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Basics ⬇

Basics

Definition

Single cardiac impulse initiated within the ventricles instead of the sinus node.

ECG Features

  • QRS complexes typically wide and bizarre
  • P waves dissociated from the QRS complexes

Pathophysiology

Mechanisms include increased automaticity, reentry, and delayed afterdepolarizations.

Systems Affected

Cardiovascular-secondary effects on other systems because of poor perfusion.

Genetics

Polygenic in German shepherd dogs-inherited ventricular arrhythmia.

Incidence/Prevalence

Unknown

Signalment

Species

Dog and cat

Breed Predilections

  • Common in large-breed dogs with cardiomyopathy, especially boxers (arrhythmogenic right ventricular cardiomyopathy) and Doberman pinschers.
  • Inherited ventricular arrhythmia in German shepherds.
  • Common in cats with cardiomyopathy; occasionally seen in cats with hyperthyroidism.

Mean Age and Range

Seen in all age groups

Signs

Historical Findings

  • Weakness
  • Exercise intolerance
  • Syncope
  • Sudden death
  • Often asymptomatic

Physical Examination Findings

  • Irregular rhythm associated with pulse deficits; may auscult splitting of the first or second heart sound.
  • May be normal if arrhythmia is intermittent and absent during examination.
  • May observe signs of CHF (e.g., cough, dyspnea) or murmur, depending on the cause of arrhythmia.

Causes

  • Cardiomyopathy
  • Congenital defects (especially subaortic stenosis)
  • Chronic valve disease
  • Gastric dilation and volvulus
  • Traumatic myocarditis (dogs)
  • Digitalis toxicity
  • Hyperthyroidism (cats)
  • Cardiac neoplasia
  • Myocarditis
  • Pancreatitis

Risk Factors

  • Hypokalemia
  • Hypomagnesemia
  • Acid-base disturbances
  • Hypoxia

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

  • Supraventricular premature beats with bundle branch block.
  • Look for P waves associated with the wide QRS complexes; an atrial premature complex with aberrant conduction has an associated P wave.
  • An atrial premature complex is usually followed by a non-compensatory pause in which the R-R interval of the two sinus complexes enclosing an APC is less than the R-R interval of three consecutive sinus complexes.
  • A ventricular premature complex is usually followed by a compensatory pause in which the R-R interval of two sinus complexes enclosing a VPC is greater than or equal to the R-R interval of three consecutive sinus complexes.

CBC/Biochemistry/Urinalysis

  • Hypokalemia and hypomagnesemia predispose animals to ventricular arrhythmias and blunt the response to class I antiarrhythmic drugs (e.g., lidocaine, procainamide, mexiletine, and quinidine).
  • High amylase and lipase if condition is secondary to pancreatitis.

Other Laboratory Tests

  • High T4 (cats) if condition is secondary to hyperthyroidism.
  • Increased cardiac troponin I, a biomarker for possible acute myocardial injury may suggest an underlying cardiac condition.

Imaging

Echocardiography may reveal structural heart disease.

Diagnostic Procedures

Long-term ambulatory (Holter) recording of the ECG to detect transient ventricular arrhythmias in patients with unexplained syncope or weakness.

Pathologic Findings

Vary with underlying cause

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

Generally outpatient basis

Activity

Restrict if the arrhythmia is accompanied by clinical signs or evidence of structural heart disease.

Client Education

Alert owner to potential for the arrhythmia worsening and syncope or sudden death.

Surgical Considerations

  • Continuous ECG monitoring recommended while anesthetized.
  • Premedicating the patient with acepromazine (0.02–0.05 mg/kg) raises the threshold for ventricular fibrillation.
  • Mask inductions not recommended; sympathetic release during mask induction can aggravate arrhythmia.
  • Avoid anticholinergics unless bradycardia develops.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

General Comments

  • Correct any hypokalemia or hypomagnesemia.
  • Drug therapy in the absence of clinical signs-controversial; studies in humans with asymptomatic VPCs and myocardial infarction demonstrated a high incidence of sudden death when treatment was initiated with class I antiarrhythmic agents; no similar studies have been conducted in veterinary patients.
  • The author generally does not prescribe antiarrhythmic drugs unless there is evidence of clinical signs of low cardiac output (e.g., episodic weakness or syncope) or the belief that the patient is at high risk of sudden death, based on presence of R on T phenomenon or breed association with VPCs and sudden death (e.g., boxers and Doberman pinschers).
  • If antiarrhythmic therapy is initiated in an attempt to lower the risk of sudden death, the author usually chooses a beta-blocker or sotalol; no studies have been done to confirm efficacy of beta-blockers for prevention of sudden death in dogs or cats.

Dogs

  • Patient not in CHF or hypotensive-initiate therapy with a beta-blocker such as propranolol (0.2–1 mg/kg PO q8h), atenolol (0.2–1 mg/kg q12h), or metoprolol (0.2–1 mg/kg PO q8–12h) or class III agent sotalol (1–3.5 mg/kg PO q12h).
  • Patient in CHF or hypotensive-initiate therapy with a class I antiarrhythmic agent such as mexiletine (5–8 mg/kg PO q8h) or procainamide (8–20 mg/kg PO q6–8h).
  • Combine a class I antiarrhythmic drug with a beta-blocker or sotalol if arrhythmia persists; especially in boxers.
  • Sotalol monotherapy may have proarrhythmic effect in German shepherds.

Cats

Atenolol (6.25–12.5 mg PO q12h)

Contraindications

Avoid atropine, catecholamines (e.g., epinephrine and dopamine) until arrhythmia is controlled.

Precautions

  • Use beta-blockers cautiously in animals with CHF; they initially depress myocardial contractility.
  • Use digoxin cautiously; it can potentially aggravate ventricular arrhythmias.
  • Drugs that prolong the action potential (e.g., sotalol) may worsen arrhythmia in German shepherds with inherited ventricular arrhythmia.

Possible Interactions

Quinidine and amiodarone raise serum digoxin levels.

Alternative Drug(s)

  • Consider amiodarone (5–10 mg/kg PO q12h) for refractory arrhythmias in dogs (generally reserved for ventricular tachycardia); may not want to use in Doberman pinschers.
  • Consider sotalol (10–20 mg/cat PO q12h) or procainamide (3–8 mg/kg PO q6–8h) for cats that do not tolerate beta-blockers.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

  • Holter monitoring preferred for monitoring severity of the arrhythmia and efficacy of antiarrhythmic therapy; the goal of antiarrhythmic therapy is to reduce the frequency of ventricular ectopy by >85%.
  • Serial ECGs are not as useful as Holter monitoring-VPCs and paroxysmal ventricular tachycardia can occur sporadically through the day.
  • Serum digoxin levels in patients receiving that medication.

Prevention/Avoidance

Correct predisposing factors such as hypokalemia, hypomagnesemia, myocardial hypoxia, and digoxin toxicity.

Possible Complications

Syncope, sudden death

Expected Course and Prognosis

  • If cause is metabolic-condition may resolve with good prognosis.
  • If condition is associated with cardiac disease-prognosis is guarded; VPCs may increase the risk of sudden death.

Miscellaneous ⬆

Miscellaneous

Abbreviations

  • APC = atrial premature complex
  • CHF = congestive heart failure
  • ECG = electrocardiogram
  • T4 = thyroxine
  • VPC = ventricular premature complex

Author Francis W.K. Smith, Jr.

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

Client Education Handout Available Online

Suggested Reading

Knight DH.Reason must supersede dogma in the management of ventricular arrhythmias. In: Bonagura JD, ed., Kirk's Current Veterinary Therapy XIII. Philadelphia: Saunders, 2000, pp. 730–733.

Kraus M.S., Ridge L.G., Gelzer A.R.M., et al. Toxicity in Doberman pinscher dogs with ventricular arrhythmias treated with amiodarone. J Vet Intern Med 2005, 19(3):407.

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).

Meurs K.M., Spier A.W., Wright N.A., et al. Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J Am Vet Med Assoc 2002, 221(4):522–527.

Moise N.S., Gilmour R.F. Jr, Riccio M.L., Flahive W.F.Jr. Diagnosis of inherited ventricular tachycardia in German shepherd dogs. J Am Vet Med Assoc 1997, 210(3):403–410.

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).