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Basics ⬇

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BASICS

Definition!!navigator!!

Ventricular arrhythmias originate in the ventricle and the term ventricular premature depolarization refers to isolated premature complexes. VPD can occur singly, or in pairs or triplets. More than 4 VPDs in succession is VT and can be either paroxysmal or sustained. Complexes that have a uniform appearance are termed monomorphic, whereas if there are more than 2 configurations the VT is described as polymorphic.

Pathophysiology!!navigator!!

  • A number of different electrophysiologic mechanisms are responsible for the development of ventricular arrhythmias, including reentry, enhanced automaticity, and accelerated conduction
  • Ventricular arrhythmias often occur in association with other systemic illness
  • Primary myocardial disease is an infrequent cause.

Systems Affected!!navigator!!

Cardiovascular

Signs!!navigator!!

General Comments

  • VPDs may be found incidentally when they are infrequent
  • VT is often associated with what is perceived to be abdominal pain

Historical Findings

  • Acute onset
  • Poor performance
  • Weakness and collapse
  • Congestive heart failure

Physical Examination Findings

  • Individual premature beats or runs of rapid, regular, or irregular rhythm
  • Loud booming heart sounds
  • Jugular pulses
  • Respiratory distress
  • Generalized venous distention and congestive heart failure

Causes!!navigator!!

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

Risk Factors!!navigator!!

  • Gastrointestinal and renal disease
  • Endotoxemia
  • Infective endocarditis
  • Aortic regurgitation
  • Aortic root rupture

Diagnosis ⬆ ⬇

Outline

DIAGNOSIS

Differential Diagnosis!!navigator!!

  • Supraventricular arrhythmias—differentiate with ECG
  • Sinus tachycardia—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!!

ECG

  • VPDs are represented by a QRS–T complex that occurs prematurely and is different in configuration from those arising in the ventricle. The QRS complex usually appears widened and bizarre, with a T wave oriented in the opposite direction to the QRS complex. It is not preceded by a P wave
  • With VT, there is a rapid ventricular rate with QRS and T complexes that are abnormal for the lead. P waves are present but occur less frequently than the ventricular depolarizations and are buried in the other complexes. The R–R interval may be regular or irregular. All ventricular QRS complexes and T waves may look identical (monomorphic; Figure 1 or vary in appearance (polymorphic; Figure 2)

Echocardiography

  • With isolated VPD and monomorphic VT and no underlying cardiac disease, the echocardiogram is often normal or there may be a slightly low shortening fraction
  • With polymorphic VT and 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, severe valvular disease, pericarditis, or aortic root rupture

Thoracic Radiology

Pulmonary edema may be detected in horses with VT.

Other Diagnostic Procedures!!navigator!!

Continuous 24 h Holter Monitoring

This is particularly helpful in identifying intermittent or paroxysmal ventricular arrhythmias, in quantifying numbers of isolated VPDs, and in assessing response to therapy.

Exercise ECG

Characterization of the effect of exercise on ventricular arrhythmias is important in assessing their clinical significance.

Pathologic Findings!!navigator!!

  • The heart may be normal, grossly and histopathologically, in horses with no underlying cardiac disease
  • Focal or diffuse myocardial necrosis, inflammation, or fibrosis may be present

Treatment ⬆ ⬇

Outline

TREATMENT

Aims!!navigator!!

  • Address any predisposing causes
  • Antiarrhythmic therapy is restricted to cases in which the rhythm is unstable and life-threatening

Appropriate Health Care!!navigator!!

Antiarrhythmic therapy is considered if the horse shows signs of low cardiac output, the ventricular rate exceeds 100 bpm, an R-on-T phenomenon is present (QRS complexes come immediately after the preceding T wave), and/or the VT is polymorphic.

Nursing Care!!navigator!!

  • Continuous ECG monitoring should be performed during antiarrhythmic therapy
  • Horses should be kept quiet and not moved during the antiarrhythmic therapy

Activity!!navigator!!

Horses with VT or frequent isolated VPDs during exercise should not be exercised.

Client Education!!navigator!!

The risks associated with the treatment need to be discussed with the owner (see Possible Complications).

Medications ⬆ ⬇

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MEDICATIONS

Drug(s) of Choice!!navigator!!

  • VPDs are not usually treated with antiarrhythmics but may respond to corticosteroids if due to primary myocarditis
  • Treatment of VT is usually an emergency and requires the use of IV preparations. The choice of the first drug used depends on the severity of the ventricular arrhythmia present and the onset of action of the drug selected, as well as the other side effects that the drug may have such as being a negative inotrope
  • IV magnesium sulfate (25 g/450 kg slowly IV over 20–30 min) is occasionally successful in correcting sustained ventricular tachycardia in both hypomagnesemic and normomagnesemic horses and has no negative inotropic effect
  • Lidocaine hydrochloride is very rapidly acting but has central nervous system side effects that limit the dose that can be administered to an awake horse (0.25 mg/kg IV as a bolus)
  • Quinidine gluconate is one of the most successful antiarrhythmic drugs for horses with sustained ventricular tachycardia. Quinidine has a negative inotropic effect that is thought to be present only at high dosages but that may be a problem in horses with severe myocardial dysfunction. Quinidine gluconate is administered is small boluses of 0.5–1 mg/kg every 5–10 min up to a total dose of 12 mg/kg. Quinidine sulfate is rarely indicated in horses with sustained ventricular tachycardia because it must be administered via nasogastric intubation
  • Procainamide 1 mg/kg/min to a total dose of 20 mg/kg IV has also been successful and its negative inotropic effect is thought to be less than that of quinidine
  • 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

Contraindications!!navigator!!

  • Antidysrhythmic drugs can have proarrhythmic effects and their effects must be monitored carefully
  • Quinidine gluconate should be administered carefully to horses with VT and severe myocardial dysfunction

Precautions!!navigator!!

  • See Possible Complications
  • IV lidocaine can cause seizures that may last for 5–10 min
  • The QRS duration should be measured prior to each quinidine treatment. A prolongation of the QRS duration >25% of the pretreatment duration should prompt discontinuation of quinidine treatment. The development of colic, ataxia, convulsions, or bizarre behavior is a sign of quinidine toxicity and should prompt discontinuation of treatment

Possible Interactions!!navigator!!

Antiarrhythmic drugs with different mechanisms of action can be used in combination, but specific guidelines are lacking and interactions are possible.

Alternative Drugs!!navigator!!

  • Most other drugs with efficacy against ventricular arrhythmias may be beneficial in converting horses with VT but have been less effective
  • Phenytoin has been effective in VT refractory to other antiarrhythmics and is given orally at a starting dose of up to 20–22 mg/kg every 12 h PO and then modified to keep the drug in the target range (usually 10–15 mg/kg). Side effects include excitement, sedation, and other neurologic signs
  • IV propafenone at a dose of 0.5–1 mg/kg in 5% dextrose given slowly to effect over 5–8 min has been successful in converting 1 horse with ventricular tachycardia but is not available in the USA in the IV formulation. Oral propafenone in conjunction with IV procainamide may have been helpful in achieving conversion in several horses
  • Propranolol can be tried at 0.03–0.1 mg/kg IV but is not as successful in correcting VT as many of the other antiarrhythmic drugs

Follow-up ⬆ ⬇

Outline

FOLLOW-UP

Patient Monitoring!!navigator!!

  • Continuous ECG monitoring should be performed in all horses being treated for VT, as the antiarrhythmic drugs administered are also arrhythmogenic
  • Following treatment of VT or VPD, continuous 24 h Holter ECGs are useful in assessing whether complete resolution has occurred. Before returning to athletic activities, an exercise ECG should be obtained
  • Owners and trainers should regularly monitor their horse's cardiac rhythm before high-intensity exercise. Any irregularities in the cardiac rhythm or poor performance should prompt a cardiac reexamination

Prevention/Avoidance!!navigator!!

The possibility of ventricular arrhythmias should be considered in horses with systemic illness, particularly if the heart rate is unexpectedly high.

Possible Complications!!navigator!!

  • With sustained VT, congestive heart failure or sudden death may ensue
  • There are a myriad of complications that have been reported in horses treated for VT that can be broken down into cardiovascular and neurologic categories

Cardiovascular

  • Other ventricular arrhythmias—may need to be treated with an antiarrhythmic unless ventricular rhythm is slow (<100 bpm) and uniform and no R-on-T detected
  • Hypotension—needs to be monitored and treated with IV polyionic fluids and, if severe, with IV phenylephrine at 0.1–0.2 μg/kg/min to effect
  • Congestive heart failure—treat with digoxin at 0.0022 mg/kg IV and furosemide at 1–2 mg/kg IV, if needed
  • Sudden death—try to prevent it with continuous ECG monitoring and treatment of arrhythmias that do occur

Neurologic

  • Indicative of quinidine, phenytoin, or lidocaine toxicity
  • Ataxia—resolves upon return of plasma quinidine concentration to negligible levels
  • Convulsions—administer anticonvulsants
  • Sedation and bizarre behavior—resolves upon return of plasma drug concentrations to negligible levels
  • Colic—indicative of quinidine toxicity, treat with analgesics as needed; has also been seen in several horses with magnesium sulfate and severe multiform ventricular tachycardia and congestive heart failure

Expected Course and Prognosis!!navigator!!

  • The majority of horses with monomorphic VT convert to sinus rhythm with antiarrhythmic therapy if there is little or no underlying cardiac disease. Recurrences of VT can occur as the antiarrhythmic medication wears off
  • Horses with sustained polymorphic VT are more difficult to convert and are more likely to have underlying myocardial disease

Miscellaneous ⬆ ⬇

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MISCELLANEOUS

Age-Related Factors!!navigator!!

Older horses that develop ventricular tachycardia are more likely to have significant underlying cardiac disease.

Pregnancy/Fertility/Breeding!!navigator!!

VT leading to low cardiac output is likely to lead to fetal compromise.

Synonyms!!navigator!!

VTach

Abbreviations!!navigator!!

  • VPD = ventricular premature depolarization
  • VT = ventricular tachycardia

Suggested Reading ⬆ ⬇

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.

Reef VB, Bonagura J, Buhl R, et al. Recommendations for management of equine athletes with cardiovascular abnormalities. J Vet Intern Med 2014;28:749–761.

Reimer JM, Reef VB, Sweeney RW. Ventricular arrhythmias in the horse: twenty-one cases (1984–1989). J Am Vet Med Assoc 1992;201:1237–1243.

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.

Wijnberg ID, Ververs FF. Phenytoin sodium as a treatment for ventricular dysrhythmia in horses. J Vet Intern Med 2004;18:350–353.

Author(s) ⬆

Author: Celia M. Marr

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

Acknowledgment: The author acknowledges the prior contribution of Virginia B. Reef.