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Basics

Basics

Definition

  • Atrial fibrillation-rapid, irregularly irregular supraventricular rhythm. Two forms recognized: primary atrial fibrillation, an uncommon disease that occurs mostly in large dogs with no underlying cardiac disease, and secondary atrial fibrillation, which occurs in dogs and cats secondary to underlying cardiac disease.
  • Atrial flutter is similar to atrial fibrillation, but the atrial rate is generally slower and is characterized by saw-toothed flutter waves in the baseline of the ECG. The ventricular response is generally rapid but may be regular or irregular.

ECG Features

Atrial Flutter

  • Atrial rhythm usually regular; rate approximately 300–400 bpm.
  • P waves usually discerned as either discrete P waves or a “saw-toothed” baseline.
  • Ventricular rhythm and rate generally depend on the atrial rate and AV nodal conduction, but are generally regular or regularly irregular and rapid.
  • Conduction pattern to the ventricles is variable-in some cases every other atrial depolarization produces a ventricular depolarization (2:1 conduction ratio), giving a regular ventricular rhythm; other times the conduction pattern appears random, giving an irregular ventricular rhythm that can mimic atrial fibrillation.

Secondary Atrial Fibrillation

  • No P waves present-baseline may be flat or may have small irregular undulations (“f” waves); some undulations may look like P waves.
  • Ventricular rate high-usually 180–240 bpm in dogs and >220 bpm in cats.
  • Interval between QRS complexes is irregularly irregular; QRS complexes usually appear normal.

Primary Atrial Fibrillation

Similar to secondary atrial fibrillation except ventricular rate usually in the normal range.

Pathophysiology

  • Atrial fibrillation-caused by numerous small reentrant pathways creating a rapid (>500 depolarizations/minute) and disorganized depolarization pattern in the atria that results in cessation of atrial contraction. Depolarizations continuously bombard the AV nodal tissue, which acts as a filter and does not allow all depolarizations to conduct to the ventricles. Many atrial depolarizations activate only a part of the atria because the rapid rate renders portions of the atria refractory, and thus they cannot reach the AV junction. Other atrial impulses penetrate into the AV junctional tissue but are not robust enough to penetrate the entire length. Blocked impulses affect the conduction properties of the AV junctional tissue and alter conduction of subsequent electrical impulses; electrical impulses are conducted through the AV junction irregularly, producing an irregular ventricular rhythm.
  • Atrial flutter-probably originates from one site of reentry that moves continuously throughout the atrial myocardium and frequently and regularly stimulates the AV node. When the atrial rate becomes sufficiently fast, the refractory period of the AV node exceeds the cycle length (P to P interval) of the SVT, and some atrial depolarizations are blocked from traversing the AV node (functional second-degree AV block).

Systems Affected

Cardiovascular

Loss of atrial contraction may result in decreased stroke volume and cardiac output depending on heart rate; high heart rate may result in deterioration in myocardial function (tachycardia-induced myocardial failure).

Genetics

No breeding studies available

Signalment

Species

Dog and cat

Breed Predilections

Large- and giant-breed dogs are more prone to primary atrial fibrillation.

Mean Age and Range

N/A

Predominant Sex

N/A

Signs

General Comments

  • Generally relate to the underlying disease process and/or CHF rather than the arrhythmia itself, but previously stable animals may decompensate.
  • Patients with primary atrial fibrillation are generally asymptomatic but may demonstrate mild exercise intolerance.

Historical Findings

  • Coughing/dyspnea/tachypnea.
  • Exercise intolerance.
  • Rarely syncope.
  • Dogs with primary atrial fibrillation are typically asymptomatic.

Physical Examination Findings

  • On auscultation, patients with atrial fibrillation have an erratic heart rhythm that sounds like “tennis shoes in a dryer.”
  • First heart sound intensity in atrial fibrillation is variable; second heart sound only heard on beats with effective ejection, not on every beat.
  • Third heart sounds (gallop sounds) may be present.
  • Patients with atrial fibrillation have pulse deficits and variable pulse quality.
  • Signs of CHF often present (e.g., cough, dyspnea, cyanosis).

Causes

  • Chronic valvular disease
  • Cardiomyopathy
  • Congenital heart disease
  • Digoxin toxicity
  • Idiopathic
  • Ventricular preexcitation (atrial flutter)

Diagnosis

Diagnosis

Differential Diagnosis

  • Frequent atrial (supraventricular) premature depolarizations
  • Supraventricular tachycardia with AV block
  • Multifocal atrial tachycardia (irregular)

CBC/Biochemistry/Urinalysis

N/A

Other Laboratory Tests

N/A

Imaging

  • Echocardiography and radiography may characterize type and severity of the underlying cardiac disease; moderate to severe left atrial enlargement common.
  • Typically normal in patients with primary atrial fibrillation, although mild left atrial enlargement may accompany the hemodynamic alterations imposed by the arrhythmia.

Diagnostic Procedures

A baseline 24-hour Holter is recommended to determine if the arrhythmia is chronic or paroxysmal. If it is chronic, drug therapy is indicated.

Treatment

Treatment

Appropriate Health Care

  • Patients with fast (secondary) atrial fibrillation are treated medically to slow the ventricular rate. Converting the atrial fibrillation to sinus rhythm would be ideal, but such attempts in patients with severe underlying heart disease or left atrial enlargement are generally futile because of a low success rate and high rate of recurrence. Consider electrical cardioversion to sinus rhythm for a dog with primary atrial fibrillation and only mild structural heart disease.
  • Patients with primary atrial fibrillation may be converted back to normal sinus rhythm. The success rate depends on chronicity. Patients that have been in atrial fibrillation for >4 months generally have a lower success rate and a higher rate of recurrence. In these patients, rate control, if necessary, is the recommended treatment.
  • Electrical (DC) cardioversion-application of a transthoracic electrical shock at a specific time in the cardiac cycle; requires special equipment, trained personnel, and general anesthesia. Using a monophasic defibrillator: Start with 4 J/kg; if no conversion occurs, increase dose by 50 J and repeat until a max of 360 J. Using a biphasic defibrillator: Start with 1 to 2 J/kg; if no cardioversion occurs, increase dose by 50 J and repeat until max of 360 J.
  • For atrial flutter, conversion to sinus rhythm can be done by drug therapy, electrical cardioversion, or rapid atrial pacing (transvenous pacing electrode).

Nursing Care

As indicated for CHF.

Activity

Restrict activity until tachycardia is controlled.

Diet

Mild to moderate sodium restriction if CHF.

Client Education

  • Secondary atrial fibrillation and atrial flutter is usually associated with severe underlying heart disease; goal of therapy is to lower heart rate and control clinical signs.
  • Sustained conversion to sinus rhythm is unlikely with secondary atrial fibrillation.

Surgical Considerations

N/A

Medications

Medications

Drug(s) Of Choice

  • Digoxin, -adrenergic blockers, esmolol, and calcium channel blockers (diltiazem) are frequently used to slow conduction through the AV node; definition of an adequate heart rate response varies among clinicians, but in dogs is generally 140–160 bpm.
  • For atrial flutter, therapy is aimed at suppressing the atrial re-entry circuit using sotlalol, amiodarone or procainamide.

Dogs

  • Digoxin-maintenance oral dose 0.005–0.01 mg/kg PO q12h; to achieve a therapeutic serum concentration more rapidly, the maintenance dose can be doubled for the first day. If digoxin is administered alone and the heart rate remains high, check the digoxin level and adjust the dose to bring the level into the therapeutic range. If the heart rate remains high, consider adding a calcium channel blocker or a -adrenergic blocker.
  • Diltiazem-initially administered at a dose of 0.5 mg/kg PO q8h, then titrated up to a maximum of 1.5 mg/kg PO q8h or until an adequate response is obtained.
  • Therapy for atrial fibrillation is aimed at suppressing the atrial reentry circuit using sotalol, amiodarone, or procainamide. The conversion to normal sinus rhythm is usually unsuccessful.

Cats

  • Diltiazem (1–2.5 mg/kg PO q8h) or atenolol (6.25–12.5 mg/cat PO q12–24h) are the drugs of choice in most cats.
  • If the heart rate is not sufficiently slowed with these drugs or if myocardial failure is present, digoxin (5 µg/kg PO q24–48h) can be added.

Contraindications

  • Digoxin, diltiazem, propranolol, and atenolol should not be used in patients with preexisting AV block.
  • Use of calcium channel blockers in combination with beta blockers should be avoided because clinically significant bradyarrhythmias and/or AV block can develop.

Precautions

  • Calcium channel blockers and -adrenergic blockers, both negative inotropes, should be used cautiously in animals with myocardial failure.
  • Using high-dose oral quinidine for conversion into sinus rhythm carries a risk of quinidine toxicity (e.g., hypotension, weakness, ataxia, and seizures)-administration of diazepam intravenously controls seizures; other signs abate within several hours of discontinuing quinidine administration.

Possible Interactions

Quinidine raises the digoxin level, generally necessitating a digoxin dose reduction.

Follow-Up

Follow-Up

Patient Monitoring

  • Monitor heart rate and ECG closely.
  • As heart rates in the hospital and those measured on the surface ECG may be inaccurate (due to patient anxiety and other environmental factors), Holter monitoring provides a more accurate means for assessing the need for heart rate control and/or the efficacy of medical therapy for heart rate control.

Possible Complications

Worsening of cardiac function with onset of arrhythmia.

Expected Course and Prognosis

  • Secondary atrial fibrillation-associated with severe heart disease, so a guarded-to-poor prognosis.
  • Primary atrial fibrillation with normal ultrasound findings-generally a good prognosis.

Miscellaneous

Miscellaneous

Abbreviations

  • AV = atrioventricular
  • CHF = congestive heart failure
  • ECG = electrocardiogram
  • SVT = supraventricular tachycardia

Suggested Reading

Bright JM, Brunnen J. Chronicity of atrial fibrillation affects duration of sinus rhythm after transthoracic cardioversion of dogs with naturally occurring atrial fibrillation. J Vet Intern Med 2008, 22(1):114119.

Gelzer R.M., Kraus M.S.. Management of atrial fibrillation. Vet Clin North Am Small Anim Pract 2004, 34:11271144.

Gelzer A.R.M., Kraus M.S., Moise N.S., Pariaut R., Charter M.E., Renaud-Farrell S. Assessment of antiarrhythmic drug efficacy to control heart rate in dogs with atrial fibrillation using 24-hour ambulatory electrocardiographic (Holter) recordings. J Vet Intern Med 2004, 18(5):779.

Kittleson MD. Electrocardiography. In: Kittleson MD, Kienle RD, eds., Small Animal Cardiovascular Medicine. St Louis, MO: Mosby, 1998, pp. 7294.

Kraus MS, Gelzer ARM, Moise S. Treatment of cardiac arrhythmias and conduction disturbances. In: Smith FWK, Tilley LP, Oyama MA, Sleeper MM, eds., Manual of Canine and Feline Cardiology, 5th ed. St. Louis, MO: Saunders Elsevier, 2015 (in press).

Tilley LP, Smith FWK, Jr. Electrocardiography. In: Smith FWK, Tilley LP, Oyama MA, Sleeper MM, eds., Manual of Canine and Feline Cardiology, 5th ed. St. Louis, MO: Saunders Elsevier, 2015 (in press).

Tilley LP, Smith , F.W.Essentials of Electrocardiography. Interpretation and Treatment, 4th ed. Ames, IA: Wiley Blackwell Publishing, 2016 (in preparation).

Author Larry P. Tilley

Consulting Editors Larry P. Tilley and Francis W.K. Smith, Jr.

Acknowledgment The author and editors acknowledge the prior contribution of Richard D. Kienle.

Client Education Handout Available Online