An 11-year-old 33.6-kg (73.9-lb) neutered male chocolate Labrador Retriever was referred to a veterinary teaching hospital for evaluation of a newly diagnosed paroxysmal arrhythmia, lethargy of 3 days' duration, and a single episode of emesis. Four days prior to the referral evaluation, the dog developed gastric dilatation volvulus and consequently underwent exploratory laparotomy and gastropexy performed at another emergency hospital. Two days after discharge from that hospital, inappetence and lethargy prompted readmission. Electrocardiography reportedly revealed paroxysms of a narrow-complex tachycardia (NCT) with instantaneous rates of 280 to 300 beats/min as well as wide-complex premature beats (no ECG tracings available). Lidocaine (2 boluses of 2.08 mg/kg [0.95 mg/lb] each) and procainamide (4.76 mg/kg [2.16 mg/lb]) were administered IV and resulted in a reported reduction in arrhythmia frequency. Maropitant citrate (0.45 mg/kg [0.20 mg/lb], PO, q 24 h), ranitidine (2.23 mg/kg [1.01 mg/lb]), PO, q 12 h), and diltiazem (0.45 mg/kg, PO, q 8 h) were prescribed, and the dog was referred to the veterinary teaching hospital.
On initial examination, the dog was bright, alert, and responsive. Thoracic auscultation revealed a heart rate of 130 beats/min with a regular rhythm, punctuated by premature beats and paroxysms of tachycardia. Femoral pulse quality was good with pulse deficits detectable during the tachyarrhythmia. The dog was tachypneic and had increased lung sounds bilaterally but normal respiratory effort. The rest of the physical examination findings were unremarkable. Echocardiography revealed moderate to severe left ventricular dilation in both diastole (52.7 mm; reference interval, 38.1 to 39.6 mm) and systole (42.1 mm; reference interval, 24.0 to 25.3 mm), with a mild increase in left atrial diameter (33.8 mm; reference interval, 25.1 to 27.5 mm). Global left ventricular systolic function was depressed with a fractional shortening of 20% (reference interval, 25% to 45%). The mitral valve appeared structurally normal with an intermittent centrally directed jet of trace insufficiency during postextrasystolic beats. Systemic blood pressure (Doppler assessment) was 120 mm Hg.
ECG Interpretation
Multiple 6-lead ECGs were acquired (Figure 1), and in all recordings, premature ventricular complexes (PVCs) with right bundle branch block or left bundle branch block morphology were observed. In addition, paroxysms of NCT were present; these were always initiated, and in some cases terminated, by an aberrant beat. The runs of NCT had QRS complexes of variable amplitude (electrical alternans), normal duration (40 milliseconds), and subtle variation in cycle length (220 to 240 milliseconds) at a heart rate of 270 to 300 beats/min. A 6-lead ECG recording of one of the NCT runs began with a normal sinus beat, followed by a PVC and another sinus beat before a PVC initiates the run of NCT. There were P’ waves in the NCT with a right cranial (superior) axis, seen as positive deflections on the T waves of lead aVR and as negative deflections on the T waves in lead II. The RP’ interval was approximately 120 milliseconds with a P'R interval of 80 milliseconds (RP':P'R interval ratio, 1.5). In 1 beat, there may have been a premature atrial complex because a P’ wave in the ST segment of the preceding beat was suspected and the QRS complex duration was normal. The ventricular mean electrical axis of the NCT was comparable to that of the sinus complexes. Some episodes of NCT were apparently triggered by a PVC of an alternate morphology and, on occasion, terminated by a PVC of alternate morphology. The NCT was interpreted as a form of supraventricular tachycardia (SVT), and 3 possible interpretations were considered including focal atrial tachycardia (FAT) initiated by a PVC, FAT with rate-dependent aberrancy on the first complex, or orthodromic atrioventricular reciprocating tachycardia (OAVRT) initiated by a PVC (Figure 2).
Electrocardiograms (all obtained at the initial referral evaluation) from an 11-year-old Labrador Retriever that was referred to a veterinary teaching hospital for evaluation of a newly diagnosed paroxysmal arrhythmia, lethargy of 3 days' duration, and a single episode of emesis. A—A 6-lead ECG recording. From the left, notice a normal sinus complex followed by a premature ventricular complex (PVC [#]), another sinus complex, and then a run of narrow-complex tachycardia (NCT). There are P’ waves in the NCT with a right cranial (superior) axis that are seen as positive deflections on the T wave in lead aVR and as negative deflections on the T wave in lead II (arrows). The third from last complex on the right (arrowhead) may represent a premature atrial complex because a P’ wave is suspected in the ST segment of the preceding complex and the QRS complex duration is normal. B—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and of a comparable morphology (#) to those in panel A. C—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and terminated by a PVC of comparable morphology (#) to that in panel A. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Electrocardiograms (all obtained at the initial referral evaluation) from an 11-year-old Labrador Retriever that was referred to a veterinary teaching hospital for evaluation of a newly diagnosed paroxysmal arrhythmia, lethargy of 3 days' duration, and a single episode of emesis. A—A 6-lead ECG recording. From the left, notice a normal sinus complex followed by a premature ventricular complex (PVC [#]), another sinus complex, and then a run of narrow-complex tachycardia (NCT). There are P’ waves in the NCT with a right cranial (superior) axis that are seen as positive deflections on the T wave in lead aVR and as negative deflections on the T wave in lead II (arrows). The third from last complex on the right (arrowhead) may represent a premature atrial complex because a P’ wave is suspected in the ST segment of the preceding complex and the QRS complex duration is normal. B—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and of a comparable morphology (#) to those in panel A. C—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and terminated by a PVC of comparable morphology (#) to that in panel A. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Electrocardiograms (all obtained at the initial referral evaluation) from an 11-year-old Labrador Retriever that was referred to a veterinary teaching hospital for evaluation of a newly diagnosed paroxysmal arrhythmia, lethargy of 3 days' duration, and a single episode of emesis. A—A 6-lead ECG recording. From the left, notice a normal sinus complex followed by a premature ventricular complex (PVC [#]), another sinus complex, and then a run of narrow-complex tachycardia (NCT). There are P’ waves in the NCT with a right cranial (superior) axis that are seen as positive deflections on the T wave in lead aVR and as negative deflections on the T wave in lead II (arrows). The third from last complex on the right (arrowhead) may represent a premature atrial complex because a P’ wave is suspected in the ST segment of the preceding complex and the QRS complex duration is normal. B—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and of a comparable morphology (#) to those in panel A. C—A lead II ECG tracing. In this recording, the NCT appears to be triggered by PVCs of an alternate morphology (*) and terminated by a PVC of comparable morphology (#) to that in panel A. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Ladder diagrams constructed for the lead II ECG tracing in panel A of Figure 1 to illustrate 3 possible interpretations for the NCT in the dog in Figure 1. In each ladder diagram, the upper zone represents atrial activation (A), the middle zone represents atrioventricular conduction (AV), and the lower zone represents ventricular activation (V). The 3 possible NCT interpretations include focal atrial tachycardia (FAT) initiated by a PVC (A), FAT with rate-dependent aberrancy on the first complex (B), or orthodromic atrioventricular reciprocating tachycardia initiated by a PVC. Paper speed = 25 mm/s; 1 cm = 1 mV. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Ladder diagrams constructed for the lead II ECG tracing in panel A of Figure 1 to illustrate 3 possible interpretations for the NCT in the dog in Figure 1. In each ladder diagram, the upper zone represents atrial activation (A), the middle zone represents atrioventricular conduction (AV), and the lower zone represents ventricular activation (V). The 3 possible NCT interpretations include focal atrial tachycardia (FAT) initiated by a PVC (A), FAT with rate-dependent aberrancy on the first complex (B), or orthodromic atrioventricular reciprocating tachycardia initiated by a PVC. Paper speed = 25 mm/s; 1 cm = 1 mV. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Ladder diagrams constructed for the lead II ECG tracing in panel A of Figure 1 to illustrate 3 possible interpretations for the NCT in the dog in Figure 1. In each ladder diagram, the upper zone represents atrial activation (A), the middle zone represents atrioventricular conduction (AV), and the lower zone represents ventricular activation (V). The 3 possible NCT interpretations include focal atrial tachycardia (FAT) initiated by a PVC (A), FAT with rate-dependent aberrancy on the first complex (B), or orthodromic atrioventricular reciprocating tachycardia initiated by a PVC. Paper speed = 25 mm/s; 1 cm = 1 mV. See Figure 1 for remainder of key.
Citation: Journal of the American Veterinary Medical Association 251, 12; 10.2460/javma.251.12.1383
Treatment with sotalol hydrochloride (2.38 mg/kg [1.1 mg/lb], PO, q 12 h) was started because of the impression that PVCs initiated the paroxysmal NCT. Pimobendan (0.30 mg/kg [0.14 mg/lb], PO, q 12 h) was also prescribed to treat the systolic dysfunction. Eighteen days later, a 24-hour Holter examination was performed during which 7 paroxysms of NCT were recorded; each NCT run was initiated by either a supraventricular premature complex or PVC. There was no evidence of ventricular pre-excitation throughout the Holter recording. There was frequent ventricular ectopy with characteristics of complexity or malignancy (multiform PVCs, paroxysmal ventricular tachycardia, couplets, triplets, and ventricular bigeminy or trigeminy). On the basis of these findings, treatment with mexiletine hydrochloride (5.95 mg/kg [2.70 mg/lb], PO, q 8 h) was initiated and administration of sotalol (dosage unchanged) was continued to better control the ventricular ectopy. After some modulation of the medical treatments (reduction of mexiletine dosage to 4.46 mg/kg [2.03 mg/lb], PO, q 8 h because of perceived lethargy), recheck ECG, echocardiographic, and Holter examinations were performed. Echocardiography revealed static structural heart changes, and the left ventricular systolic dysfunction was presumed to be related to either a primary cardiomyopathy or persistent tachycardia-induced cardiomyopathy. There were occasional single PVCs and paroxysms of NCT on the ECG recording. No medication changes were made, and 24-hour Holter monitoring was performed. Results of the second Holter examination indicated poor control of the dog's ventricular arrhythmia with 12,574 ventricular ectopic beats (an increase of 24.7% from the previous Holter findings) and increasing complexity of the ventricular ectopy (multiform PVCs and ventricular tachycardia). An increase in the mexiletine dosage was discussed, but given the lethargy and a possible proarrhythmic effect associated with the mexiletine treatment initiation, administrations of sotalol and mexiletine were discontinued. After a 2-day washout, treatment with amiodarone hydrochloride was initiated (11.9 mg/kg [5.4 mg/lb], PO, q 24 h for 2 weeks, then 5.95 mg/kg [2.70 mg/lb], PO, q 24 h thereafter). Within 2 weeks after the change in drug regimen, the owner reported that the dog's energy level and exercise tolerance were improved. The owner declined a recheck Holter examination after initiation of treatment with amiodarone, and adequate control of the dog's supraventricular and ventricular ectopy was not confirmed. Although the dog had been doing well, it died 11 months after diagnosis.
Discussion
Supraventricular tachycardia represents a broad category of dysrhythmia that includes rhythms emanating from the sinus node, atrial myocardium, atrioventricular (AV) and junctional tissues, and accessory pathway–mediated tachycardias.1,2 Regular SVTs include FAT tachycardia, atrial flutter, AV nodal reentrant tachycardia, and AV reentrant tachycardias. The AV reentrant tachycardias are caused by bypass tracts (accessory pathways) in which conduction can be anterograde (antidromic AV conduction), retrograde (orthodromic AV conduction), or in both directions.1,3–5 Irregular SVTs include atrial fibrillation, atrial flutter with variable AV block, and multifocal atrial tachycardias. In people, the most common type of reentrant SVT is AV nodal reentrant tachycardia, whereas orthodromic AV reentrant tachycardia (ie, OAVRT) is the most commonly reported reentrant SVT for dogs.3,4,6 Because antegrade conduction in most SVTs occurs along the AV node-His-Purkinje system, the QRS complex duration remains within normal limits in the absence of functional or anatomic conduction abnormalities. For the dog of the present report, the normal QRS duration (40 milliseconds) during the NCTs supported conduction along the AV-node His-Purkinje system and an absence of conduction abnormalities.
The top 2 differential diagnoses for the NCTs in the dog of the present report were FAT and OAVRT. Focal atrial tachycardias originate from a single focus in the atrial myocardium and can be caused by enhanced automatism, microreentrant circuits, and, rarely, triggered activity.4,7 The ECG findings are characterized by P’ wave configuration and polarity that vary with the location of the ectopic origin. In dogs, it is common to see positive P’ waves in leads II, III, and aVF; slight warm-up (ie, rate becomes faster) and cool-down (ie, rate becomes slower) of the P'-P’ interval; and, frequently, just before termination of the tachycardia, an increase in the duration of the P'R interval.7 Orthodromic AV reciprocating tachycardia is a macroreentrant circuit involving an AV bypass tract and the AV node. The circuit used to maintain the macroreentrant in OAVRT has a concealed accessory AV pathway as the retrograde limb and the AV node as the anterograde limb. Orthodromic AV reciprocating tachycardia is characterized by a rapid ventricular response, retrograde P waves in the late part of the ST segment, a RP':P'R interval ratio < 1, and a high incidence of QRS complex alternans because of oscillations in the relative refractory period of the specialized conduction system, resulting in altered action potential duration.4,8
Focal atrial tachycardia and OAVRT are difficult to differentiate in surface ECG tracings. On the basis of results of a study4 in 23 dogs with either FAT or OAVRT that underwent 12-lead ECG examinations, there were 2 findings for the dog of the present report that supported FAT as the mechanism for the NCTs. First, there was the presence of P’ waves in the late part of the ST segment with a relatively long RP’ interval (used to measure ventriculo-atrial conduction time) of 120 milliseconds and an RP':P'R ratio of 1.5.4 Second, there was a lack of pre-excitation during sinus rhythm. However, these findings did not rule out OAVRT, because many dogs with accessory pathway–mediated SVT have concealed conduction.6,9
The ECG findings for the dog of the present report also included features that supported OAVRT as the mechanism for the NCTs. Electrical alternans (as noted in this dog's ECG tracings) can occur during both OAVRT and FAT, yet is more common during the former.4,5 The P’ wave polarity in the NCT of this dog had a right cranial (superior) axis. This is common during OAVRT in dogs because the most common accessory pathways are in the caudal (posterior)-septal tricuspid valve annulus or right ventricular free wall.1,4 Negative P’ waves in the caudal (inferior) leads, as seen in the case described in the present report, supported a caudal origin of a FAT.
For the dog of the present report, the presence of P’ waves made a third possible differential diagnosis (ie, AV nodal reentrant tachycardia) less likely. Overall, the surface ECG characteristics of this rhythm supported FAT with aberrancy on the initiating beat as the more likely mechanism, but results of an electrophysiologic assessment of the dog would have had to be available to definitively differentiate between OAVRT and FAT.
An unusual aspect of the arrhythmia in the dog of the present report was that the paroxysms of SVT appeared to be initiated by a PVC. This led to initial suspicion that an accessory pathway was accessed by the PVCs. To the authors' knowledge, initiation of an accessory pathway–mediated SVT by a PVC in a dog has been reported only once.10 In humans, initiation of an atrial re-entrant tachycardia by ventricular premature beats has been reported.11 In the dog of the present report, however, the presence of P waves in the late part of the ST segment, a RP':P'R interval ratio > 1, and the warm-up and cool-down variation in cycle duration made the diagnosis of OAVRT less likely.4,5
References
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