Supraventricular premature beats (SVPB) in cats

© Rand, J (2006) Problem-based feline medicine. Saunders Elsevier, Sydney

SVPB shows classically as pulse deficits and interruptions of rhythm regularity. Premature beats result from two mechanisms; alterations in impulse formation and alterations in impulse conduction. 

Alterations in impulse formation depend on the intrinsic automaticity of diseased cardiac cells. Diseased myocardial cells outside the specialised conduction system can acquire automaticity because of changes in the resting membrane potential.

Alterations of impulse conduction result from re-entry and by-pass tracts. Re-entry is a self-sustaining electrical circuit that repeatedly depolarises surrounding tissue. By-pass tracts alter the normal pathway of conduction by providing an alternative pathway around the AV node.

Clinical signs

Most patients show no evidence of clinical disease. In some cases panting, restlessness and anxiety may be seen.

Diagnosis

The heart rate is normal and the cardiac rhythm is irregular because of the premature beats. The ectopic P wave is premature, the configuration may be different from normal sinus beats. The morphology of the QRS complex is similar to a normal sinus beat. The QRS complex is usually narrow, but in very premature beats it may be wider (longer duration) than normal. There is association between P waves and the QRS complex. Supraventricular premature beats cause re-setting of the sinoatrial node. SVT is always irregular.

Differential diagnosis

Marked respiratory sinus arrhythmia is rare in cats but may mimic the presence of premature beats. Sinus arrhythmia is rare in cats and only occurs at slow heart rates. Increasing the heart rate above 180 bpm by excitement or atropine (0.04 mg/kg parenterally) will abolish sinus arrhythmia.

Motion artefact

Ventricular premature beats without a wide QRS complex may be erroneously classified as supraventricular premature beats. SVPB will usually reset the sinus rate.

Treatment

Isolated premature beats do not require therapy unless they present with other more severe arrhythmias. If there is a suggestion of hemodynamic compromise therapy may be considered:

Atenolol at 6.25 - 12.5 mg/cat PO q 12hrs

Diltiazem at 7.5 - 15mg / cat PO q 8 hrs

Propanolol at 0.5-1.0 mg/cat PO q 8 hrs

Sotalol at 10-20 mg/cat PO q 12 hrs

Prognosis

The prognosis depends on the underlying disease, but in general this class of arrhythmias is not likely to severely compromise the patient's outcome. If the arrhythmia is frequent and is a result of severe left atrial enlargement, these beats may reflect atrial electrical instability and precede the development of atrial fibrillation.