversion to atrial fibrillation.

A unique supraventricular rhythm disturbance that is not precisely of "atrial" origin is the re-entrant supraventricular tachycardia7. This rhythm disturbance is created from a circuit path using (most often) the atria, atrioventricular node, and an accessory pathway (+/- ventricle tissues). The tachycardia is often triggered by an atrial or ventricular premature complex. The atrial premature complex conducts down the AV node, but not the accessory pathway. The ventricular extrasystole transmits up the accessory path, into the atrium, and then down the AV node to return to the ventricle. In most cases the circuit tachycardia is a macro-reentrant arrhythmia that is "orthodromic"; i.e., dependent on conduction down the atrioventricular node. Once the current exits the atrioventricular conduction ventricular activation proceeds with a normal (narrow) QRS. Current then proceeds up the accessory pathway in a retrograde manner to depolarize the atria before descending again through the atrioventricular node. The QRS complexes are typically narrow during the supraventricular tachycardia and retrograde P-waves are identified in the ST segment (an R - P' as opposed to a P'-R). There are very strict "rules" for recognizing these in human patients, but such guidelines are unavailable for dogs and cats. In some dogs with atrioventricular nodal dependent supraventricular tachycardia, periods of sinus rhythm are associated with ventricular pre-excitation, a very helpful clue to the presence of an accessory pathway (the so-called Wolff-Parkinson-White syndrome). Pre-excitation is characterized by a short PR interval and an early ventricular activation (delta wave), which in dogs and cats can appear as a discrete small deflection immediately preceding the QRS. Management of reentrant supraventricular tachycardia is done with drugs initially (see below) and then referral to a specialist in radiofrequency catheter ablation of the accessory path.

The final two atrial rhythm abnormalities for consideration are quite different from those above and involve situations wherein atrial muscle is rendered inexcitable. These conditions are caused by high serum potassium concentrations, severe atrial muscle disease, or marked atrial dilation (typically in cats). In these cases, no P-waves will be evident (atrial standstill) or only very small amplitude, non-conducted impulses observed. Persistent silent atrium is most common in English Springer spaniels, but can also occur in other breeds, including larger retrievers. In cats apparent atrial standstill can be observed with dilated cardiomyopathy, right ventricular (and atrial) cardiomyopathy, and in advanced restrictive cardiomyopathy.

Junctional (Nodal) Rhythms

Cardiac rhythm disturbances arising in the atrioventricular node and atrioventricular junction are relatively uncommon in dogs and cats. Junctional escape rhythms can be observed in sinus arrest and in some cases of "high" complete atrioventricular block. Certainly, digoxin toxicity can lead to an automatic junctional tachycardia with atrioventricular block. Occasionally junctional (or low atrial) tachycardias are seen in heart disease, including right sided diseases. These are often normal in rate, with inverted P-waves, and may be clinically benign. Some re-entrant supraventricular tachycardias are confined to the atrioventricular conduction system and involve infranodal pathways (longitudinal dissociation of the atrioventricular node) with current spreading from the atrioventricular circuit into the ventricle and then the atria. A pearl of diagnosis is related to the onset of longitudinal dissociation wherein a sudden prolongation of the PR interval precedes the onset of the tachycardia.

Ventricular Rhythms

Arrhythmias arising in the ventricle parallel those of the atria, but with two important differences: 1) the atrioventricular node need not be activated to generate a QRS complex, and 2) there is greater potential for sudden death as the rhythm may degenerate into ventricular fibrillation or asystole. Normal ventricular tissues are quiet and only discharge if no other impulse arrives in a suitable period. In that case, a ventricular escape complex or escape rhythm will be produced. This is observed most often when the sinus node arrests or if impulses coming from the atria are blocked in the atrioventricular node or bundle of His (atrioventricular block). The typical idioventricular rhythm in the dog discharges at 20 to 40/minute, but in the cat, the rate is much faster, approach 120/minute in many cats with complete atrioventricular block. When impulses originate in the ventricular tissues, the QRS complexes are abnormal and wider. This is explained by the need for ectopic impulses to forego rapid-conduction in the His-Purkinje system and for current spread that proceeds more slowly across myocardial cells. Two other pointers regarding ventricular ectopic beats are these: the T-wave is usually very large and in the opposite direction of the QRS (secondary T-wave change), and there is not a related P-wave preceding the QRS.

If an impulse originates prematurely in the ventricular tissues, the resultant complex is called a ventricular premature complex (VPC) or premature ventricular complex (PVC). Ventricular premature complexes can be uniform or multiform in morphology. Fusion complexes between ventricular premature complex and sinus impulses also can create intermediate forms. When ventricular premature complexes occur in a series, the rhythm is termed ventricular tachycardia. Ventricular tachycardia (VT) can be paroxysmal (non-sustained) or sustained (>30 seconds); monomorphic or polymorphic; and rapidly varying in orientation (torsade de pointes). The ventricles also can flutter (producing sine-wave QRS-T complexes), or fibrillate (creating a disorganized and lethal electrical activity). In very sick animals, death may occur due to asystole, which is essentially ventricular standstill.

Clearly ventricular premature complexes are among the most common rhythm disturbances, and often develop in apparently healthy dogs and cats8. As indicated above, causes include primary electrical or structural heart diseases, electrolyte and metabolic disturbances, autonomic imbalance, drugs and toxins, and the "usual suspects", such as splenic masses. It can be very difficult to decide if ventricular premature complexes are "clinically significant" or not. The issue is important in many cases. For example, most cats with chronic ventricular ectopy have structural heart disease or at least elevated serum troponins suggestive of active myocardial disease. A Doberman pinscher (at least one from North America) with premature ventricular complexes on a routine ECG is likely to progress towards overt dilated cardiomyopathy. Furthermore, when an ECG demonstrates even a few premature ventricular complexes in a Doberman pinscher that has collapsed or fainted, the risk of sudden cardiac death within the year is very high. Such information may prompt antiarrhythmic therapy, recognizing that there is no proof treatment will prolong life.

ECG diagnosis of ventricular premature complexes or of VT is generally straightforward. In many cases a full workup including drug history, history of clinical signs such as collapse or syncope, echo findings, blood tests (CBC, chemistries, serum troponin-I), and abdominal ultrasound may be needed to determine the cause and likely significance. The ambulatory (Holter) ECG is useful for assessing the severity of arrhythmias, complexity of the disturbance, and response to therapy. The absolute number of "normal" premature ventricular complexes (not simply ectopics) per day is controversial, but in the author's (arbitrary) opinion >10/day in cats and >50/day in dogs should be considered abnormal. Day to day variation is common (up to ~85%) and this must be taken into account when considering "response" to treatment9.

Management of ventricular ectopy involves determining the most likely cause, advancing an educated guess about the significance of the rhythm disturbance and need for therapy, and selecting one or more drugs with potential for side effects and worsening of the arrhythmia (pro-arrhythmia). In general, lidocaine remains the drug of choice for acute management with procainamide, esmolol, magnesium salts, and amiodarone back up treatments. For chronic treatment, the best therapy for a specific situation is still unresolved. Most antiarrhythmics carry significant proarrhythmic potential. This can relate to prolongation of repolarization (sotalol, amiodarone, procainamide) or effects on heart rate (beta-blockers). Overall, sotalol is often effective for reducing ectopy on Holter ECGs10, and is probably the best in terms of overall tolerance and convenience (b.i.d.) of treatment. However, as with any beta-blocker, care must be exercise relative to negative inotropy in LV dysfunction or congestive heart failure. However, the best drug in any given patient may not be what is first prescribed, and combinations are sometimes more effective than single drugs. For example, mexiletine plus sotalol, mexiletine plus atenolol, and amiodarone represent reasonable alternative treatments for many canine patients. The author still uses long-acting procainamide (+/- a beta-blocker) in some dogs with impaired LV function or in those who are unresponsive or intolerant of other therapies. Amiodarone is a potent antiarrhythmic drug in some dogs, but does deserve respect, especially in terms impairing liver function, creating ocular lesions, and altering thyroid function. The drug's very long half life makes elimination a many day event. Control of ventricular ectopy in cats generally starts with a beta-blocker or sotalol.

Conduction Disturbances

The heart rhythm is also influenced by conduction of impulses across the atria, atrioventricular node, and His-Purkinje system. SA block and atrial standstill were considered previously. The next level of potential conduction delay is along the atrioventricular conduction system, or the atrioventricular blocks. When P-waves are followed by the QRS complex, but the PR interval is abnormally long, the diagnosis is first-degree atrioventricular block. If P waves are intermittently blocked from conduction, this incomplete block is called second-degree atrioventricular block. There are variants of Mobitz type I (progressively longer PR before block), Mobitz type II (consistent PR before block or 2:1 P:QRS block), and Types A (normal QRS duration) and B (wide QRS duration) that describe the appearance of the QRS following conducted impulses. Type B suggests more diffuse conduction disease. When no P-waves are conducted into the ventricle, the heart relies on an "escape" pacemaker rhythm, and the condition is called complete or third-degree atrioventricular block. Unstable escape rhythms or intermittent ventricular tachycardias are commonly associated with overdrive suppression of the escape focus resulting in recurrent syncopal attacks11,12; this is one clear indication for immediate transvenous pacing prior to implant of the permanent system13,14.

Conduction delay also can develop in the ventricles. For example, if either bundle branch is diseased the current will travel to the other ventricle first, finally activating the blocked area via slow myocardial cell to cell spread. This leads to a wide and often abnormally oriented QRS complex that was actually created by a supraventricular stimulus, but resembles an ectopic ventricular beat. The axis shifts towards the blocked bundle or fascicle in the case of right bundle branch block and left anterior fascicular block. The key is identification of an associated P-wave (or atrial fibrillation wave) that precedes the QRS and appears to be related. Phasic aberrant conduction (usually of right or left bundle branch block morphology), is related to varying cycle lengths. This can develop in atrial fibrillation or with disease of the bundle branches. Electrical alternans is common in "rapid" and regular supraventricular tachycardias.

Ventricular pre-excitation is a conduction disturbance caused by an accessory "by-pass" tract. When current spreads down both the accessory pathway and the normal atrioventricular tissues, the ventricle is "pre-excited" by the accessory tract resulting in a short PR interval along with a widened QRS with initial QRS slurring caused by early ventricular activation ("delta wave"). If a circuit movement supraventricular tachycardia occurs as well (down the atrioventricular node, into the ventricle, up the accessory pathway, into the atrium and then re-entering the atrioventricular node), the condition is called the Wolff-Parkinson-White syndrome. The accessory pathway may only conduct in the retrograde direction resulting in periodic re-entrant supraventricular tachycardia with normal QRS complexes during sinus rhythm.

Antiarrhythmic Therapy

Drugs, electrolytes, pacing, direct current shock, and radiofrequency energy can be used to treat disorders of heart rhythm. Antiarrhythmic drugs can be classified based on their electrophysiologic characteristics (the Vaughn-Williams classification); however, this ordering is not ideal, and other schemes have been proposed but not widely adopted. The Vaughn-Williams classification places antiarrhythmic drugs into one of four classes (and subclasses). As with any classification, it is limited, and does not consider other potentially useful drugs with antiarrhythmic effects (see the Sicialian Gambit Group classification). For example, the anticholinergic effects of atropine; the parasympathetic effects of digoxin; the delayed atrioventricular nodal conduction caused by adenosine; and the membrane stabilizing effects of the magnesium salts are not included. Nevertheless, there is some convenience in grouping drugs according to the traditional system.

Class I antiarrhythmic drugs reduce the rate of Na+ influx by blocking sodium channels. These drugs generally decrease the rate of depolarization, slow conduction, and increase overall refractoriness of cells; these are subdivided as follows: IA drugs (quinidine, procainamide, disopyramide) lengthen the action potential duration and the refractory period; IB drugs (lidocaine, mexiletine) shorten the action potential duration but increase the refractory period; IC drugs (flecainide, propafenone) produce little effect on action potential duration but slow conduction. Class II antiarrhythmic drugs block beta adrenoceptors and decrease sinus node rate, slow atrioventricular nodal conduction, and reduce arrhythmias related to high sympathetic tone and calcium influx. Central effects may also be evident with some lipophilic drugs. Class III antiarrhythmic drugs (sotalol, amiodarone, dofetilide) prolong the action potential duration by blocking potassium channels and also increase cell refractoriness. These drugs generally do not change automaticity or conduction velocity but often exert some beta-blocking effects. Class IV antiarrhythmic drugs (verapamil, diltiazem) block the movement of calcium ions across the slow calcium channels. Effects are a decreased heart rate, slowing of atrioventricular nodal conduction, and other less well-defined antiarrhythmic effects.

Antiarrhythmic drug dosing varies and drug safety is highly dependent on ventricular function and proarrhythmic effects. General canine dosing guidelines are:

 Amiodarone (5 mg/kg IV as a slow infusion; 10 mg/kg PO daily x 2 weeks; thereafter 4-6 mg/kg PO daily).

 Atenolol (0.5-1 mg/kg PO q12h; reduce dosage at least 50% in congestive heart failure).

 Diltiazem (0.1 mg/kg slow IV boluses repeated to 0.4 to 0.5 mg/kg cumulative dose with BP monitoring; 3-6 mg/kg PO, total daily dose, divided b.i.d. or t.i.d. depending on the preparation. Initial doses in congestive heart failure should be lower--1.5 mg/kg total daily dose--and then can be rapidly uptitrated).

 Esmolol (50-200 micrograms/kg/minute IV infusion); use care with anesthesia or LV dysfunction.

 Lidocaine (2 mg/kg boluses IV to 8 mg/kg cumulative dose; thereafter, 25-75 micrograms/kg/min constant rate infusion).

 Mexiletine (5-8 mg/kg PO q8h)--can be combined with a beta blocker or sotalol.

 Procainamide (2 mg/kg slow IV boluses to 20 mg/kg cumulative dose; 10-20 mg/kg PO q8h of long-acting preparation).

 Sotalol (1-2 mg/kg PO q12h); higher dosages may be tolerated in some dogs.

Effective use of any antiarrhythmic drug depends on clinical response and experience. Hypokalemia and hypomagnesemia can nullify the beneficial effects of class I agents while exacerbating pro-arrhythmic effects of Class III agents. Some drugs are more effective at particular heart rates (use dependence) and may worsen an arrhythmia by changing the rate. Every drug used to treat arrhythmias is considered an extralabel drug use in veterinary practice and treatment recommendations are based mainly on clinical experience; specific recommendations have been included above. Additional effects from activation/block of the autonomic nervous system and depression of myocardial contractility may occur. Most antiarrhythmic drugs demonstrate a proarrhythmic effects in a percentage of patients. Even beta-blockers can be proarrhythmic indirectly by slowing heart rate and prolonging cell cycle length. Thus antiarrhythmic therapy a true risk: benefit proposition.

References

1.  Abbott JA. J Feline Med Surg. 2005; 7(3):195.

2.  Moneva-Jordan A, et al. Vet Rec. 2001; 3;148(5):142.

3.  Cote E, et al. J Am Vet Med Assoc. 2004; 225(2):256.

4.  Menaut P, et al. J Vet Cardiology 2005; 7(2):75

5.  Johnson MS, et al. J Vet Intern Med. 2006; 20(2):272.

6.  Bright JM, et al. J Vet Cardiology 2005; 7(2):85.

7.  Santilli RA, et al. J Am Vet Med Assoc. 2007; 231(3):393.

8.  Duerr FM, et al. Can Vet J. 2007 Feb;48(2):169.

9.  Spier AW, Meurs KM. J Am Vet Med Assoc. 2004; 15;224(4):538.

10. Meurs KM, et al. J Am Vet Med Assoc. 2002; 221(4):522.

11. Kellum HB and Stepien RL. J Vet Intern Med. 2006; 20(1):97.

12. Schrope DP, et al. J Am Vet Med Assoc. 2006; 228(11):1710.

13. Johnson MS, et al. J Small Anim Pract. 2007; 48(1):4.

14. Wess G, et al. J Vet Intern Med. 2006; 20(4):877.

Speaker Information
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John Bonagura, DVM, DACVIM (Cardiology, Internal Medicine-SA)
The Ohio State University
Columbus, OH


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