Atrial fibrillation tough to manage at times due to many other concurring problems
Q: Please provide a brief review of the clinical management of atrial fibrillation in older dogs and cats.
A: Atrial fibrillation is a commonly diagnosed supraventricular arrhythmia in older dogs and cats. Atrial fibrillation is usually associated with underlying heart disease - advanced stages of atrial enlargement secondary to dilated or hypertrophic cardiomyopathy or volume overload from chronic atrioventricular valve regurgitation. Atrial fibrillation may also occur in the absence of organic heart disease and is referred to as idiopathic or lone atrial fibrillation. The following articles describe current experiences in the clinical management of atrial fibrillation in dogs and cats: Gelzer A: the challenges of atrial fibrillation. Proc 20th Annual Forum ACVIM 20: 92, 2002 and Bright JM, Martin JM: treatment of atrial fibrillation: challenging the paradigm. Proc 20th Annual Forum ACVIM 20: 103-105, 2002.
atrial fibrillation produces several clinical consequences as a result of cessation of effective atrial contraction, and from the irregular and often rapid ventricular rate frequently induced. With underlying heart disease, the onset of atrial fibrillation usually coincides with deterioration in the animal's clinical signs such as onset of weakness, anorexia and congestive heart failure. atrial fibrillation in dogs with cardiac disease decreases cardiac output by 25-39 percent and increases ventricular filling pressures. These deleterious hemodynamic consequences occur even without a significant change in heart rate.
In addition, atrial fibrillation reduces coronary flow relative to myocardial oxygen demand, and the characteristically rapid ventricular rate of atrial fibrillation will cause myocardial systolic dysfunction (tachycardia-induced cardiomyopathy). Even in healthy dogs, induction of atrial fibrillation reduces cardiac output by 25 percent. Although the long-term effects of lone atrial fibrillation in dogs are unclear at this time, it is conceivable that in atrial fibrillation, wide fluctuations of heart rate with peak heart rates exceeding those that occur during sinus rhythm may produce cardiomyopathy.
Clinical signs of animals with atrial fibrillation depend largely on the presence and severity of an underlying heart disease. Dogs may present with congestive heart failure with signs of coughing, dyspnea or weakness due to advanced stages of dilated cardiomyopathy, atrioventricular valve insufficiency or cardiac enlargement due to left-to-right shunting.
In giant-breed dogs, atrial fibrillation may be an incidental finding with no clinical signs pertaining to the cardiovascular system. Cats with atrial fibrillation may have various forms of cardiomyopathy, with significant left atrial or biatrial enlargement secondary to diastolic dysfunction.
Physical examination findings for atrial fibrillation include an irregular heart rate, with a rate of 70270 beats/min depending on the severity of the underlying heart disease and the autonomic tone. The intensity of S1 is inconsistent and the femoral pulses quality can vary from normal to weak, depending on the heart rate and underlying heart disease. atrial fibrillation is recognizable on the electrocardiogram by the absence of distinct atrial activity (P waves), replaced by a baseline of undulating wavelets occurring at a rate greater than 500 beats/min (F waves).
Additionally, there is no predictable relationship present between atrial and ventricular complexes; therefore, the ventricular response is irregular. Very rapid atrial fibrillation may appear to be regular. On the electrocardiogram, atrial fibrillation may be confused with a rapid supraventricular tachycardia where P waves are buried in the previous QRS complex. atrial fibrillation with aberrant ventricular conduction may mimic ventricular tachycardia with invisible P waves.
Evaluation of an animal with suspected atrial fibrillation should include thoracic radiographs and an echocardiogram for determination of chamber dimensions and cardiac function to diagnose or confirm presence of underlying heart disease.
The development of atrial fibrillation in animals with severe underlying heart disease can be a serious sequel, due to the complete absence of coordinated atrial systole (loss of atrial contraction) and, therefore, decreased ventricular filling. In addition, if the ventricular response rate is fast, the increase in heart rate results in a deterioration of systolic function.
The combined effects cause a decrease in cardiac output and can progress to overt congestive heart failure. Chronically elevated heart rates during atrial fibrillation in an animal with no underlying heart disease may eventually progress to a primary tachycardiomyopathy with systolic dysfunction and chamber enlargement similar to dilated cardiomyopathy.
Remember that increased sympathetic tone - during obtaining an electrocardiographic tracing (animals are restrained and may be very stressed) and during hospitalization - is in part responsible for acceleration of atrioventricular nodal conduction and may result in transiently increased heart rates.
In such cases, a 24-hour Holter recording may be used to obtain a more accurate heart-rate assessment in a home environment. In dogs with atrial fibrillation secondary to heart disease, the average heart rate often exceeds 160 beats/min and can be as high as 220 beats/min (range 150-320 beats/min). Dogs with very mild or occult underlying heart disease as well as dogs with lone atrial fibrillation may present with heart rates within normal limits. Cats with atrial fibrillation invariably have severe underlying heart disease - very rapid heart rates.
Heart rate reduction is still the preferred treatment for atrial fibrillation. Adequate heart rate control may be achieved in a dog in a range of 80 beats/min during rest and 150 beats/min during exercise.
If concurrent heart failure is present, a dog may require a relatively higher average heart rate to maintain adequate blood pressure than a dog with uncompromised ventricular function. Currently, there is no data proving that dogs with atrial fibrillation with slow ventricular response rates have a higher death rate than dogs that are converted from atrial fibrillation to sinus rhythm. Conversion to sinus rhythm in dogs can be a difficult task, even in lone atrial fibrillation with slow ventricular response rates, depending on how chronic the condition is.
Success of pharmacologic restoration of sinus rhythm in dogs and cats is nil. Pharmacologic conversion is most promising in very recent onset atrial fibrillation in animals with minimal or no underlying heart disease (lone atrial fibrillation). Unfortunately, the time of onset of atrial fibrillation is usually not known, and atrial fibrillation may be an incidental finding if clinical signs are absent.
Controlling the heart rate
In dogs with atrial fibrillation and an elevated ventricular response, rate-control is initiated with digoxin (0.005 mg/kg BID). Digoxin works by enhancing vagal tone and slowing the atrioventricular node conduction velocity.
If heart rates are markedly elevated or overt congestive heart failure is present, digoxin alone is unlikely to achieve adequate rate control. These animals are sympathetically stimulated and the vagomimetic effects of digoxin are subjugated. Successful management of congestive heart failure with ACE-inhibitors and diuretics may contribute to improved heart rate control, because overall sympathetic tone may be lessened. In this situation, a combination of digoxin with a calcium channel blocker or a beta-blocker is effective.
Diltiazem (1.5-6 mg/kg PO SID or divided BID) or atenolol (0.25-1 mg/kg PO SID to BID) is a good choice. The mild negative inotropic effects of these two drugs are offset by the positive effects of heart rate reduction, resulting in prolonged diastole, improved filling pressures and reduced myocardial oxygen consumption.
Blood pressure and renal status should be monitored, because hypotension and prerenal azotemia may be induced with aggressive medical management in these animals.
In giant-breed dogs with lone atrial fibrillation and heart rates within normal limits (in hospital or by Holter monitoring during 24 hours: range 60-150 beats/min, with an average of less than 120 beats/min), there is no need to reduce the ventricular rate any further.
However, many dogs with lone atrial fibrillation go on to develop signs of heart failure later in life. Therefore, administration of digoxin or a beta blocker alone in dogs with normal ventricular rates may improve long-term outcome and is usually of no detriment to the animal. This concept remains to be proven.
In cats, rate-control is targeted with beta blockers (atenolol 6.25-12.5 mg PO SID) or calcium channel blockers (diltiazem 7.5 mg/kg PO SID or divided BID); heart rate reduction to 170-220 beats/min would be desirable.
Monotherapy with amiodarone or sotalol has not resulted in successful conversion of atrial fibrillation to sinus rhythm in most affected dogs. Transthoracic, synchronized DC cardioversion (50-300J) alone or in combination with pharmacologic loading with sotalol or amiodarone or propafenone or flecainide antiarrhythmic drug may be helpful. However, success can be limited and recurrence of atrial fibrillation is common immediately or shortly after conversion. In animals with lone atrial fibrillation, radiofrequency ablation of pulmonary vein foci that trigger atrial fibrillation can lead to a permanent cure.
A surgical therapy involves isolation of the pulmonary veins and atrial appendage (maze procedure) to reduce the electrical atrial surface area and abolish re-entry. In the clinical setting, these therapeutic approaches have not been tested in animals.
Atrial fibrillation can be a challenging arrhythmia to manage because most affected animals have numerous other concurring problems associated with the underlying heart disease that influence the veterinarian's choice of treatment and monitoring strategy for each individual animal.