Problem Definition

Disturbances of heart rate and cardiac rhythm are commonly present with both cardiac and noncardiac disorders. While some arrhythmias have no clinical consequence, some cause significant hemodynamic compromise, resulting in pulse deficits, weakness, syncope, or even sudden death. The decision to treat abnormalities of heart rate and rhythm must be made on the basis of the clinical circumstances.

Normal Anatomy and Physiology

Pathophysiology

Classification

Although it is common to classify arrhythmias according to anatomic origin and/or mechanism, clinically it is more logical to utilize a classification on the basis of heart rate. Arrhythmias are divided into tachyarrhythmias (elevated heart rates), bradyarrhythmias (slow heart rates), and those rhythms with a normal heart rate (Table 17-1).

Tachyarrhythmias

Sinus Tachycardia. Sinus tachycardia is the most common arrhythmia in both the dog and the cat (Tilley 1992). It is a regular sinus rhythm that occurs at an elevated rate. Since there is a wide range ofresting heart rates for normal dogs and cats, the distinction between sinus rhythm and sinus tachycardia is not always clear. In general, a sinus tachycardia occurs at a rate greater than 160 bpm for dogs and greater than 240 bpm for cats (Tilley 1992). On electrocardiographic examination, the P-waves are normal in morphology and the QRS complexes are narrow. Gradual speeding up and slowing of the heart rate is characteristic of this rhythm. The underlying mechanism of sinus tachycardia is elevated sympathetic tone, and the causes are numerous. Common physiologic causes include stress, exercise, and pain.

Table 17-1. Differential diagnoses of arrhythmias and conduction disturbances on the basis of rate and regularity during physical examination.

Pathologic causes include, but are not limited to, the following conditions: hypotension/ hypovolemia, fever, anemia, hypoxia, congestive heart failure, hyperthyroidism, sepsis, and toxicities/drugs (Tilley 1992; Côté and Ettinger 2005). Treatment is not aimed at the arrhythmia itself but at the underlying cause.

Atrial Tachycardia. Atrial tachycardia consists of three or more consecutive ectopic atrial complexes that occur faster than the normal sinus rhythm. Ectopic atrial complexes are impulses that arise within the atrial myocardium but outside of the sinus node. The rate of atrial tachycardia is usually above 200 bpm and may reach over 300 bpm. This rhythm is almost always regular. Atrial tachycardia is usually paroxysmal, but may be sustained in some cases. The morphology of the QRS complex is similar to that of a normal sinus complex, unless aberrant conduction exists. The waveform associated with atrial depolarization from the ectopic focus differs from a normal sinus P-wave and is termed a “P′-wave.” The morphology of the P^;-wave depends on the atrial location of the ectopic origin. This difference in morphology between P′-waves and sinus P-wave may be helpful in making an ECG diagnosis. In some cases, the atrial tachycardia may be rapid enough that the P′-waves summate over the T-waves of the previous complex, obscuring their identification (Fig. 17-1) (Tilley 1992; Côté and Ettinger 2005).

Causes of atrial tachycardia most commonly involve atrial dilatation or stretch secondary to mitral valvular endocardiosis or dilated cardiomyopathy in the dog or various types of cardiomyopathy in the cat. Less common causes of atrial ectopy include cardiac masses (e.g., right atrial hemangiosarcoma), atrial dilation due to other cardiac diseases (e.g., congenital heart disease), and drug toxicities (e.g., digoxin) (Tilley 1992; Côté and Ettinger 2005). Uncommonly, atrial tachycardia is associated with a congenital accessory pathway that bypasses the AV node. In these patients, tachyarrhythmias may result from a macroreentrant circuit utilizing the AV node and the bypass tract as limbs of the circuit. Catheter ablation of such pathways is curative. The reader is referred to other sources for a more detailed description of these unusual cases (Wright et al. 1999; Wright 2000, 2004).

Use of a vagal maneuver (i.e., carotid massage) or intravenous drugs blocking AV nodal conduction (e.g., diltiazem) may terminate the rhythm or cause block of some of the atrial impulses through the AV node, providing both therapeutic and diagnostic benefit. Treatment of atrial tachycardia may involve two approaches: suppressing the atrial focus or slowing the ventricular response rate by decreasing conduction through the AV node. Class Ia (e.g., procainamide) or class III (e.g., sotalol and amiodarone) antiarrhythmic drugs are used to suppress an atrial ectopic focus. Class Ic drugs are also effective but are not commonly used due to their frequent and serious side effects (e.g., renal failure). Digoxin, diltiazem, and beta-blockers are used to slow down conduction through the AV node, resulting in a slower ventricular response rate. Adjunct treatment should be directed toward the underlying cause (Wright 2000, 2004).

FIGURE 17-1. Paroxysmal atrial tachycardia (PAT) in a 7-year-old female Irish wolfhound with dilated cardiomyopathy. Within the run of atrial tachycardia, most of the P′-waves are summated over the T-wave of the previous complex. Lead II; 25 mm/s, 10 mm/mV

FIGURE 17-2. Atrial flutter (F-waves) at a rate of over 400/minute in an English bulldog with right ventricular cardiomyopathy. There are varying degrees of conduction to the ventricles resulting in a ventricular rate that ranges from 120 to 200 bpm. Telemetry lead; 25 mm/s.

Atrial Flutter. Atrial flutter is an uncommon arrhythmia in both dogs and cats. This rhythm involves a macroreentrant circuit within the right atrium. This circus movement creates rapid and regular atrial depolarizations. The electrocardiographic hallmark of atrial flutter is the replacement of P-waves by “flutter waves.” Flutter waves have a sawtooth appearance with an absence of a return to baseline (Fig. 17-2). The atrial rate of depolarization usually ranges from 300 to 600 impulses per minute. The QRS morphology should be narrow unless conduction disease or aberrancy exists. As with most supraventricular tachycardias, the AV node ultimately determines the number of impulses reaching the ventricle. Most often there is 2:1 physiologic block within the AV node, resulting in only one QRS complex for every two flutter waves. There can be higher grades of physiologic block (e.g., 3:1, and 4:1) whereby fewer atrial impulses reach the ventricle. If there is 2:1 conduction, the ventricular rate is very rapid and most of the flutter waves are buried in the QRS complexes, making ECG diagnosis difficult (Tilley 1992; Moïse 1999; Côté and Ettinger 2005).

Atrial flutter most commonly occurs as a result of atrial pathology (i.e., right atrial stretch), but can also develop secondary to myocardial irritation as may occur during surgery or cardiac catheterization. Atrial flutter is an unstable rhythm that often degenerates into atrial fibrillation fairly rapidly. Treatment may involve electrical cardioversion back to a normal sinus rhythm or rate control using pharmacologic means of slowing AV nodal conduction (i.e., digoxin, diltiazem, beta-blockers) (Moïse 1999; Côté and Ettinger 2005).

Atrial Fibrillation. Atrial fibrillation is a very common and important arrhythmia in dogs but is very rare in cats. In this rhythm, the sinus node no longer controls atrial depolarization. Instead, there is chaotic electrical disorganization of atrial impulses. The electrophysiological mechanism of atrial fibrillation is not completely understood but likely involves a primary reentry circuit that fragments into multiple microreentrant circuits within the atria. This involves more than 400–500 atrial impulses traveling through the atrial myocardium per minute (Jalife 2003; Everett and Olgin 2004; Brundel et al. 2005). The AV node acts as the “gate keeper” of the ventricle, allowing only some of these atrial impulses to reach the ventricles. Electrocardiographic diagnosis of atrial fibrillation is made on the basis of the following features: lack of discernible P-waves, irregularly irregular R-to-R intervals, narrow QRS complexes (unless aberrancy or a bundle branch block exists), and the presence of coarse or fine flutter waves (Fig. 17-3). Slight variation in QRS morphology or height is not unusual due to slight differences in conduction of impulses down the AV node (Tilley 1992; Côté and Ettinger 2005). These ECG features translate into physical examination findings of a rapid, irregularly irregular rhythm (“tennis shoes in a dryer”) on thoracic auscultation. The irregularly irregular rhythm results in variable time for diastolic filling and correlates with the presence of variable pulse quality and frequent pulse deficits.

FIGURE 17-3. Coarse atrial fibrillation (f waves) with a ventricular response rate of 100-120/minute in a 5-year-old male Newfoundland dog. This patient was diagnosed with lone atrial fibrillation due to the absence of structural heart disease evident on echocardiography. Lead II; 25 mm/s, 10 mm/mV.

Because a certain critical mass is needed to support this rhythm, atrial fibrillation is most commonly diagnosed in small animal patients with structural heart disease and atrial dilatation. The most common diseases associated with atrial fibrillation are mitral valvular endocardiosis and dilated cardiomyopathy in the dog and hypertrophic cardiomyopathy or restrictive cardiomyopathy in the cat. The ventricular response rate in canine patients is almost always rapid due to the high sympathetic tone associated with severe structural cardiac disease (Moïse 1999; Côté and Ettinger 2005). Patients who present in congestive heart failure often have rates of 180–240 bpm or higher (Fig. 17-4). Occasionally there are patients who develop atrial fibrillation without any underlying cardiac disease (“lone atrial fibrillation”). The ventricular response rate associated with atrial fibrillation in these patients is near normal. Patients with lone atrial fibrillation are most commonly giant-breed dogs such as Irish wolfhounds or Scottish deerhounds (Tilley 1992; Côté and Ettinger 2005). Atrial fibrillation may also develop in normal canine patients during general anesthesia, pericardiocentesis, or with gastrointestinal disease (Côté and Ettinger 2005). In contrast to dogs, almost all cats with atrial fibrillation have severe cardiac pathology (Côté el al. 2004).

Patients with atrial fibrillation secondary to structural heart disease often present in congestive heart failure due to the hemodynamic compromise caused by this rhythm. Due to loss of the atrial contraction, ventricular filling decreases and cardiac output subsequently declines. The often rapid rate that results from this rhythm shortens the time allowed for diastolic filling, resulting in a further decline in cardiac output (Côté and Ettinger 2005). Furthermore, cats with this rhythm are at high risk for thromboembolic events due to stasis of blood within the atria (Côté et al. 2004).

Sustained tachycardia can lead to progressive myocardial dysfunction (“tachycardia-induced cardiomyopathy”) (Moïse 1999; Power and Tonkin 1999; Wright et al. 1999; Wright 2004; Foster et al. 2006). For this reason, rate control is very important in the long-term management of patients with atrial fibrillation. Since the conduction properties of the AV node ultimately determine the ventricular response rate in atrial fibrillation, treatment of atrial fibrillation involves drugs that target the AV node. Medical therapy involves administration of drugs that slow down conduction through the AV node and prolong the node refractory period (Tilley 1992; Gelzer and Kraus 2004; Côté and Ettinger 2005). Digoxin is most commonly used in conjunction with calcium-channel blockers (i.e., diltiazem). Beta-blockers must be used with great caution in those patients with severe underlying cardiac disease, as such drugs can exacerbate congestive heart failure as a result of their negative inotropic effects. The target in-hospital heart rate for patients receiving medical therapy is approximately 120—150 bpm. In patients with lone atrial fibrillation, electrical cardioversion may be attempted. Direct current electrical cardioversion involves the delivery of a low-energy shock timed with the QRS complex while the patient is under general anesthesia. This technique is ineffective in individuals with significant cardiac pathology or with a chronic duration of the arrhythmia (Gelzer and Kraus 2004; Ziv and Choudhary 2005). Rarely, pharmacologic cardioversion using class Ia, Ic, or III antiarrhythmic agents is successful (Moïse 1999).

FIGURE 17-4. Fine atrial fibrillation (f waves) with an average ventricular response rate of 200/minute in a 6-month-old German shepherd dog diagnosed with patent ductus arteriosus and congestive heart failure. Lead II; 50 mm/s, 5 mm/mV.

Junctional Tachycardia. Junctional tachycardia is a rapid, regular rhythm whereby the origin of the impulse is the AV junction. The mechanism for the arrhythmia is either enhanced automaticity or a reentry circuit, as the rate is faster than the inherent rate of this region of the conduction system. It is difficult to distinguish this rhythm from other supraventricular arrhythmias (i.e., atrial tachycardia, sinus tachycardia) on a surface ECG because the P′-waves are often buried within the QRS complexes. As with other supraventricular tachyarrhythmias, the QRS morphology should be narrow unless conduction disease or aberrancy exists. Common causes of junctional tachycardia are similar to that of atrial tachycardia and include digoxin toxicity and cardiac disease resulting in atrial dilatation. Treatment is identical to that for atrial tachycardia (Tilley 1992; Côté and Ettinger 2005).

Ventricular Tachycardia. Ventricular tachycardia is defined as a series of three or more ectopic impulses originating from the ventricle. It can be paroxysmal or sustained. Ventricular tachycardia is identified on ECG by the typical appearance of the QRS complex (Fig. 17-5). Because ventricular depolarization occurs by cell-to-cell conduction, the resulting QRS complexes are wide and bizarre. Because depolarization is abnormal, repolarization is also abnormal, resulting in giant T-waves. It should be noted that supraventricular impulses may appear widened if a conduction disturbance, such as a left bundle branch block, exists. Differentiation between ventricular tachycardia and supraventricular tachycardia becomes more difficult in this situation, and accurate identification is made easier if the arrhythmia is paroxysmal. The presence of fusion beats (QRS complexes with a morphology intermediate between sinus and ventricular complexes), capture beats (sinus QRS complex immediately following termination of VT), or atrioventricular dissociation (presence of

FIGURE 17-5. Paroxysmal ventricular tachycardia (VT) in a 3-year-old male Doberman pinscher with a history of collapsing episodes. Capture beats (C) are normal sinus complexes that occur immediately following termination of the VT. Lead I; 50 mm/s, 10 mm/mV.

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