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Ventricular tachycardia (ventricular arrhythmia) is a heart disease of dogs characterized by a series of ventricular premature complexes (VPC) usually greater than 100 beats per minute.
In this condition, the RR interval on the ECG is usually regular, but nonconducted sinus P waves may be superimposed on or between the ventricular complexes. This is usually unrelated to the VPCs because the AV node and/or ventricles are in a refractory period (physiological AV dissociation).
The term 'capture beat' refers to the successful conduction of a sinus P wave into the ventricles uninterrupted by another VPC. If the normal ventricular activation sequence is interrupted by another VPC, a fusion complex can result.
- Breed predisposition in the Boxer and autosomal-recessive genetic in German Shepherd
- Trypanosoma cruzi infection
- Drug overdoses - e.g. phenylpropanolamine, albuterol, digitalis
- Dilated cardiomyopathy - breed predisposition in the Doberman
- Congestive heart failure
- Cardiac hemangiosarcoma
- Subaortic stenosis
- Cor triatriatum
- Right ventricular outflow tract obstruction
- Mitral valve endocardiosis
- Gastric dilatation-volvulus
Clinically affected dogs present frequently with syncope, weak femoral pulses, pale mucous membranes, panting, weakness, exercise intolerance, sudden death and tachycardia audible on auscultation. The syncope, commonly seen in the Boxer dog with normal echocardiograms, is thought to be due to secondary ischemic bradycardia which ensues as a result of ventricular tachycardia.
This condition is life-threatening as ventricular tachycardia can quickly degenerate into ventricular fibrillation, which leads invariably to poor cardiac contractility, reduced ventricular diastolic functioning and eventual congestive heart failure.
Diagnosis can be rapidly achieved on ECG examination, but 24-hour Holter monitors are usually required to definitively confirm the suspicion.
The underlying cause of ventricular fibrillation must be address for long-term survival of cardiac patients.
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