Introduction

Arrhythmia means, in simple words, "no rhythm". An arrhythmia (also called dysrhythmia) is a deviation from the normal cardiac rate and rhythm, site of origin of the cardiac impulse, or sequence of activation of the atria or the ventricles. Consequently, any heart rhythm that does not originate from the sinus node at a normal rate and at regular interval is classified as an arrhythmia. Mechanisms of arrhythmogenesis primarily include disorders of cardiac electrical impulse formation and electrical impulse conduction. Abnormalities of impulse formation can produce both tachyarrhythmias and bradyarrhythmias. Conduction abnormalities may result in delayed conduction or block, but may also contribute to the formation of ectopy (premature or ectopic depolarizations). There are 3 basic mechanisms that may explain the initiation and maintenance of tachyarrhythmias: Reentry ("retaking possession" or "coming back"), enhanced automaticity ("cells fire or depolarize faster than normal"), and triggered activity ("get kicked by something else"). Determination of the underlying mechanisms is not always possible using the surface ECG and multiple mechanisms may be present with a given arrhythmia, however, certain more specific ECG features make a specific mechanism likely which may help making a decision on specific antiarrhythmic treatments. Surface ECG characteristics of arrhythmias whose underlying mechanism is reentry include 1) paroxysmal onset and cessation, 2) very rapid rates (400 to 500 min^-1 possible), and 3) initiation and termination by a premature beat (most often). In contrast, automatic SVT is characterized by "warm-up" (relatively slowly rising heart rate over a time period of several heart beats) and 'cool down' phenomena (gradual decrease of heart rate at termination of the arrhythmia). Tachyarrhythmias secondary to triggered activity may not have specific morphologic ECG characteristics, however, Torsade de Pointes (polymorphic ventricular tachyarrhythmia with "twisting of the points") and inherited superfast ventricular tachycardia in German shepherds are examples of triggered activity caused by early or delayed after depolarizations. Certain drugs (e.g., sotalol, procainamide), hypokalemia, and conditions associated with intracellular calcium overload (e.g., advanced myocardial disease) may induce triggered activity. There are 3 proposed prerequisites for induction and maintenance of tachyarrhythmias: 1) A substrate such as an area of myocardial ischemia, fibrosis, and inflammation, or an accessory pathway; 2) A trigger such as a premature beat; and 3) modulators such as drugs, toxins, electrolytes, myocardial stretch, autonomic imbalance, hypothermia, or ischemia. If all 3 are present, the development of an arrhythmia is very likely. Moreover, strategies for successful treatment of most tachyarrhythmias are based on addressing either the substrate (e.g., relieve the ischemia), suppress the trigger (e.g., treat APCs and VPCs), and influence the modulators (e.g., correct electrolyte imbalances), or address all three. Based upon site of origin, tachyarrhythmias may be divided into supraventricular and ventricular.

Supraventricular Tachyarrhythmias (SVT)

As the name implies, SVT's are fast (> 160 bpm in dogs and > 240 bpm in cats) and require atrial or atrioventricular junctional tissue for its initiation and maintenance. Although sinus tachycardia also originates in that geographic region many cardiologists do not consider sinus tachycardia as a type of SVT as sinus tachycardia is, in almost all instances, a temporary physiologic response to external stimuli (e.g., stress, excitement, exercise, or hypovolemia). Different types of SVT may be observed (see below). Causes of SVT (and ventricular tachyarrhythmias) may for ease of remembrance be divided into 5 categories: 1) cardiac, 2) drugs and toxins, 3) autonomic imbalance, 4) metabolic / endocrine, and 5) usual suspects (e.g., GDV, head trauma, neurologic disease). Typical ECG findings with SVT include narrow-complex tachycardia, electrical alternans, evidence of atrial activation (P', F, or f waves), and response to treatments that slow down AV conduction. In rare cases (< 5%), SVTs may have a wide QRS complex (e.g., if the ventricles are severely dilated or if aberrant conduction is present). Sustained SVT with 1:1 AV conduction is a life threatening rhythm disturbance and should, therefore, be immediately corrected. Clinical signs such as weakness, dyspnea, lethargy, and syncope related to reduced cardiac output, hypotension, and congestion are consequences of prolonged tachycardic events. If sustained, tachycardia-induced cardiomyopathy may be the long-term consequence. Physical, electrical, and pharmacological maneuvers may all be initiated to treat SVTs. This summary only discusses pharmacological treatment options (see drug class and dose in Table 1).

Sinus tachycardia (ST): Correct underlying cause; treat of thyrotoxicosis and give atenolol if persistent ST in hyperT4.

Atrial tachycardia: Both sotalol, amiodarone (use only in dogs), and atenolol have effects on atrial ectopy. However, due to its negative inotropic effects, Atenolol should not be used in animals with congestive heart failure (CHF). Oral procainamide (regular, q8h and extended release, q12h) may also be effective. Digitalis may enhance atrial ectopy and should, therefore, not be administered. Although diltiazem's main antiarrhythmic effect is blockade of L-type Ca-channels of the AV node and related reduction of AV nodal conduction, we have observed dogs in which the addition of diltiazem to sotalol led to a considerable reduction of atrial ectopy.

Atrial flutter / atrial fibrillation (Afib): The combination of digoxin and diltiazem is preferred by most to control ventricular response rate in Afib in dogs. Only one drug (either/or) is preferred by the author in cats. Digoxin should not be administered if relevant ventricular ectopy is present as digoxin may enhance automaticity of the His-Purkinje system favoring the genesis of ventricular arrhythmias. If ventricular rate cannot be controlled sufficiently enough and clinical status and myocardial function allow, addition of atenolol is indicated. In situations where Afib is accompanied by CHF or severe systolic dysfunction, preference may be given to amiodarone (and sometimes sotalol). In rare cases of acute vagally-induced Afib (e.g., in dogs with GDV or in animals treated with fentanyl), intravenous lidocaine may convert Afib into normal sinus rhythm promptly (after 1 or 2 IV-doses of lidocaine).

Junctional tachycardia: This is a rare type of SVT most commonly associated with digitalis toxicity. Treatments aim at relief of the underlying cause. Diltiazem, sotalol, atenolol, and amiodarone may also be effective.

AV-nodal and AV-reentrant tachycardia: Both types of SVT are AV nodal-dependent and should be interrupted by drugs that slow down AV nodal conduction. Repeated doses of diltiazem and esmolol are preferred. Chronic treatment would include diltiazem, atenolol, or sotalol. Sometimes, the combination of pharmacological and physical (gentle eyeball pressure, carotid sinus massage) procedures may be more effective in abolishing the arrhythmia than drugs alone. If an accessory pathway is involved in maintaining the arrhythmia, drugs such as procainamide, sotalol, and amiodarone may slow or interrupt conduction through the bypass tract.

As SVTs are most often due to left heart disease associated with arrhythmia-favoring LA dilatation, any means to reduce LA size (e.g., preload-lowering drugs) may be associated with a reduction of atrial ectopy. Also, Enalapril and Fish oil have been shown in rodents and humans to have a negative impact on atrial arrhythmogenesis. If symptomatic, fast (> 250 min^-1), and potentially life-threatening SVT cannot be "broken" by physical maneuvers and pharmacologic agents synchronized DC cardioversion, performed by a certified specialist in cardiology, may be mandated.

Ventricular Tachyarrhythmias (VT)

With ventricular ectopy, the abnormal impulse arises distal to the bifurcation of the bundle of His. Depending on the proximity of the impulse origin to the bundle and its branches, the ECG appearance of the beat varies from a nearly normal QRS morphology to a wide, bizarre, aberrant complex. The latter results from slow muscle fiber-to-fiber impulse propagation, whereas the former is due to rapid Purkinje fiber transmission. By definition, VT means a series of 3 or more consecutive beats of ventricular origin. Sustained VT is prolonged (> 30 sec), whereas paroxysmal VT has short bursts of fast regular rhythms that terminate spontaneously. The hemodynamic consequences of VT depend on their rate, duration, and the severity of cardiovascular disease. Reduced cardiac output leading to hypotension, collapse, CHF, renal failure, and further progression of myocardial disease due to ischemia and calcium overload may result. Mechanisms leading to VT are similar to mechanisms leading to SVT. VT is almost always a wide-complex tachycardia. The ECG hallmarks of VT include the presence of A-V dissociation, fusion beats, and capture beats. When a P wave reaches the ventricle at the same time as the ectopic focus fires, a QRS complex with a morphology that combines features of both the ectopic and the capture beat occur. This complex is termed a fusion beat and is evidence that ventricular ectopy is present. VT originating from the right ventricle is commonly associated with upright QRS complexes in lead II, whereas ventricular ectopy originating from the left ventricle is characterized by negative QRS complexes in lead II. VT may be monomorphic (all ectopic complexes look alike) or polymorphic. The latter indicates more electrical heterogeneity and more malignant ectopy. Finally, dogs may develop ventricular flutter (fast but still organized ventricular activity) or ventricular fibrillation (fast, unorganized, chaotic ventricular activity). Both types of arrhythmias are common precursors of sudden cardiac death and require immediate attention. Accelerated idioventricular rhythm is a benign type of VT which is frequently seen in animals with autonomic imbalance, does not relevantly affect hemodynamics, is self limiting, and does NOT need to be specifically treated. However, from a differential diagnostic point of view identification of accelerated idioventricular rhythms is of utmost importance.

Treatment of ventricular ectopy is still a matter of debate and depends on 1) the underlying disease, 2) its hemodynamic consequences, 3) clinical signs associated, and 4) the presumed risk of sudden cardiac death. In all cases, an attempt to identify and resolve underlying and correctable predisposing factors should be made. If this is not possible or the patient's condition dictates immediate relief, specific antiarrhythmic intervention is warranted.

Intravenous treatment: If the patient is clinically stable, the blood pressure is within the normal range, the VT is less than 180 min^-1, and the complexes are monomorphic immediate IV or other intervention is usually not needed. Remember that almost all antiarrhythmics have intrinsic pro-arrhythmic properties and are hemodynamically depressing, therefore, unless there is clear clinical indication such compounds should be avoided. Ventricular flutter or fibrillation should be corrected immediately with precordial thumps, IV lidocaine, IV procainamide, and magnesium, or transthoracic electrical defibrillation. Due to the potential for severe adverse effects IV amiodarone is not recommended anymore. Keep in mind that the effects of lidocaine and procainamide depend on the blood concentration of potassium--hypokalemia makes both drugs ineffective.

Oral treatment: For chronic oral treatment of ventricular arrhythmias, the "ASPAM" drugs are most commonly used (Atenolol, Sotalol, Procainamide, Amiodarone, and Mexiletine). Combinations of Atenolol and Mexiletine or Sotalol and Mexiletine may be considered when each of the single drugs fails. Also, the addition of Carvedilol or Fish oil to one-or-two-drug treatment protocols may be beneficial. Holter ECG monitoring is needed at baseline and under the influence of the drug to verify treatment success. As the presence of ventricular ectopy may have considerable day to day variation only a significant reduction of the number of VPCs (most cardiologists consider 85% or more) or the observation of less malignancy of the ectopics (less couplets, less triplets, less runs of VT) are considered treatment success. Also, elimination of clinical signs such as syncope means successful treatment. Complete elimination of the arrhythmia cannot be a realistic treatment goal. Remember that sotalol as well as amiodarone have increased toxicity in the presence of hypokalemia. As Mexiletine may soon go out of production and may not be available anymore, another class-I antiarrhythmic drug (Flecainide), may become a useful alternative.

Table 1. Selected drugs and doses commonly used for the treatment of SVT and VT in dogs and cats.

NPD, no published dose (Do not use). Vaughan-Williams classification: Class I (Sodium channel antagonist), Class II (Beta receptor blocker), Class III (Potassium channel antagonist), Class IV (Calcium channel blocker). Please note: The antiarrhythmic class based on mechanism of action represents only the main effect of the drug. Many antiarrhythmic drugs have additional, auxiliary effects. *Additional alpha-1 blocking activity and antioxidative properties. (Data from Bonagura JD, Twedt DC. Kirk's Current Veterinary Therapy. St. Louis: Saunders Elsevier, 2009, pp 1306-1336.)

References

References are available upon request.