During this presentation case examples of coexisting heart failure and arrhythmias will be discussed. The approach to the diagnosis and management will be addressed. The most common arrhythmias and clinical scenarios will be illustrated with emphasis on treatment. We will discuss the treatment of (1) atrial fibrillation with heart failure and (2) ventricular tachycardia with heart failure.

Atrial fibrillation and heart failure

The most common arrhythmia that requires treatment is atrial fibrillation and it is usually found in conjunction with dilated cardiomyopathy and mitral valve regurgitation in the dog. Atrial fibrillation is usually a rapid irregular rhythm associated with chaotic heart sounds and variable pulse quality. The baseline may have fine undulations due to the fibrillating atria. The QRS complexes may have slight variability in their size and shape. Although some giant breed dogs such as Irish wolfhounds can have atrial fibrillation without heart disease, it is most commonly associated with cardiomegaly, particularly of the atria. Small breed dogs and cats that have atrial fibrillation almost exclusively have atrial dilation.

The danger of atrial fibrillation rest in the rapid ventricular response rate; that is, the tachycardia. Although the rapid rate compromises cardiac output, the major concern is the tachycardiomyopathy that can result with sustained rapid rates for too long. Tachycardiomyopathy simply means that the myocardium can actually develop structural and functional compromise because the ventricle is forced to beat too rapidly. These alterations can lead to further deterioration of myocardial reserve in an animal that is already compromised. The tachycardia of atrial fibrillation is most severe when congestive heart failure is present either as pulmonary edema or ascites. Throughout the day the ventricular response rate is not constant as seen with 24-hour recordings of dogs in atrial fibrillation. During the hours of excitement or exercise the heart rate is greater than the time of rest and sleep. These results are because the conduction of the impulses from the atrium through the atrioventricular (AV) node is influenced by sympathetic and parasympathetic tone. With heart failure sympathetic tone is increased, and therefore, the conduction through the AV node is faster.

Control of the ventricular response rate usually is the first goal in the treatment of atrial fibrillation. There are several approaches to meeting this objective. First, in animals with congestive heart failure, controlling the retention of fluid and poor cardiac output will diminish the sympathetic tone and secondarily decrease the heart rate. This is always a priority in treating an animal with both heart failure and atrial fibrillation. However, this is usually inadequate in the management of dogs with atrial fibrillation (the heart rate remains too high), whether the situation is acute or chronic decompensated failure. Therefore, other pharmacologic interventions are required. Three drug categories are most frequently used to treat atrial fibrillation and these include: cardiac glycosides, beta-adrenergic blockade, and calcium channel blockade. The specific choice of drug, route and dose are dictated by the urgency of the situation.

Dogs in a congestive heart failure crisis that are suffering from pulmonary edema, poor cardiac output and the tachycardia of atrial fibrillation, frequently require intravenous medication. Because dogs with dilated cardiomyopathy represent the vast majority of such cases, the points made here are with these animals considered. Dogs with class IV heart failure and atrial fibrillation represent a therapeutic challenge. The drugs that are available for decreasing the ventricular heart rate can frequently affect the cardiovascular system beyond rate control. Although digoxin can decrease the heart rate, it is not desirable as a first line intravenous drug for the treatment of atrial fibrillation. Digoxin to be effective intravenously must be loaded and this can cause adverse effects. Importantly, digoxin slows the rate of atrial fibrillation by increasing parasympathetic tone; however, in class IV heart failure sympathetic stimulation is too high to be overridden adequately by digoxin. Beta-adrenergic drugs can be used intravenously (e.g., esmolol) in to slow the heart rate of atrial fibrillation. However, the negative inotropic effect of these agents may be too compromising for this class of drugs and this is particularly true if higher doses are required to control the heart rate. Finally, the calcium channel blockers can slow the heart rate by an effect on the slow calcium channels of the AV node. These agents (most commonly used today are diltiazem or verapamil) also have a negative inotropic effect, but this effect is less dramatic if the drugs are given slowly intravenously rather than as a rapid bolus. Therefore, diltiazem can be given as a slow bolus (to assess its effectiveness) and then as a constant rate infusion. Sometimes in the management of dogs with coexisting heart failure and atrial fibrillation it is difficult to optimize the balance between decreasing the heart rate and improving myocardial function. This is true because in many dogs the dose of diltiazem required to decrease the ventricular response rate still causes a drop in systemic blood pressure. Although concurrent treatment with digoxin has the potential to help in this situation, the time to digitalization is not immediate and the actual positive inotropic effect to minimal to importantly maintain an adequate blood pressure. Therefore, in such cases clinicians may find themselves administering simultaneously drugs that are having opposing effects. Such is the case when dobutamine must be used to improve function and systemic blood pressure while diltiazem is used to slow the ventricular response rate. During the presentation we will discuss the details of treating a case that encompasses the concepts of severe heart failure with concurrent atrial fibrillation.

The basic principal of treating the underlying heart failure simultaneously while treating the atrial fibrillation applies to dogs that have compensated heart failure too. Today, the pharmaceutical list of drugs to treat heart failure includes diuretics, angiotensin converting enzyme inhibitors, digoxin, pimobendan, nitrates and others. Of these drugs, only digoxin has enough of a negative dromotrophic effect in the AV node to slow the ventricular response rate. But just as in acute heart failure, the magnitude of this effect usually is not strong enough to drop the heart rate to levels that would assure the maximum benefit to the dog. Therefore, frequently, digoxin needs to be combined with another drug. Recently, beta-adrenergic blockers have found favor in the treatment of heart failure in humans with heart failure and these drugs are beginning to be used more frequently in dogs. These agents can also decrease the heart rate in atrial fibrillation, although the dose that is used for failure, may be too low to slow AV node conduction enough. Therefore, today, for most dogs with heart failure we have found the optimal success in combining orally administered digoxin (0.005 mg/kg twice daily, imperative that digoxin levels are determined 7 days later, 8 hours after pilling) and diltiazem (2 to 3 mg/kg sustained release form twice daily) together. With this combined treatment digoxin has the mild positive inotropic effect and positive effect to increase parasympathetic tone while diltiazem directly slows the conduction in the AV node by blocking the calcium channels.

There is an ideal method of monitoring the heart rate of dogs with heart failure and atrial fibrillation. Such a method entails the use of repeated 24-hour electrocardiographic monitoring (Holter monitoring) before treatment is started and then one week after drug therapy has begun and when medication is changed or the disease progresses. Subsequent examinations are determined by the response to the treatment. With the 24-hour electrocardiographic monitoring multiple measures of heart rate can be evaluated. These include (1) average heart rate per hour or over the entire duration of the recording, (2) time that the heart rate is above a certain set rate (frequently set at 120 bpm), and (3) tachygrams that give a graph of the heart rate and its variability averaged every second over the 24 hour period. By accounting for all the daily events of sleeping, behavior and time of day a full appreciated of the baseline heart rate and the response to treatment can be ascertained. This is the optimal way to manage the dogs, but this is not always possible due to costs or availability of the monitors. Consequently, we must rely on each of the following in the monitoring: (1) at home ausculted heart rate (owners taught to take heart rate with stethoscope), (2) in hospital ausculted heart rate, and (3) electrocardiogram in hospital. It should be emphasized that each method is going to give a different heart rate and the goal of the heart rate must be determined based on the means that it is taken. During the presentation the process of determining the target heart rate will be discussed and case examples will be shown to illustrate when this heart rate is met and when it is not.

Heart failure and ventricular tachycardia

Although ventricular tachycardia that demands treatment is less frequent than atrial fibrillation in the presence of heart failure, dedicated attention to this arrhythmia is needed to prevent sudden death. Ventricular tachycardia can occur in many cardiac conditions, but the most frequent situations are found in two dog breeds: boxers with arrhythmogenic right ventricular dysplasia (ARVD) and Doberman pinchers with dilated cardiomyopathy (DCM).

Arrhythmogenic right ventricular dysplasia is a disease that results in the replacement of myocardium with fat and fibrous tissue. It is similar to the same disease in humans and may have abnormal gene expression in cell to cell junction proteins. Boxers with ARVD can present with 3 different clinical scenarios although they are all the same disease: (1) no clinical signs but ventricular arrhythmias detected, (2) clinical signs of syncope or sudden death associated with ventricular tachycardia, and (3) clinical signs of congestive heart failure with ventricular tachycardia. The ventricular arrhythmias are most often monomorphic, rapid rhythms with a left bundle branch block pattern indicating an origin most likely from the right ventricle. Dogs can have variable numbers of arrhythmia from single premature complexes to ventricular tachycardia. Dogs that have heart failure can also have ventricular arrhythmias that are polymorphic indicating origin from multiple regions of the ventricles. Holter monitoring has shown that when boxers faint it is associated with ventricular tachycardia. This is not absolute; however, because on occasion boxers have been identified that have both ventricular tachycardia and sick sinus syndrome. Although some proof exists to say that treatment of the ventricular arrhythmias decreases the arrhythmia count, inadequate proof exists to state that sudden death is prevented. However, sotalol (2 to 2.5 mg/kg twice daily) when given at the proper dose for a given dog does decrease the ventricular tachycardia frequency. Most commonly dogs without heart failure are treated. This is simply because these dogs are more commonly seen. When heart failure coexists with ventricular tachycardia in boxers we still use sotalol as the first treatment of choice, despite the risk of excessive negative inotropic effects from the beta-adrenergic blockade component of sotalol. This is done because of the high risk of sudden death. Just as described above, treatment of heart failure is conscientious and follow-up is methodical. Baseline and after treatment 24-hour electrocardiographic monitoring is the ideal tool for determining an adequate response to treatment. Although an elimination of the ventricular arrhythmias is ideal, the first goal is the eradication of ventricular tachycardia. Commonly the heart rate, number of pauses, and duration of pauses increase during the treatment with sotalol and this is most likely due to the beta-adrenergic blockade.

Doberman pinchers with DCM have rapid polymorphic ventricular tachycardia associated with myocardial failure. Although the arrhythmias certainly meet the criteria for treatment, effective treatment of these dogs is more difficult. We still use sotalol, but the response is more varied than in the boxers and the antiarrhythmic effect less apparent. Also, some Dobermans may actually die of a sudden bradycardia, although this is likely less frequent than ventricular fibrillation as the ventricular tachycardia degenerates before death. Treatment of the underlying cardiac disease and congestive heart failure as usual is paramount, yet difficult.

In boxers, Doberman pinchers and other breeds with ventricular tachycardia that do not respond to sotalol, we have found success with mexiletine combined with atenolol. Most recently a combination of sotalol and mexiletine can be antiarrhythmic in selected cases. It is imperative that if such combinations are used, careful monitoring is used.