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.
Q: Please provide a brief review of the clinical management of atrialfibrillation in older dogs and cats.
A: Atrial fibrillation is a commonly diagnosed supraventriculararrhythmia in older dogs and cats. Atrial fibrillation is usually associatedwith underlying heart disease - advanced stages of atrial enlargement secondaryto dilated or hypertrophic cardiomyopathy or volume overload from chronicatrioventricular valve regurgitation. Atrial fibrillation may also occurin the absence of organic heart disease and is referred to as idiopathicor lone atrial fibrillation. The following articles describe current experiencesin the clinical management of atrial fibrillation in dogs and cats: GelzerA: the challenges of atrial fibrillation. Proc 20th Annual Forum ACVIM 20:92, 2002 and Bright JM, Martin JM: treatment of atrial fibrillation: challengingthe paradigm. Proc 20th Annual Forum ACVIM 20: 103-105, 2002.
atrial fibrillation produces several clinical consequences as a resultof cessation of effective atrial contraction, and from the irregular andoften rapid ventricular rate frequently induced. With underlying heart disease,the onset of atrial fibrillation usually coincides with deterioration inthe animal's clinical signs such as onset of weakness, anorexia and congestiveheart failure. atrial fibrillation in dogs with cardiac disease decreasescardiac output by 25-39 percent and increases ventricular filling pressures.These deleterious hemodynamic consequences occur even without a significantchange in heart rate.
In addition, atrial fibrillation reduces coronary flow relative to myocardialoxygen demand, and the characteristically rapid ventricular rate of atrialfibrillation will cause myocardial systolic dysfunction (tachycardia-inducedcardiomyopathy). Even in healthy dogs, induction of atrial fibrillationreduces cardiac output by 25 percent. Although the long-term effects oflone atrial fibrillation in dogs are unclear at this time, it is conceivablethat in atrial fibrillation, wide fluctuations of heart rate with peak heartrates exceeding those that occur during sinus rhythm may produce cardiomyopathy.
Clinical signs of animals with atrial fibrillation depend largely onthe presence and severity of an underlying heart disease. Dogs may presentwith congestive heart failure with signs of coughing, dyspnea or weaknessdue to advanced stages of dilated cardiomyopathy, atrioventricular valveinsufficiency or cardiac enlargement due to left-to-right shunting.
In giant-breed dogs, atrial fibrillation may be an incidental findingwith no clinical signs pertaining to the cardiovascular system. Cats withatrial fibrillation may have various forms of cardiomyopathy, with significantleft atrial or biatrial enlargement secondary to diastolic dysfunction.
Physical examination findings for atrial fibrillation include an irregularheart rate, with a rate of 70270 beats/min depending on the severityof the underlying heart disease and the autonomic tone. The intensity ofS1 is inconsistent and the femoral pulses quality can vary from normal toweak, depending on the heart rate and underlying heart disease. atrial fibrillationis recognizable on the electrocardiogram by the absence of distinct atrialactivity (P waves), replaced by a baseline of undulating wavelets occurringat a rate greater than 500 beats/min (F waves).
Additionally, there is no predictable relationship present between atrialand 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 tachycardiawhere P waves are buried in the previous QRS complex. atrial fibrillationwith aberrant ventricular conduction may mimic ventricular tachycardia withinvisible P waves.
Evaluation of an animal with suspected atrial fibrillation should includethoracic radiographs and an echocardiogram for determination of chamberdimensions and cardiac function to diagnose or confirm presence of underlyingheart disease.
The development of atrial fibrillation in animals with severe underlyingheart disease can be a serious sequel, due to the complete absence of coordinatedatrial systole (loss of atrial contraction) and, therefore, decreased ventricularfilling. In addition, if the ventricular response rate is fast, the increasein heart rate results in a deterioration of systolic function.
The combined effects cause a decrease in cardiac output and can progressto overt congestive heart failure. Chronically elevated heart rates duringatrial fibrillation in an animal with no underlying heart disease may eventuallyprogress to a primary tachycardiomyopathy with systolic dysfunction andchamber enlargement similar to dilated cardiomyopathy.
Remember that increased sympathetic tone - during obtaining an electrocardiographictracing (animals are restrained and may be very stressed) and during hospitalization- is in part responsible for acceleration of atrioventricular nodal conductionand may result in transiently increased heart rates.
In such cases, a 24-hour Holter recording may be used to obtain a moreaccurate heart-rate assessment in a home environment. In dogs with atrialfibrillation secondary to heart disease, the average heart rate often exceeds160 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 withlone 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/minduring rest and 150 beats/min during exercise.
If concurrent heart failure is present, a dog may require a relativelyhigher average heart rate to maintain adequate blood pressure than a dogwith uncompromised ventricular function. Currently, there is no data provingthat dogs with atrial fibrillation with slow ventricular response rateshave a higher death rate than dogs that are converted from atrial fibrillationto sinus rhythm. Conversion to sinus rhythm in dogs can be a difficult task,even in lone atrial fibrillation with slow ventricular response rates, dependingon how chronic the condition is.
Success of pharmacologic restoration of sinus rhythm in dogs and catsis nil. Pharmacologic conversion is most promising in very recent onsetatrial fibrillation in animals with minimal or no underlying heart disease(lone atrial fibrillation). Unfortunately, the time of onset of atrial fibrillationis usually not known, and atrial fibrillation may be an incidental findingif 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 worksby enhancing vagal tone and slowing the atrioventricular node conductionvelocity.
If heart rates are markedly elevated or overt congestive heart failureis present, digoxin alone is unlikely to achieve adequate rate control.These animals are sympathetically stimulated and the vagomimetic effectsof digoxin are subjugated. Successful management of congestive heart failurewith ACE-inhibitors and diuretics may contribute to improved heart ratecontrol, because overall sympathetic tone may be lessened. In this situation,a combination of digoxin with a calcium channel blocker or a beta-blockeris effective.
Diltiazem (1.5-6 mg/kg PO SID or divided BID) or atenolol (0.25-1 mg/kgPO SID to BID) is a good choice. The mild negative inotropic effects ofthese two drugs are offset by the positive effects of heart rate reduction,resulting in prolonged diastole, improved filling pressures and reducedmyocardial oxygen consumption.
Blood pressure and renal status should be monitored, because hypotensionand prerenal azotemia may be induced with aggressive medical managementin these animals.
In giant-breed dogs with lone atrial fibrillation and heart rates withinnormal limits (in hospital or by Holter monitoring during 24 hours: range60-150 beats/min, with an average of less than 120 beats/min), there isno need to reduce the ventricular rate any further.
However, many dogs with lone atrial fibrillation go on to develop signsof heart failure later in life. Therefore, administration of digoxin ora beta blocker alone in dogs with normal ventricular rates may improve long-termoutcome and is usually of no detriment to the animal. This concept remainsto be proven.
In cats, rate-control is targeted with beta blockers (atenolol 6.25-12.5mg PO SID) or calcium channel blockers (diltiazem 7.5 mg/kg PO SID or dividedBID); heart rate reduction to 170-220 beats/min would be desirable.
Monotherapy with amiodarone or sotalol has not resulted in successfulconversion of atrial fibrillation to sinus rhythm in most affected dogs.Transthoracic, synchronized DC cardioversion (50-300J) alone or in combinationwith pharmacologic loading with sotalol or amiodarone or propafenone orflecainide antiarrhythmic drug may be helpful. However, success can be limitedand recurrence of atrial fibrillation is common immediately or shortly afterconversion. In animals with lone atrial fibrillation, radiofrequency ablationof pulmonary vein foci that trigger atrial fibrillation can lead to a permanentcure.
A surgical therapy involves isolation of the pulmonary veins and atrialappendage (maze procedure) to reduce the electrical atrial surface areaand abolish re-entry. In the clinical setting, these therapeutic approacheshave not been tested in animals.
Atrial fibrillation can be a challenging arrhythmia to manage becausemost affected animals have numerous other concurring problems associatedwith the underlying heart disease that influence the veterinarian's choiceof treatment and monitoring strategy for each individual animal.