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Basics ⬇

Outline

BASICS

Definition!!navigator!!

  • Supraventricular arrhythmias originate in the atria or atrioventricular junction
  • The term supraventricular premature depolarization refers to isolated premature complexes. More than 4 SVPDs in succession is SVT, and this can be paroxysmal or sustained
  • AF is also a supraventricular arrhythmia but is described elsewhere (see chapter Atrial fibrillation)

Pathophysiology!!navigator!!

  • Reentry, enhanced automaticity, and accelerated conduction can lead to supraventricular arrhythmias
  • Primary myocardial disease is an infrequent cause
  • Horses are often able to block conduction of SVPD into the ventricles at the atrioventricular node, a vagal effect, and there is rarely a rapid ventricular rate in the presence of supraventricular arrhythmias

Systems Affected!!navigator!!

Cardiovascular

Signalment!!navigator!!

There are no specific predilections.

Signs!!navigator!!

General Comments

  • SVPDs are common but often incidental during routine examinations
  • SVPDs occurring during or after strenuous exercise are rarely of any immediate clinical significance, but may be a risk factor for AF
  • SVT is uncommon, but may be associated with poor performance

Historical Findings

Poor performance.

Physical Examination Findings

Individual premature beats or runs of rapid rhythm, usually with a rapid onset and offset.

Causes!!navigator!!

  • Hypoxia
  • Sepsis
  • Toxemia
  • Drugs such as quinidine sulfate
  • Autonomic imbalance
  • Metabolic and electrolyte imbalance
  • Primary myocardial disease

Risk Factors!!navigator!!

  • Mitral or tricuspid valvular disease and congenital cardiac disease leading to atrial enlargement
  • Infective endocarditis

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Ventricular premature depolarizations—differentiate with ECG
  • Sinus tachycardia—usually speeds up and slows down more subtly with sinus tachycardia than with SVT; differentiate with ECG

CBC/Biochemistry/Urinalysis!!navigator!!

Electrolyte or metabolic abnormalities may be present.

Other Laboratory Tests!!navigator!!

  • Increased serum concentration of cardiac troponin I may be present
  • Blood culture may be indicated in some cases

Imaging!!navigator!!

Echocardiography

  • The echocardiogram is most often normal, or there may be a slightly low shortening fraction, particularly with SVT
  • With primary myocardial disease, there are more profound decreases in fractional shortening and abnormalities of myocardial wall motion (dyskinesis or akinesis) and mitral and aortic valve motion
  • Foci of increased or decreased echogenicity are occasionally seen within the myocardium
  • Echocardiography may reveal evidence of other cardiac diseases such as infective endocarditis or severe valvular disease

Other Diagnostic Procedures!!navigator!!

ECG

  • SVPDs are represented by a premature P wave, which may (conducted) or may not (unconducted) be followed by a QRS-T complex (Figure 1)
  • The shape of the premature P wave is different from those of sinus origin, but the configurations of the premature QRS complex and T wave are the same as those of sinus origin as conduction through the ventricle is not affected
  • The premature P wave may not be visible if it occurs sufficiently early that it is buried in the preceding T wave
  • Junctional complexes do not have a P wave but do have the same QRS configuration as those of sinus origin
  • Occasionally, SVPDs have QRS complexes that are of slightly larger duration and morphology compared to the sinus QRS complexes
  • Characterizing the frequency with an ambulatory ECG over prolonged periods and presence or absence during exercise are invaluable for assessing the clinical significance and assessing response to therapy
  • It can be helpful to examine multiple leads to differentiate premature P waves and confirm that all premature QRS complexes have a configuration that is identical to those of sinus origin

Pathologic Findings!!navigator!!

  • There is often no underlying cardiac disease
  • Focal or diffuse myocardial necrosis, inflammation, or fibrosis may be present
  • Atrial enlargement and valvular pathology may be identified

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Address any predisposing causes
  • Antiarrhythmic therapy in selected cases

Appropriate Health Care!!navigator!!

  • Emergency antiarrhythmic therapy is restricted to cases in which the rhythm is unstable and life-threatening. This is very rarely necessary except in cases in which the rapid SVT is due to drug treatment such as quinidine sulfate
  • Oral antiarrhythmic therapy is occasionally used for frequent SVPDs and/or SVT

Nursing Care!!navigator!!

Continuous ECG monitoring is indicated and horses should be kept quiet and not moved during the antiarrhythmic therapy.

Activity!!navigator!!

  • SVPDs are not an important cause of collapse during exercise; and if there is no poor performance, horses with SVPDs can be exercised normally
  • Horses with poor performance may benefit from rest
  • Horses with SVT during exercise should not be exercised

Diet!!navigator!!

N/A

Client Education!!navigator!!

Clients should be counseled that the main risk associated with SVPD is that it may predispose the horse to developing AF in the future. Normal exercise can be performed in most horses with SVPD providing there is no poor performance.

Surgical Considerations!!navigator!!

Surgical ablation techniques have been performed successfully in horses with supraventricular arrhythmias.

Medications ⬆ ⬇

Outline

MEDICATIONS

Drug(s) of Choice!!navigator!!

  • In the absence of any predisposing causes precluding their use, such as infective endocarditis, corticosteroids are often used in horses with SVPD. Either prednisolone 1 mg/kg PO every 48 h or dexamethasone 0.05–0.1 mg/kg IV, or 0.1 mg/kg PO every 24 h for 3 or 4 days and then continued every 3–4 days in decreasing dosages, is recommended. Vitamin C (20 mg/kg PO every 24 h) and vitamin E (10 IU/kg PO every 24 h) may also be beneficial owing to their antioxidant effect
  • Phenytoin given orally at doses of 5–15 mg/kg every 12 h may be effective in suppressing SVPD, but the arrhythmia may recur on discontinuation of therapy
  • Digoxin is given IV at 0.0022 mg/kg for emergency treatment of rapid SVT, particularly when it is associated with quinidine administration. For less rapid SVT during quinidine therapy, digoxin can be given at 0.011 mg/kg PO every 12 h. Digoxin is less likely to be effective against SVPD, although occasionally favorable responses have been observed when it is used orally
  • Propranolol given IV at 0.03–2 mg/kg can be used for emergency treatment of rapid SVT, particularly if digoxin is unsuccessful
  • Quinidine sulfate (single dose of up to 22 mg/kg PO) and quinidine gluconate (0.5–2.2 mg/kg IV boluses to a maximum of 12 mg/kg) are indicated for treating rare cases of rapid SVT when it is not associated with quinidine administration

Contraindications!!navigator!!

Corticosteroids should not be used in horses with concurrent pituitary pars intermedia dysfunction or active laminitis.

Precautions!!navigator!!

  • Horses should be monitored for signs of laminitis if receiving corticosteroid therapy
  • Adverse effects of digoxin include anorexia, depression, abdominal pain, and ventricular arrhythmias. Ideally, therapeutic drug monitoring should be used to ensure that plasma digoxin concentrations remain at therapeutic levels (1–2 μg/mL)
  • Adverse effects of phenytoin include excitement, sedation, and other neurologic signs. Ideally, therapeutic drug monitoring should be used to ensure that plasma phenytoin concentrations remain at therapeutic levels (5–10 ug/ml)
  • Adverse effects of quinidine include myocardial depression, colic, diarrhea, and ventricular arrhythmias. Ideally, therapeutic drug monitoring should be used to ensure that plasma phenytoin concentrations remain at therapeutic levels (3–5 μg/mL)

Possible Interactions!!navigator!!

There is interaction between quinidine and digoxin.

Alternative Drugs!!navigator!!

Other drugs used in humans for treatment of SVT may be beneficial in horses, but protocols for their use have yet to be defined. Sotalol is often prescribed for long-term oral antiarrhythmic therapy in humans and has intermediate bioavailability in horses. Doses of 1–4 mg/kg sotalol PO every 12 hours have been used, gradually increasing the dose. Sweating can occur with larger doses.

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

24 h Holter monitoring and exercise ECG are the most useful tools to assess the success of therapy and, when no treatment has been recommended, to monitor for any progression of the supraventricular arrhythmia.

Possible Complications!!navigator!!

  • The main risk associated with SVPD is that it may predispose the horse to developing AF in the future. However, the magnitude of this risk in horses that have not previously had paroxysmal or sustained AF has not been quantified. Horses that have previously had AF are more likely to have recurrences if SVPDs are detected after treatment of the AF or SVT occurs during treatment. AF is also more likely to develop if there is underlying heart disease
  • Horses that develop SVPDs in association with atrial enlargement and severe underlying cardiac disease are at particular risk of developing AF and this often marks the onset of declining clinical status and congestive heart failure. In these cases, the SVPDs can be regarded as a complication of the underlying condition rather than a cause of AF

Expected Course and Prognosis!!navigator!!

Horses in which SVPDs are detected as an incidental finding may frequently remain asymptomatic in work for prolonged periods.

Miscellaneous ⬆ ⬇

Outline

MISCELLANEOUS

Associated Conditions!!navigator!!

  • Tricuspid and mitral regurgitation
  • Atrial septal defect
  • Infective endocarditis

Abbreviations!!navigator!!

  • AF = atrial fibrillation
  • SVPD = supraventricular premature depolarization
  • SVT = supraventricular tachycardia

Suggested Reading ⬆ ⬇

Broux B, De Clercq D, Decloedt A, et al. Pharmacokinetics of intravenously and orally administered sotalol hydrochloride in horses and effects on surface electrocardiogram and left ventricular systolic function. Vet J 2016;208:60–64.

Dembek KA, Hurcombe SD, Schober KE, Toribio RE. Sudden death of a horse with supraventricular tachycardia following oral administration of flecainide acetate. J Vet Emerg Crit Care 2014;24:759–763.

Reef VB, Marr CM. Dysrhythmias: assessment and medical management. In: Marr CM, Bowen M, eds. Cardiology of the Horse, 2e. Edinburgh, UK: Saunders Elsevier, 2010:159–178.

Sage A, Mogg TD. Pharmacology of drugs used to treat cardiac disease. In: Marr CM, Bowen M, eds. Cardiology of the Horse, 2e. Edinburgh, UK: Saunders Elsevier, 2010:75–87.

Author(s) ⬆

Author: Celia M. Marr

Consulting Editors: Celia M. Marr and Virginia B. Reef