Overview

Ventricular tachycardia may occur in structurally normal hearts (hereditary arrhythmias) or may occur due to myocardial abnormalities associated with cardiomyopathy, significant valvular disease, or myocarditis. To date, there is no medical therapy available that is known to prevent sudden death in animals afflicted with ventricular tachyarrhythmias.

Pathophysiology

Potentially life-threatening arrhythmia because it can degenerate into ventricular fibrillation, resulting in sudden death. Usually signifies underlying myocardial disease or metabolic/electrolyte derangement; mechanisms include increased automaticity, reentry, and triggered activity.

Systems Affected

Cardiovascular system, with secondary effects on other systems because of poor perfusion.

Genetics

• Arrhythmogenic right ventricular cardiomyopathy (ARVC) in boxer dogs and dilated cardiomyopathy with VT in Doberman pinschers are both inherited as autosomal dominant traits.
• There is an association with a striatin mutation with the development of DCM in boxers. Striatin is desmosomal protein (scaffolding protein) that has been associated with ARVC in humans. In addition, the Wnt signaling pathway is now implicated in boxer dogs with ARVC. In brief, WnT signaling pathways play essential roles in in cell behavior, survival, and proliferation.
• There is a mutation in Doberman pinschers in the PDK4 gene. However, there are more than 20 different mutations in humans that can cause DCM.
• Ventricular arrhythmias and sudden cardiac death are hereditary in German shepherd dogs; mode of inheritance is polygenic due to an abnormality in a major gene with modifiers.
• In the Maine Coon and Ragdoll cat a mutation in the myosin binding protein C (MYBPC3) has been identified. However, the Ragdoll mutation is different from the Maine Coon mutation as it is located in a different region of the gene.
• Testing positive for the genetic defect does not mean all animals will express the phenotype of the disease.

Incidence/Prevalence

Common arrhythmia in dogs; uncommon in cats

Geographic Distribution

None

Signalment

Signs

Causes

• Cardiomyopathy
• Congenital defects (especially subaortic stenosis)
• Chronic degenerative valve disease
• Traumatic or infectious myocarditis
• Cardiac neoplasia
• Gastric dilation and volvulus
• Splenic neoplasia/hemorrhage
• Hyperthyroidism (cats)
• Digitalis toxicity
• Pancreatitis

Risk Factors

• Hypokalemia, hyperkalemia
• Hypomagnesemia
• Acid-base disturbances
• Hypoxemia
• Neoplasia (e.g., cardiac or splenic hemangiosarcoma)
• Anemia

Differential Diagnosis

Supraventricular tachycardia with bundle branch block. If P waves can be identified, look for association between P waves and QRS complexes. If there is a consistent PR interval, then the rhythm is supraventricular with bundle branch block. If there is no association between P waves and QRS complexes, the rhythm is probably ventricular tachycardia. If P waves cannot be identified due to a fast rate (P buried in preceding T wave), lidocaine administration may result in slowing of the VT rate and P waves may be identified if present. Termination of a tachyarrhythmia after administration of lidocaine supports diagnosis of ventricular tachycardia. If no effect with lidocaine, esmolol administration may result in slowing of a supraventricular tachycardia with bundle branch block, so that P waves associated with QRS complexes can be identified.

CBC/Biochemistry/Urinalysis

• Hypokalemia and hypomagnesemia predispose animal to ventricular tachycardia and blunt response to class I antiarrhythmic drugs (e.g., lidocaine, procainamide, mexiletine, and quinidine).
• High amylase and lipase if arrhythmia is secondary to pancreatitis.
• Inflammatory changes may occur on CBC such as increased neutrophil count if arrhythmias secondary to myocarditis.

Other Laboratory Tests

• Increased troponin (cTnI) with myocarditis. Cardiac troponin is a highly sensitive and specific biomarker of myocardial injury.
• High T₄ (cats) if arrhythmia is secondary to hyperthyroidism.
• Lyme or tick titers in myocarditis.
• Genetic testing if suspect DCM as the cause for VT:
  • Striatin mutation can be tested for in boxers.
  • There is one genetic mutation that can be tested for in Doberman pinschers-mutation in in the PDK4 gene.
• Genetic testing if suspect HCM in cats:
  • In the Maine Coon and Ragdoll genetic testing can be performed. There is a mutation in the cardiac myosin binding protein C gene (MYBPC3).
• Increased TLI (trypsin-like immunoreactivity) and PLI (pancreatic lipase immunoreactivity) if suspect pancreatitis is a cause for the VT.

Imaging

Echocardiography may reveal presence of underlying structural heart disease.

Diagnostic Procedures

Pathologic Findings

Vary with underlying cause

Appropriate Health Care

• Most patients with intermittent VT can safely be evaluated for underlying diseases (echocardiogram, lab work) and it is ideal to establish a true baseline of the arrhythmia quantity and quality by a 24-hour Holter prior to initiating therapy.
• If an animal is unstable (lateral recumbent, weak, or has frequent syncope), immediate intravenous treatment in a hospital setting with continuous ECG monitoring may be required. Once the arrhythmia is controlled and patient is hemodynamically stable, oral medication should be instituted. A follow-up 24-hour Holter is required to test efficacy and possible pro-arrhythmic effects of antiarrhythmic therapy.

Nursing Care

Varies with underlying cause

Activity

• Generally speaking, there is no known benefit to exercise restriction.
• Boxer dogs tend to have an increased incidence of VT during excitement, so in some cases owners should know what specific situations to avoid.

Diet

N/A

Client Education

Alert the owner to the potential for sudden death.

Surgical Considerations

• When possible, determine the cause of the arrhythmia and treat it prior to inducing general anesthesia.
• Assess if VT is correctable with a test dose of lidocaine; if it is, treat as necessary with lidocaine, either using IV boluses or CRI.
• Premedication with acepromazine (0.02–0.05 mg/kg) raises the threshold for ventricular fibrillation.
• Avoid pro-arrhythmic drugs such as alpha-2 agonists (xylazine and medetomidine) and thiopental.
• Mask inductions are not recommended in inadequately sedated patients with ventricular arrhythmias because increased sympathetic tone during mask induction will aggravate the arrhythmia.
• Continuous ECG monitoring while animal is anesthetized.

Drug(s) Of Choice

Correct any hypokalemia or hypomagnesemia, if possible, prior to instituting medical therapy.

Contraindications

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

Precautions

• Use beta-blockers cautiously in animals with CHF. Monitoring by echocardiogram is recommended to check for worsening of myocardial function due to beta blockade.
• Sotalol when used as a sole agent and other drugs that prolong the action potential duration may worsen VT in German shepherd dogs with inherited ventricular arrhythmias.

Possible Interactions

Quinidine and amiodarone raise digoxin levels.

Alternative Drug(s)

• For extremely refractory life-threatening VT in dogs consider amiodarone, 10 mg/kg q12h for 1 week (loading dose), then 5 mg/kg q24h (maintenance dose. Although amiodarone is a potent antiarrhythmic drug, its benefits must be balanced against its slow onset to action and adverse effects, which include hepatic toxicity, gastrointestinal disturbances, and blood dyscrasias in dogs. Caution is advised when considering amiodarone therapy because of its adverse effects. Signs of toxicity include anorexia, vomiting, lethargy, and hepatic enzyme elevation. Amiodarone hepatopathy is reversible after reduction of dosage or discontinuation of the drug. Overt clinical signs of toxicity resolve within a few days of stopping amiodarone. Hepatic enzyme activity gradually returns to normal within 3 months after amiodarone is discontinued or the dosage is reduced.
• Monitoring of serial serum chemistries is recommended, since increases in liver enzyme activities usually precede the onset of clinical signs of amiodarone toxicity. Liver enzymes should be measured after 7 days of drug loading and once monthly during maintenance therapy.
• Consider sotalol (10–20 mg/cat q12h) for refractory arrhythmias in cats.

Patient Monitoring

• Holter monitoring is 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 and telemetry can be used cautiously-not as useful as Holter monitoring because ventricular premature complexes and paroxysmal ventricular tachycardia can occur sporadically through the day.
• To avoid digoxin toxicity, serum digoxin levels should be measured after 1 week, 8–10 hours post-pill in patients receiving that medication due to its narrow therapeutic range (0.5–1.5 ng/mL).

Prevention/Avoidance

• Correct predisposing factors such as hypokalemia, hypomagnesemia, myocardial hypoxia, and digoxin toxicity.
• In boxer dogs, limit significant stress or excitement as the increase in sympathetic tone may exacerbate the arrhythmia.

Possible Complications

• Syncope
• Sudden death

Expected Course and Prognosis

• If cause is metabolic-condition may resolve with a good prognosis.
• If condition is associated with cardiac disease-prognosis is guarded because the underlying heart disease is likely chronic and progressive and therefore the arrhythmias may also worsen over time; presence of significant VT increases the risk of sudden death.
• If VT associated with hemangiosarcoma (cardiac or splenic)-the long-term outcome is grave due to the poor prognosis of the underlying disease.
• Approximately 50% of German shepherds with more than 10 runs of ventricular tachycardia/24 hours die suddenly.
• If German shepherd dogs reach the age of 18 months, the probability of sudden death decreases.
• Unlike boxers with ARVC, Doberman pinschers with VT and DCM may die suddenly during their first syncopal episode.

Associated Conditions

N/A

Age-Related Factors

N/A

Zoonotic Potential

None

Pregnancy/Fertility/Breeding

N/A

See Also

• Chagas Disease (American Trypanosomiasis)
• Digoxin Toxicity
• Myocarditis
• Ventricular Arrhythmias/Sudden Death in German Shepherds
• Ventricular Premature Complexes

Abbreviations

• ARVC = arrhythmogenic right ventricular cardiomyopathy
• CHF = congestive heart failure
• DCM = dilated cardiomyopathy
• ECG = electrocardiogram
• T₄ = thyroxine
• VT = ventricular tachycardia

Client Education Handout Available Online