Ventricular premature beats (VPBs)

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

Classical signs are pulse deficits and interruptions of rhythm regularity, and VPBs are often secondary to underlying heart disease, which may be secondary to other systemic illnesses.

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 morphology of the QRS complex is abnormal (appears inverted) when compared with the normal sinus beat. The QRS complex is wider than normal and has a bizarre appearance. VPBs may occur as a fusion beat or an interpolated beat. There is no association between P waves and the QRS complex. VPBs do not re-set the sinoatrial node.

Treatment

If there is a large number of ventricular premature beats wher the premature QRS falls within the preceding T wave, therapy should be considered;

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

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

Procainamide at 10-20 mg/kg PO q 8-12 hrs

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