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Basics ⬇

Basics

Definition

Repetitive supraventricular premature depolarizations that originate from a site other than the sinus node, such as the atrial myocardium or atrioventricular nodal tissue.

ECG Features

  • Heart rate-rapid, 150–350 bpm in dogs. The lower rate of supraventricular tachycardia depends on the size of the patient. Smaller dogs typically have higher sinus nodal rates than larger dogs.
  • Rhythm usually very regular (R-R interval is constant) and may be sustained, but there can be frequent or infrequent short runs of supraventricular tachycardia, so-called paroxysmal SVT. Rarely, the rhythm during the tachycardia will be irregular, suggesting abnormal automaticity as the etiology.
  • Usually the QRS complexes are typical of normal sinus complexes, narrow with a normal mean electrical axis. In some cases a coexisting bundle branch block or aberrant ventricular conduction makes it difficult, if not impossible, to differentiate an SVT from a ventricular tachycardia by examining the ECG.
  • P waves can be normal or abnormal and typically differ in configuration from the sinus P waves. P waves may be buried in the previous T wave and therefore not visualized.
  • Atrioventricular conduction is usually normal (1:1), but various levels of functional second-degree AV block may occur at higher atrial rates (2:1, 3:1, 4:1, etc.).

Pathophysiology

  • SVT may be primary (idiopathic) or secondary to other cardiac disease, generally those creating atrial enlargement.
  • May result from a reentrant mechanism or from abnormal automaticity in an ectopic focus. Reentrant SVT typically produces a very regular rhythm; SVT due to an automatic focus in atrial myocardium can produce an irregular rhythm.
  • Most cases in dogs respond to drugs that specifically alter conduction and refractoriness in the AV nodal tissue, suggesting AV nodal reentry as the mechanism.
  • Recent electrophysiologic studies revealed that some SVT in dogs is related to a congenital accessory pathway between the atria and ventricles that allows the electrical impulses to travel freely between the atria and ventricles without traversing the AV node and without conduction delay; in these patients, the SVT is caused by reentry through the accessory pathway and the AV node.

Systems Affected

  • Cardiovascular-CHF may develop secondary to progressive myocardial failure associated with a chronically high heart rate (so-called tachycardia-induced myocardial failure).
  • Neuromuscular-syncope or generalized episodic weakness due to reduced cardiac output and oxygen delivery.

Signalment

Species

Dog and rarely cat

Signs

General Comments

  • Clinical signs may relate to the underlying cause.
  • Dogs with slow SVT or infrequent paroxysmal SVT may exhibit no clinical signs.
  • Dogs with fast SVT (heart rate usually > 300 bpm) generally exhibit episodic weakness or syncope.

Historical Findings

  • Owners are generally unaware of the arrhythmia.
  • Coughing or breathing abnormalities in dogs with CHF.
  • Episodic weakness or syncope.

Physical Examination Findings

  • Rapid, usually regular heart rhythm. However, in dogs with paroxysmal SVT the rhythm may be normal and regular during the physical exam.
  • May have evidence of poor peripheral perfusion-pale mucous membranes, a prolonged capillary refill time, and weak pulses.
  • May have no signs other than the rapid heart rate.
  • Findings may reflect an underlying cardiac condition (e.g., heart murmur).

Causes

  • Chronic valvular disease
  • Cardiomyopathy
  • Congenital heart disease
  • Cardiac neoplasia
  • Systemic disorders
  • Ventricular preexcitation
  • Electrolyte imbalances
  • Digoxin toxicity
  • Idiopathic

Risk Factors

Heart disease

Diagnosis ⬆ ⬇

Diagnosis

Differential Diagnosis

  • Sinus tachycardia.
  • Atrial flutter.
  • Atrial fibrillation.
  • Ventricular tachycardia (SVT with right bundle branch block or aberrant conduction can look like ventricular tachycardia; resolution of arrhythmia after lidocaine administration usually confirms ventricular tachycardia).

Imaging

  • Echocardiography (including Doppler studies) may help characterize the type and severity of underlying cardiac disorders. Echocardiography is also important for assessing myocardial function in patients with idiopathic SVT.
  • When viewed on an echocardiogram during bursts of SVT, the left ventricle has a normal end-systolic diameter and a small end-diastolic diameter, resulting in a decreased shortening fraction because of inadequate filling.
  • Usually left or right atrial enlargement in dogs with SVT secondary to other cardiac disorders.

Diagnostic Procedures

  • Long-term ambulatory (Holter) recording of the ECG may detect paroxysmal SVT in cases of unexplained syncope. This is generally only helpful if syncope is occurring regularly within a 24- to 48-hour period. Holter monitors may also help characterize the rate and frequency of sustained SVT and are useful in evaluating the efficacy of therapy.
  • Event (loop) recorders may detect paroxysmal SVT in patients with infrequent episodes of syncope (<q24–48h).
  • Sustained SVT must be distinguished from sinus tachycardia because the two arrhythmias have different implications and treatment. A precordial thump may help differentiate sinus tachycardia from SVT when the heart rate is in the 150–250 bpm range; it will usually stop an SVT for at least 1 or 2 beats, while a sinus tachycardia will not slow. A vagal maneuver (e.g., ocular pressure or carotid sinus massage) may break an SVT abruptly but only gradually slows sinus tachycardia.

Treatment ⬆ ⬇

Treatment

Appropriate Health Care

  • Asymptomatic patients can be managed on an outpatient basis; patients with a sustained SVT or signs of congestive heart failure should be hospitalized until stable.
  • SVT is a medical emergency in dogs that exhibit weakness and collapse; non-pharmacologic interventions that may break an SVT include vagal maneuvers, precordial thump, and electrical cardioversion.
  • Vagal maneuvers are often unsuccessful but may be used initially because of their ease of administration and non-invasive nature.
  • Delivering a precordial thump can successfully (>90% of the time) terminate an SVT in dogs, but this maneuver may break the rhythm for only a brief period. At other times the rhythm remains converted. To perform a precordial thump, the dog is placed on its right side and the left apex beat is located. This region is then “thumped” with a fist while recording the ECG.
  • Emergency medical therapy is required in patients in which a precordial thump is unsuccessful (see below).

Nursing Care

Treat CHF and correct any underlying electrolyte or acid-base disturbances.

Activity

Restrict until arrhythmia has been controlled.

Diet

Mild to moderate sodium restriction if in CHF.

Client Education

Owners should observe patients closely for signs of low cardiac output such as weakness and collapse.

Surgical Considerations

Consider transvenous catheter ablation for patients with accessory pathways.

Medications ⬆ ⬇

Medications

Drug(s) Of Choice

Emergency Therapy

  • Administer one of the following drugs:
    • Calcium channel blockers-verapamil (0.05 mg/kg boluses IV over 3–5 minutes up to three times) or diltiazem (0.05–0.25 mg/kg IV over 5–15 minutes).
    • -adrenergic blockers-esmolol (0.25–0.5 mg/kg slow IV bolus administration followed by a constant-rate infusion of 50–200 µg/kg/min); moderate-to-severe myocardial failure is a relative contraindication to the administration of these drugs at these doses.
    • Electrical cardioversion or intracardiac electrophysiologic pacing methods may be considered in extreme cases.

Long-Term Therapy

  • Digoxin-administer at either a maintenance oral dose or double the maintenance dose for the first day to produce a therapeutic serum concentration more rapidly; contraindicated in patients with accessory pathways.
  • -adrenergic blocker-atenolol (0.2–1 mg/kg PO q12–24h) can be administered as long as the patient does not have underlying moderate-to-severe myocardial failure.
  • Diltiazem is the calcium channel blocker of choice for long-term control of SVT. The dosage required to control SVT has not been reported in the dog. Diltiazem is used more frequently to control the ventricular rate in patients with atrial fibrillation at a dosage of 0.5–1.5 mg/kg PO q8h. In our clinic, we generally start in this dosage range but almost always need to increase the dose to 2–3 mg/kg PO q8h to effect control of SVT.
  • Class I antiarrhythmic agents such as quinidine and procainamide can be tried when the aforementioned drugs are ineffective or when the SVT is thought to be due to an automatic, rather than a reentrant, rhythm. SVT caused by an automatic atrial focus may produce an irregular rhythm and may be refractory to conventional drug therapy. When the SVT is due to an accessory pathway, these drugs are more effective.

Contraindications

Avoid use of calcium channel blockers in combination with beta-blockers; clinically significant bradyarrhythmias can develop.

Precautions

Calcium channel blockers and -adrenergic blockers have negative inotropic properties and should be used cautiously in dogs with documented myocardial failure.

Alternative Drug(s)

Emergency treatment-intravenous adenosine (1–12 mg IV rapidly). Adenosine is very expensive and short-lived; propranolol (0.02 mg/kg slow IV boluses up to a total dose of 0.1 mg/kg). Propranolol has a long half-life after IV administration and also has significant 2 blocking effects and is generally not recommended unless no other alternative is available.

Follow-Up ⬆ ⬇

Follow-Up

Patient Monitoring

Serial ECG or Holter monitoring

Possible Complications

Syncope and CHF

Expected Course and Prognosis

Most is controlled effectively with medication

Miscellaneous ⬆

Miscellaneous

Associated Conditions

Accessory pathways in some patients

Age-Related Factors

In young dogs without evidence of structural heart disease, suspect a reentrant tachycardia involving an accessory pathway.

Synonyms

Atrial tachycardia, junctional tachycardia

See Also

Atrial Fibrillation and Atrial Flutter

ABBREVIATIONS

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

Author Larry P. Tilley

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

Client Education Handout Available Online

Suggested Reading

Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds., Small Animal Cardiovascular Medicine. St. Louis: Mosby, 1998, pp. 449–494.

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).

Wright KN. Assessment and treatment of supraventricular tachyarrhythmias. In: Bonagura JD, ed., Kirk's Current Veterinary Therapy XIII. Philadelphia: Saunders, 1999, pp. 726–730.