ECG Interpretation

The initial ECG trace revealed evidence of a regular tachycardia of 420 beats/min with upright, narrow QRS complexes (Figure 1). In the lead II trace, there was a small positive deflection immediately after each S wave (J point); this deflection was identified as the P wave. On the basis of the QRS complex morphology and duration, the rhythm was classified as supraventricular tachycardia (SVT). An IV bolus of diltiazem hydrochloride’¹ (0.05 mg/kg [0.023 mg/lb]) was administered, and the tachycardia was terminated. Electrocardiogra-phy was repeated (Figure 2). In the lead II trace, the appearance of the first 2 QRS complexes was consistent with ventricular preexcitation secondary to an accessory pathway. The PR interval was abnormally short (0.03 seconds; reference limits,¹ 0.06 to 0.13 seconds). The morphology of the 2 complexes appeared abnormal, each having a negative deflection and an increased duration of 0.06 seconds (reference limits,¹ < 0.05 seconds). During these 2 complexes, the sinus impulse was conducted across the accessory pathway in an antero-grade direction into the ventricles, bypassing the atrio-ventricular (AV) node with resultant early ventricular activation or preexcitation. The initial activation of the ventricles occurred outside of the His-Purkinje system, resulting in abnormal conduction of the wave of depolarization over a prolonged period, alteration of QRS complex morphology, and prolongation of complex duration. The third, fifth, and sixth complexes in the lead II trace had no evidence of ventricular preexcitation, and the PR interval and QRS complex duration were considered normal. The fourth and eighth complexes were supraventricular premature contractions. These complexes occurred prematurely, with a fixed coupling interval of 180 milliseconds. The morphology of the fourth and eighth QRS complexes was slightly different from the preceding sinus beat, in that the R and Q wave amplitudes were decreased, compared with the preceding sinus beat, but the durations of each complex were still considered normal. These findings indicated that the ectopic impulse was generated within the supra-ventricular region or proximal to the bundle branches. A paroxysmal tachycardia with a rate of 428 beats/min developed following the second premature contraction. The QRS complex morphology during the tachycardia appeared similar to that of the immediately preceding sinus beats—complex duration was apparently normal, indicating supraventricular origin. P waves again became evident at the J point during the SVT.

View Full Size

Lead II ECG tracing obtained from a 9-year-old dog that had a 6-week history of episodes of collapse. Notice the regular tachycardia (heart rate, 420 beats/min) with upright and narrow QRS complexes. A P wave is evident as a small positive deflection (arrow) immediately following each S wave at the J point. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 237, 6; 10.2460/javma.237.6.641

• Download Figure
• Download figure as PowerPoint slide

View Full Size

Lead II ECG tracing obtained from the dog in Figure 1 following administration of diltiazem hydrochloride and subsequent termination of supraventricular tachycardia (SVT). The appearance of the first 2 QRS complexes (arrows) is consistent with ventricular preexcitation secondary to an accessory pathway. The appearance of the third, fifth, and sixth complexes is not indicative of preexcitation. The fourth and eighth complexes (arrowheads) are supraventricular premature contractions. Development of paroxysmal SVT (heart rate, 428 beats/min) is evident following the second premature complex. A P wave is present at each J point during SVT Paper speed = 50 mm/s; 1 cm = 1 mV

Citation: Journal of the American Veterinary Medical Association 237, 6; 10.2460/javma.237.6.641

• Download Figure
• Download figure as PowerPoint slide

Discussion

In mammals, the AV node is the only site of electrical connection between the atria and ventricles because of the insulating properties of the fibrous base of the heart.² Rarely, aberrant tracts of myocardium transverse this fibrous base. An accessory pathway is created if cardiac electrical impulses are conducted between the atria and ventricles via the aberrant myocardial tissue, rather than via the AV node.³ The accessory pathway conducts more rapidly than does AV nodal tissue because AV nodal tissue has a relatively slow impulse conduction velocity and higher electrical resistance, compared with the myocardium. If the sinoatrial nodal impulse were conducted across the bypass tract, it would enter the ventricles prematurely and outside of the conduction system. This is termed ventricular preexcitation. On ECG tracings, preexcitation appears as a shorter-than-normal PR interval and an abnormally shaped QRS complex, which includes a delta wave.⁴ The delta wave is generated by the portion of the ventricle that is activated early and outside of the normal conduction system secondary to propagation of the impulse across the accessory pathway. The remainder of the QRS complex is a hybrid complex because the ventricles are depolarized by the combination of the impulse that is carried across the bypass tract and the impulse that was transmitted in a normal manner across the AV node and the ventricular conduction system.^3,5

Wolff-Parkinson-White syndrome is defined as the concurrent presence of SVT and ventricular preexcitation secondary to an accessory pathway.¹ In dogs, the most commonly affected breeds are Labrador Retriever and Boxer.⁶ Often, an SVT is initiated by premature contractions in the presence of an accessory pathway; the premature contractions are a consequence of the differences in the conduction velocity and refractory period between the accessory pathway and AV node. An atrial premature contraction may encounter the accessory pathway when it is refractory to conduction because of the early timing of the ectopic beat. Impulse propagation may then proceed through the AV node to reach the ventricles because the refractory period of the AV node is shorter than that of an accessory pathway. During ventricular depolarization, the electrical impulse may reach the bypass tract when the tract is excitable; as a result, the impulse conducts in a retrograde direction back to the atria. Upon entering the atria, the impulse may conduct across the atria to the AV node and reenter the ventricles. This reentrant cycle establishes an SVT as the impulse reaches the ventricles through the AV node and conducts back into the atria through the accessory pathway. Alternatively, a ventricular premature beat may reach the AV node when the node is refractory to conduction; as a result, the beat is conducted retrograde through the accessory pathway to the atria. The electrical impulse can then reenter the ventricles through the now excitable AV node and then return to the atria through the accessory pathway.³ In the dog of this report, the SVT was initiated from an atrial premature beat. During the SVT, the delta wave was not evident on the ECG trace because the impulse reached the ventricles only through the AV node. Therefore, ventricular depolarization occurred through the conduction system, resulting in QRS complexes of normal appearance on the ECG trace. However, during SVT, P waves may be evident within the ST segment as a result of the impulse reentering and propagating across the atria through the accessory pathway.² With other types of SVT, P waves are not typically detected in the ST segment; thus, the presence of P waves in the ST segment is highly suggestive of an accessory pathway.

Treatment of Wolff-Parkinson-White syndrome involves administration of antiarrhythmic agents or radiofrequency ablation of the accessory pathway. Anti-arrhythmics that are traditionally administered include β-adrenergic receptor blockers (Vaughan-Williams classification, class II) or calcium channel blockers (class IV). These drugs slow AV nodal conduction and interrupt the reentrant circuit, thereby terminating the SVT.^7,8 Recently, treatment regimens involving administration of lidocaine IV followed by mexiletine (class Ib) PO have been reported⁹ to terminate and prevent SVT, even though use of class Ib antiarrhythmic drugs has been typically limited to the treatment of ventricular rather than supraventricular arrhythmias. Ablation of the accessory pathway can effectively eliminate the reentry pathway without the need for long-term antiarrhythmic treatment, but the availability of equipment and clinicians with the expertise needed to perform the ablation is limited.¹⁰

Diltiazem, a class IV antiarrhythmic, was used for initial management of SVT in the dog of this report. The patient was initially administered a dose of 8 mg (0.75 mg/kg [0.34 mg/lb]), PO, every 8 hours. After 48 hours, the dose was increased to 16 mg (1.5 mg/kg [0.68 mg/lb]), PO, every 8 hours because of the persistence of SVT. Ablation of the accessory pathway was then recommended for this patient. During the procedure, a very rapid SVT developed (rate, 430 beats/min). Ventricular pacing was performed in attempt to interrupt the reentry circuit and restore sinus rhythm. Unfortunately, ventricular fibrillation developed when the second pacing stimulus occurred on a T wave, and the dog could not be resuscitated. Before the dog's cardiac arrest, the accessory pathway was identified along the right ventricular free wall, which is the most common location in dogs.⁶ The behavior of this accessory pathway differed from the typical pathways in dogs in that it was capable of bidirectional conduction, whereas most pathways conduct only in a retrograde direction. Anterograde conduction across the pathway is necessary for ventricular preexcitation to develop, but it is not needed to maintain SVT. Therefore, the absence of ventricular preexcitation does not exclude the possibility that an accessory pathway has created a reentrant circuit between the atria and ventricles, resulting in subsequent development of SVT.