Introduction
A 17-year-old 4.59-kg castrated male domestic medium-hair cat was presented for a recheck cardiac evaluation of previously diagnosed second-degree atrioventricular (2° AV) block (atropine responsive) and idiopathic systemic hypertension (well controlled with amlodipine, 1.25 mg, PO, q 24 h). An arrhythmia was auscultated on physical examination, and echocardiography revealed mild hypertrophic cardiomyopathy with no evidence of chamber enlargement. Six-lead ECG was performed (Figure 1).
ECG Interpretation
The ECG tracing revealed an underlying sinus rhythm. Narrow QRS complexes were followed by a single wide QRS complex with a consistent PR interval and deep S wave in leads II, III, and aVF, consistent with a right bundle branch block (RBBB).1 An initial wide QRS complex is followed by a blocked P wave, suggestive of 2° AV block, and then subsequent, successive wide QRS complexes were followed by a blocked P wave, again consistent with 2° AV block. Prior to each blocked P wave, there was a constant PR interval, as with Mobitz type II 2° AV block. The development of transient RBBB in association with a change in ventricular rate produced by the 2° AV block was consistent with aberrant conduction. The diagnosis was sinus rhythm with Mobitz type II 2° AV block with linking phenomenon.
Discussion
Aberrant conduction is a ventricular conduction phenomenon defined as a transient block of the ventricular conduction system. This differs from a bundle branch block, which is an anatomic (fixed) block. Aberrant conduction occurs when an impulse reaches the conduction system before the interventricular conduction system has had time to completely repolarize.1 The duration of a refractory period changes with cycle length; the refractory period is shortened when there is an increase in heart rate and is prolonged when there is a decrease in heart rate. There are 2 forms of aberrant conduction, namely tachycardia-dependent (phase 3 aberrancy) and bradycardia-dependent (phase 4 aberrancy) blocks.2
A form of phase 3 aberrancy, Ashman phenomenon, was first described by Gouaux et al3 in association with atrial fibrillation. The generation of this aberrancy is dependent on the duration of the preceding cycle. A longer cycle preceding a shorter cycle can cause the right bundle branch to become refractory.3 If the conduction of the next impulse after a shorter R-R interval occurs, the right bundle branch will become refractory.3 The resulting aberrant conduction is termed Ashman phenomenon. For the cat of the present report, because the RBBB occurred when the cycle duration decreased and the heart rate accelerated, tachycardia-dependent RBBB with phase 3 aberrancy was initially considered; however, this would not explain the second aberrantly conducted QRS complex.
The underlying mechanism of the transient but sustained nature of the tachycardia-induced aberrant conduction in the cat of the present report can be explained by the linking phenomenon. The linking phenomenon requires a macroreentrant circuit where there are 2 branches with different properties.3–5 There is a dominant and a dependent pathway, which in this cat were the left bundle branch and right bundle branch, with preferential conduction through the dominant pathway and a dependent pathway that is characterized by a longer refractory period.2 An impulse can travel down the dominant pathway but is blocked in the dependent pathway; however, it can retrogradely travel back up the dependent pathway, resulting in prolonging the right bundle branch refractory state.2 The next antegrade impulse is not able to travel down the dependent pathway but conducts through the dominant branch and then reenters retrogradely.4,5 This will occur alternately until a change in cycle duration occurs and allows for full recovery of the pathways, thus resulting in a transient and nonsustained aberrancy.4
For the cat of the present report, the other ECG abnormality was Mobitz type II 2° AV block. Second-degree AV block in cats has been associated with cardiac disease and systemic illness, such as hyperthyroidism.6–8 Given that this cat had hypertrophic cardiomyopathy, that condition may have been an underlying contributing cause of the 2° AV block.
References
- 1. ↑
Santilli R, Moise S, Pariaut R, et al. Conduction disorders. In: Electrocardiography of the Dog and Cat: Diagnosis of Arrhythmias. 2nd ed. Prienter Trento; 2018:259–292.
- 2. ↑
Marriot H, Conover M. Aberrancy vs ectopia. In: Advanced Concepts in Arrhythmias. 3rd ed. Mosby Inc; 1998:330–343.
- 3. ↑
Gouaux JL, Ashman R. Auricular fibrillation with aberration simulating ventricular paroxysmal tachycardia. Am Heart J. 1947;34(3):366–373.
- 4. ↑
Lhemann M, Denker S, Mahmud R, Addas A, Akhtar M. Linking: a dynamic electrophysiological phenomenon in macroreentry circuits. Circulation. 1985;71(2):254–265.
- 5. ↑
Chenevert M, Lewis RJ. Ashman’s phenomenon—a source of nonsustained wide-complex tachycardia: a case report and discussion. J Emerg Med. 1992;10(2):179–183.
- 6. ↑
Fisher JD, Aronson RS. Rate-dependent bundle branch block: occurrence. J Am Coll Cardiol. 1990;16(1):240–243.
- 7.
Kaneshige T, Machida M, Itoh H, Yamane Y. The anatomical basis of complete atrioventricular block in cats with hypertrophic cardiomyopathy. J Comp Pathol. 2006;135(1):25–31.
- 8. ↑
Harvey AM, Battesby IA, Faena M, Fews D, Darke PGG, Ferasin L. Arrhythmogenic right ventricular cardiomyopathy in two cats. J Small Anim Pract. 2005;46(3):151–156.