INTRODUCTION

Physiologically, specialized ventricular cells, known as Purkinje fibers, may work as a pacemaker when the sinus and atrioventricular nodes fail to function appropriately, resulting in a ventricular escape rhythm or idioventricular rhythm at a rate of about 30 to 40 beats/min in dogs and 60 to 130 beats/min in cats.^1,2 Three arrhythmogenic mechanisms known as enhanced automaticity, triggered activity, and reentry (Box 47-1) may affect Purkinje cells or any excitable ventricular myocyte and result in ventricular tachycardia (VT).³ They result in a ventricular rhythm faster than the physiologic idioventricular rhythm. Most human cardiologists define VT as three or more consecutive ventricular beats occurring at a rate faster than 100 beats/min, the conventional upper limit for normal sinus rhythm. In our patients, normal sinus rhythm can probably reach 150 to 180 beats/min in dogs and 220 beats/min in cats. These rates define the lower limit for VT. If a ventricular rhythm is faster than the physiologic idioventricular rhythm and slower than VT, it is called accelerated idioventricular rhythm (AIVR). The rate of an AIVR is within the range of the underlying sinus rhythm. Therefore both rhythms are seen competing on a surface electrocardiogram (ECG) because the faster pacemaker inhibits the slower one, a property known as overdrive suppression.² Besides rate, an important feature of VT is duration, because both determine the clinical consequences of the arrhythmia. VT is described as nonsustained if it lasts less than 30 seconds and sustained if it lasts longer.

Box 47-1 Electrophysiologic Mechanismsof Ventricular Tachycardia

Reentry: Requires an impulse to leave a point of departure and return to its starting point with a sufficient delay that the cardiac tissue has recovered its excitability. It usually circles around an area of nonconductive tissue (fibrosis, vessel). Shortening of the refractory period and slow conduction favor this self-perpetuating mechanism.

Enhanced automaticity: A myocardial cell that never possessed the property of automaticity while healthy gets the ability to depolarize spontaneously when depressed. Its membrane potential is less negative, and the action potential becomes similar to that of the sinus node.

Triggered activity: Results from small membrane depolarizations that appear after and are dependent on the upstroke of the action potential. They trigger an action potential when they reach the threshold potential. When they occur during the process of repolarization they are called early afterdepolarizations (EADs), and when they occur after full repolarization they are called delayed afterdepolarizations (DADs). Hypokalemia and drug-induced prolongation of the QT segment increase the risk of EADs. DADs occur secondary to intracellular calcium overload associated with sustained tachycardia and digoxin toxicity.

ELECTROCARDIOGRAPHIC DIAGNOSIS

In the intensive care unit, VT is first suspected on physical examination or detected on a continuous ECG monitor. Confirmation of VT relies on a good-quality 6-lead to 12-lead surface ECG recording with the patient placed in right lateral recumbency.

Ventricular tachycardia is identified as a broad QRS tachycardia with complexes wider than 0.06 second in dogs and 0.04 second in cats. Each QRS complex is followed by a large T wave, directed opposite to the QRS deflection.

The challenge of ECG interpretation is to differentiate VT from supraventricular tachycardias (SVTs) with broad QRS complexes because of aberrant conduction of the electrical impulse within the ventricles. Aberrant ventricular conduction results from a structural bundle branch block, a functional or rate-related bundle branch block, or finally an accessory atrioventricular pathway causing preexcitation.⁴

The three most reliable diagnostic criteria of VT are atrioventricular dissociation, fusion beats, and capture beats (Figure 47-1). Atrioventricular dissociation is demonstrated when P waves are occasionally seen on the ECG tracing but are not related to ventricular complexes. These P waves reflect atrial activity independently from the ventricle. On occasion apparent atrioventricular association may be seen, or ventricular beats can conduct in a retrograde fashion to the atrium in a 1:1 ratio. Therefore signs of atrioventricular association do not rule out VT. Fusion beats and capture beats are seen with paroxysmal VT and AIVR. Fusion beats result from the summation of a ventricular impulse and a simultaneous supraventricular impulse resulting in a QRS complex of intermediate morphology and preceded by a P wave (unless there is concurrent atrial fibrillation). A capture beat is a supraventricular impulse conducting through the normal conduction pathways to the ventricle during an episode of VT or AIVR. This complex occurs earlier than expected and is narrow if the conduction system is intact.⁴