A13-year-old 7.3-kg (16.06-lb) sexually intact male Dachshund was evaluated because of acute pulmonary edema that developed during the preceding night. The dog was admitted to the emergency room and treated with furosemide and supplemental oxygen. A history of dry cough of 2 weeks’ duration was reported. The next day, the dog was examined by the cardiology service, at which time it was eupneic, bright, and alert. Cardiac auscultation revealed a grade 5/6 left apical systolic murmur; the heart rate was 160 beats/min with a regular rhythm. Femoral pulse quality was fair, and some asynchronous beats were noted. Lung sounds were considered normal. Other physical examination findings were unremarkable. Results of a serum biochemical panel and CBC were within reference ranges. Echocardiography revealed mild and moderate tricuspid and mitral valve insufficiencies, respectively, in addition to moderate left ventricular and atrial dilation and systolic dysfunction. The owners declined an ECG examination of the dog at this time. The dog was discharged from the hospital, and the owners were instructed to administer enalapril maleate (0.5 mg/kg [0.23 mg/lb], PO, q 12 h), furosemide (2 mg/kg [0.91 mg/lb], PO, q 12 h), and pimobendan (0.3 mg/kg [0.14 mg/lb], PO, q 12 h).
One week later, the dog was admitted to the emergency room because of another episode of pulmonary edema and tachycardia with an irregular rhythm. The dog had been doing well during the week with rare episodes of dry cough at night, but had suddenly become lethargic and dyspneic. During evaluation, the heart rate was 180 beats/min and the femoral pulses were weak and asynchronous with the heartbeat. Doppler ultrasonographic systolic blood pressure measurement was 110 mm Hg. An ECG recording was obtained for assessment of the rhythm (Figure 1).
Initial ECG tracings (leads II, III, and aVF) obtained from a dog during cardiologie evaluation the day after development of acute pulmonary edema during the preceding night, for which the dog was admitted to the emergency room. In these tracings, notice the wide QRS complex tachycardia (heart rate, 174 beats/min) with a right bundle branch block pattern. P waves are intermittent. The R-wave variation is respiratory artifact. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 249, 8; 10.2460/javma.249.8.898
ECG Interpretation
The 6-lead surface ECG tracing (Figure 1) revealed a wide QRS complex tachycardia and heart rate of 174 beats/min. The ventricular coupling interval was regular (340 milliseconds), and the QRS complex duration was 73 milliseconds (reference range, ≤ 60 milliseconds). The inability to clearly identify P waves made differentiation between ventricular tachycardia and supraventricular tachycardia with ventricular conduction disturbance difficult. At this point, the 3 differential diagnoses were accelerated idioventricular rhythm (AIVR), ventricular tachycardia (VT), or supraventricular tachycardia with wide QRS complexes. However, because the dog had an acute hemodynamic compromise, VT was most probable, even though the heart rate was not as fast as it would be expected.
The presence of a capture beat (Figure 2) with narrow QRS complex (duration, 50 milliseconds) and a fast run of narrow QRS complex tachycardia (Figure 3) illustrated the morphology of this dog's normal QRS complexes. Given the ECG findings, the diagnosis of ventricular tachyarrhythmia was supported. Pharmacological cardioversion was performed initially via IV administration of lidocaine hydrochloride (2 mg/kg); however, this procedure failed to achieve conversion to sinus rhythm. An attempt at rhythm conversion was then made via bolus administration of amiodarone hydrochloride (5 mg/kg [2.27 mg/lb], IV). After this treatment, a 6-lead surface ECG revealed VT, a heart rate of 186 beats/min, some QRS complexes with R-on-T phenomenon, and fusion beats. Unfortunately, because of the dog's uncooperative behavior, a constant rate infusion of amiodarone could not be performed. The dog was discharged from the hospital, and the owners were instructed to administer amiodarone (13.7 mg/kg [6.2 mg/lb], q 12 h) orally. During a recheck evaluation following 7 days of medical treatment with amiodarone, the owners reported the dog's condition appeared excellent. On physical examination, heart rhythm was regular, heart rate was 144 beats/min, and femoral pulse quality was strong and synchronous with the heartbeat. An ECG examination was declined by the owners. The amiodarone dosage was reduced (6.8 mg/kg [3.1 mg/lb], PO, q 12 h). The owners were instructed to maintain administration of the previously prescribed drugs and return the dog for a recheck examination 1 week later.
Lead II ECG tracing obtained from the dog in Figure 1 almost immediately after the initial recording. Notice the predominant rhythm is ventricular and there is a captured beat (arrow). The captured beat had normal QRS complex morphology (duration, 50 milliseconds) for this dog. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 249, 8; 10.2460/javma.249.8.898
Additional ECG tracings (leads II, III, and aVF) obtained from the dog in Figure 1 at 2 minutes and 41 seconds after the initial recording. Notice a fast run of supraventricular tachycardia (arrow) with a heart rate of 233 beats/min. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 249, 8; 10.2460/javma.249.8.898
At the second recheck evaluation (7 days after amiodarone dosage reduction), another 6-lead surface ECG examination was performed (Figure 4). On the ECG tracings, the sinus rhythm appeared normal, heart rate was 160 beats/min, QRS complex duration was 60 milliseconds, and PR interval duration was 90 milliseconds.
Follow-up ECG tracings (leads II, III, and aVF) obtained from the dog in Figure 1 after 2 weeks of treatment with amiodarone hydrochloride. Notice the normal sinus rhythm, QRS complex duration of 60 milliseconds, PR interval duration of 90 milliseconds, and heart rate of 160 beats/min. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 249, 8; 10.2460/javma.249.8.898
Discussion
The case described in the present report illustrates the difficulty in differentiating VT, AIVR, and wide QRS complex tachycardia of supraventricular origin. Supraventricular tachyarrhythmias are most commonly confused with VTs when the QRS complexes are wide. Wide QRS complex tachycardia of supraventricular origin may develop when there is marked left and right ventricular enlargement, preexistent left or right bundle branch block, atrioventricular nodal conduction over an accessory pathway, or functional left or right bundle branch block (aberrancy conduction).1
To date, no specific algorithm for differentiation of VT from supraventricular tachycardia is available for use in veterinary medicine. However, the morphology of the QRS complexes, association of P waves with QRS complexes, and presence of fusion beats can be considered the most reliable distinguishing criteria.1 For the dog of this report, the initial data from the first ECG monitoring (Figure 1) did not clearly identify whether the rhythm was VT, AIVR, or supraventricular tachycardia with wide QRS complexes. However, the subsequent presence of a captured beat with narrow QRS complex and a very fast narrow QRS complex tachycardia ruled out a supraventricular origin with aberrant conduction.
Ventricular arrhythmias are common in dogs with congestive heart failure attributable to dilated cardiomyopathy and chronic atrioventricular valve disease.1 Myocardial hypertrophy and fibrosis,2 local and acute ischemia,3 electrolyte imbalance (particularly hypokalemia and hypomagnesemia),4 cathecolamines,5 and myocardial stretch6 are considered underlying mechanisms for ventricular arrhythmias in dogs with heart failure. On the basis of additional ECG findings, VT and AIVR became the 2 major possible diagnoses for the dog of the present report. Accelerated idioventricular rhythm is an ectopic cardiac rhythm characterized by 3 or more consecutive ventricular complexes with a rate faster than the normal ventricular intrinsic escape rate (30 to 40 beats/min), but slower than the VT rate.7 An AIVR becomes evident when a focus that should normally be suppressed increases to a rate faster than that of the sinus node or AV node. The underlying electrophysiological mechanism is associated with abnormalities of the ventricular myocardium (high vagal tone and decreased sympathetic nervous system activity) and altered automatism of the Purkinje fibers. When the enhanced automaticity in the His-Purkinje fibers or myocardium surpasses that of the sinus node, AIVR becomes the dominant rhythm. Sinus bradycardia may facilitate the appearance of AIVR. Generally, it is an intermittent and transient rhythm (although it may persist for some days), which is well tolerated and rarely causes hemodynamic compromise or hypotension. Additionally, AIVR does not require treatment. An exact determination of the upper cutoff heart rate limit that differentiates AIVR from VT is not provided in the veterinary medical literature. Some researchers have suggested a ventricular rate limit > 180 beats/min8,9 can be used to differentiate AIVR from VT. As a general rule, dogs with ventricular arrhythmia and a heart rate > 160 beats/min should be treated; those with a heart rate < 120 beats/min are usually not treated, and those with a heart rate between 120 and 160 beats/min may sometimes be treated.a
However, AIVR or VT should not be diagnosed on the basis of heart rate alone. A ventricular arrhythmia is judged to be dangerous when it causes hemodynamic compromise (congestive heart failure, hypotension, syncope, or weakness) and when it may degenerate into a more electrically unstable and fatal arrhythmia.a Even so, heart rate is the most important determinant of hemodynamic compromise because it pertains to the arrhythmia itself. As a general guide,a most dogs will have substantial hemodynamic compromise when the arrhythmia is sustained (duration, > 30 seconds) at a rate > 250 beats/min. The dog of the present report had a heart rate of 175 beats/min, and the echocardiogram indicated systolic dysfunction. Myocardial failure combined with a fast heart rate has an important role in the development of congestive heart failure.a For this dog, acute conversion to sinus rhythm after the IV administration of a single dose of lidocaine and amiodarone was not achieved. Several reasons could have accounted for the failure of this therapeutic protocol, such as choice of dosage and method of administration1 (ie, bolus vs constant rate infusion). A gradual 25% increase in the lidocaine dose might have abolished the arrhythmia. Likewise, a constant rate infusion of amiodarone instead of an IV bolus might have achieved a better effect. The aggressive treatment of pulmonary edema that the dog underwent hours before the cardioversion attempt may have caused electrolyte imbalance and pharmacokinetic complications, which reduced serum drug concentration and consequently hindered the antiarrhythmic action.1
Footnotes
Moïse NS. Chronic management of tachyarrhythmias in the dog, in Proceedings. 26th Annual Waltham Diets/OSU Symposium for the Treatment of Small Animals: Cardiology, 2002.
References
1. Moïse NS. Diagnosis and management of canine arrhythmias. In: Fox PR, Sisson D, Moïse NS, eds. Textbook of canine and feline cardiology: principles and clinical practice. 2nd ed. Philadelphia: WB Saunders Co, 1999;331–385.
2. Singh SN. Congestive heart failure and arrhythmias: therapeutic modalities. J Cardiovasc Electrophysiol 1997; 8:89–97.
3. Gabriel Filho SJ, Ribeiro CA. ECG of the month. Multiform ventricular tachycardia. J Am Vet Med Assoc 2012; 241:1288–1290.
4. El-Sherif N, Turitto G. Electrolyte disorders and arrhythmogenesis. Cardiol J 2011; 18:233–245.
5. Bhagat BD, Rhao PD, Dhalla NS. Role of catecholamine in the genesis of arrhythmias. Adv Myocardiol 1980; 2:117–132.
6. Hansen DE, Craig CS, Hondeghem LM. Stretch-induced arrhythmias in the isolated canine ventricle. Evidence for the importance of mechanoelectrical feedback. Circulation 1990; 81:1094–1105.
7. Grimm W, Marhlinski FE. Accelerated idioventricular rhythm: bidirectional ventricular tachycardia. In: Zipes DP, Jalife J, eds. Cardiac electrophysiology from cell to bedside. 3rd ed. Philadelphia: Elsevier Inc, 2004;700–704.
8. Ilvento JP, Provet J, Danilo P Jr, et al. Fast and slow idioventricular rhythm in the canine heart: a study of their mechanism using antiarrhythmic drugs and electrophysiologic testing. Am J Cardiol 1982; 49:1909–1916.
9. Vassalle M, Knobb RE, Cummings M, et al. An analysis of fast idioventricular rhythm in the dog. Circ Res 1977; 41:218–226.
