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Carrie Goldkamp Section of Cardiology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126.

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Amara H. Estrada Section of Cardiology, Department of Small Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32610-0126.

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A 12-year-old 10-kg (22-lb) spayed female mixed-breed dog was evaluated at the Veterinary Medical Center of the University of Florida because of chronic renal failure. On initial physical examination, a grade 3/6 left apical systolic murmur was ausculted, which had previously been diagnosed by the hospital clinicians as mild mitral regurgitation secondary to chronic degenerative valvular disease. The dog was admitted to the hospital, and crystalloid solutions were administered IV. After 3 days of diuresis, tachycardia was detected on physical examination and an ECG was obtained (Figure 1).

Figure 1—
Figure 1—

Lead II ECG trace obtained from a dog that was evaluated because of chronic renal failure during an episode of tachycardia. A supraventricular tachycardia is present with a heart rate of approximately 270 beats/min; p waves cannot be identified. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 230, 5; 10.2460/javma.230.5.668

ECG Interpretations

Evaluation of the initial ECG revealed supraventricular tachycardia (SVT) and a heart rate of approximately 270 beats/min (Figure 1). The mechanism of the SVT could not be determined because p waves were not visible. Two boluses of esmolol (0.5 mg/kg [0.23 mg/lb]) were administered IV at a 10-minute interval with no effect. Administration of diltiazem hydrochloride (0.1 mg/kg [0.05 mg/lb], IV) resulted in termination of the SVT, followed by a short period (2.8 seconds’ duration) of second-degree atrioventricular (AV) block (Figure 2). On the ECG trace, negative pa waves were evident and blocking of the pa waves was detectable just prior to termination of the rhythm. The dog was discharged, and the owner was instructed to administer diltiazem (3.0 mg/kg [1.36 mg/lb], PO, q 12 h). The dog was to be returned to the hospital for reevaluation in 1 week.

Figure 2—
Figure 2—

Lead II ECG trace obtained from the dog in Figure 1 following IV administration of diltiazem (0.1 mg/kg [0.05 mg/lb], IV). Notice negative pa waves (arrows) are visible during the SVT with block of the pa waves just before the rhythm is terminated. Once the SVT terminates, the sinus node begins to fire slowly again and then eventually recovers to a normal rate. This was likely attributable to overdrive suppression by the arrhythmia on the sinus node. A period of AV block is then followed by a ventricular escape complex, then recovery of the AV node and normal conduction, followed by another period of AV block. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 230, 5; 10.2460/javma.230.5.668

Three days later (ie, after 4 days of treatment with diltiazem), the dog was examined at the hospital’s emergency service following 4 episodes of syncope. According to the owner, the duration of each episode was approximately 10 seconds. There was no previous history of cardiovascular events. An ECG was again performed (Figure 3). Evaluation of the third ECG trace revealed frequent episodes of paroxysmal nonsustained SVT (heart rate, 270 beats/min), followed each time by long periods of AV block (longest period represented in the ECG trace was 4.8 seconds’ duration). Each episode of AV block was subsequently followed by a regular rhythm. During this tachycardia, negative pa waves were identified with a long RP interval.1 Just prior to termination of the arrhythmia, there was 2:1 block; hence, this was most likely indicative of atrial tachycardia. Echocardiographic evaluation revealed that the left ventricle had mild to moderate volume overload but apparently normal systolic function. Mild mitral valve regurgitation attributable to degenerative mitral valve disease was again detected. Diastolic mitral valve regurgitation was also evident during periods of AV block.

Figure 3—
Figure 3—

Lead II ECG trace obtained from the dog in Figure 1 after 3 days of treatment with diltiazem (3 mg/kg [1.36 mg/lb], PO, q 12 h). Paroxysmal nonsustained SVT is again identified (heart rate, 270 beats/min), followed by a long period (4.8 seconds) of AV block and then gradual recovery of the sinus node. The block is again followed by a ventricular escape beat and then normal sinus rhythm (heart rate, 120 beats/min). During this tachycardia, negative pa waves are again identified (arrows) with a long RP interval. Just prior to termination of the arrhythmia, there is 2:1 block; thus, this is most likely an atrial tachycardia. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 230, 5; 10.2460/javma.230.5.668

Discussion

Supraventricular tachycardia occurs when an ectopic pacemaker fires more quickly than the sinoatrial node, causing an accelerated heart rate. The depolarizations may originate in the atria or AV junction (proximal AV bundle, AV node, or bundle of His).2 To distinguish between atrial and AV node-dependent tachyarrhythmias, drugs can be given to affect conduction and refractoriness in the AV junctional tissue.2 In the dog of this report, diltiazem was administered and AV block was induced. This suggests that the ectopic depolarization originated from the atrial myocardium rather than from junctional tissue. If the ectopic focus were in the junctional tissue, diltiazem would have eliminated the tachyarrhythmia without AV block.

The drugs used commonly to treat atrial tachycardia are class II and class IV antiarrhythmics. Class II antiarrhythmics are β-adrenergic receptor blockers that work by indirectly blocking the proarrhythmic effects of catecholamines on the heart.3,4 Dogs with atrial tachycardia often have high sympathetic β-adrenergic receptor activity. A β-adrenergic receptor blocker will affect the AV junctional tissue, increasing the conduction time through the AV junction and prolonging the refractory period.4 If there is a reentrant circuit in the AV nodal region, it can be disrupted by the β-adrenergic receptor blocker and the number of depolarizations that reach the ventricles is reduced. The effect that a β-adrenergic receptor blocker has on a dog with atrial tachycardia varies and depends on the sympathetic tone and the number and sensitivity of β-adrenergic receptors present in that patient.4 In the dog of this report, esmolol (an ultra–short-acting class II antiarrhythmic drug) was initially administered IV repeatedly with no effect.

Because treatment with esmolol was unsuccessful, a class IV antiarrhythmic agent was administered. Class IV antiarrhythmic agents are calcium-channel blockers that interfere with the movement of calcium ions from the extracellular space through calcium channels into the intracellular space. Movement of calcium ions through calcium channels is necessary for depolarization in the sinus node and in parts of the AV node because sodium channels are not involved in depolarization in these areas. Thus, calcium-channel blockers slow conduction through the AV node and prolong the refractory period. In this manner, they slow the ventricular response to the atrial tachycardia.3,4 Diltiazem (a calcium-channel blocker) was administered IV to the dog of this report following the attempt to convert the arrhythmia with esmolol. Diltiazem was successful in terminating the atrial tachycardia. The AV block detected after administration of diltiazem was thought to be temporary because the drug may have been given too rapidly; reduction of AV nodal conduction and increase in refractoriness of the AV node have been reported to develop after IV infusion of calcium-channel blockers.5

Although diltiazem decreased the duration and frequency of the SVT, the dog developed profound AV block. The development of AV block prevented oral administration of diltiazem or other drugs that affect AV nodal conduction; therefore, another treatment plan was necessary. Implantation of a permanent pacemaker followed by antiarrhythmic therapy was 1 option, which the owner declined because of the dog’s chronic renal failure and expense of the procedure. An alternative antiarrhythmic agent that slowed atrial reentry or automaticity, without slowing AV nodal conduction, was therefore sought.

Although class I agents can theoretically prolong AV conduction time by blocking sodium channels in the internodal pathways and His-Purkinje fibers, these drugs have fewer effects on the AV node because conduction is more calcium-channel dependent.3 Class Ia drugs (eg, quinidine or procainamide) prolong repolarization in atrial, ventricular, and Purkinje cells, which may interrupt reentrant pathways. Those agents are generally effective against supraventricular tachyarrhythmias.3,4 Both quinidine and procainamide also inhibit muscarinic receptors, resulting in increased sympathetic tone; this vagolytic effect may increase AV node conduction and result in increased ventricular response to atrial tachycardia.3 Furthermore, both drugs inhibit α-adrenergic receptors and may cause hypotension after IV administration; this may be clinically important in a dog with renal impairment. Procainamide has less effect on sympathetic tone, blood pressure, and the QT interval, and its use may be preferable to that of quinidine.3

Class Ib drugs (eg, lidocaine and mexiletine) have previously been considered ineffective for cardioversion of supraventricular tachycardia; however, a recent study6 indicated that IV administration of lidocaine followed by oral administration of mexiletine was effective in 5 dogs. Class Ib drugs selectively prolong conduction velocity in ischemic or diseased myocardial tissue while having little effect on normal tissue; in the Purkinje fibers, repolarization is accelerated and action potential duration is shortened.3,4 Class Ib drugs have little effect on atrial myocardium and AV conduction. It has been suggested that lidocaine may successfully terminate arrhythmias in dogs with SVT because of accessory pathways or focal atrial tachycardia.6 However, when SVT and AV block are present concurrently, caution is advised6; in such instances, lidocaine has been reported6 to reduce the AV block, causing increased ventricular rate.

Class Ic drugs have acquired a poor reputation because of proarrhythmic effects associated with flecainide and propafenone identified in a cardiac arrhythmia suppression trial (CAST study) and a study3 known as the CASH (cardiac arrest study Hamburg) study, respectively, in humans. However, these effects have not been reported in dogs. Class Ic drugs are potent antiarrhythmic agents that are indicated for use in the treatment of supraventricular arrhythmias that are unresponsive to treatment with other drugs.3 Like other class I drugs, flecainide and propafenone inhibit fast sodium channels and thus depress the upstroke of the action potential and slow conduction velocity.3 Those drugs can also delay inactivation of slow sodium channels and inhibit repolarization, causing variable prolongation of action potentials.3

Because of the potent antiarrhythmic effects of class Ic drugs on supraventricular tachyarrhythmias, these drugs would have been the best alternative to oral administration of diltiazem in the dog of this report. Unfortunately, the dog was not returned to the hospital for reevaluation and was subsequently euthanized because of increased frequency of syncope and inappetence.

Atrial tachycardias are notoriously difficult to control and complicated even further when there is either functional or structural AV nodal conduction delay, which limits the effective use of various classes of drugs. The ECG traces obtained in the dog of this report illustrate the necessity of a logical, mechanistic approach to evaluation of SVTs and the selection of antiarrhythmic drugs for treatment of affected dogs.

References

  • 1

    Wright KN. Assessment and treatment of supraventricular tachycardias. In: Bonagura JD, ed. Kirk's current veterinary therapy XIII. Philadelphia: WB Saunders Co, 2000;726733.

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  • 2

    Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;449494.

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    • Export Citation
  • 3

    DiMarco JP, Gersh BJ, Opie LH. Antiarrhythmic drugs and strategies. In: Opie LH, Gersh BJ, eds. Drugs for the heart. 6th ed. Philadelphia: WB Saunders Co, 2005;218274.

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    • Export Citation
  • 4

    Kittleson MD. Drugs used in treatment of cardiac arrhythmias. In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;502524.

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    • Export Citation
  • 5

    Talajic M, Nattel S. Frequency-dependent effects of calcium antagonists on atrioventricular conduction and refractoriness: demonstration and characterization in anesthetized dogs. Circulation 1986;74:11561167.

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    • Export Citation
  • 6

    Johnson MS, Martin M, Smith P. Cardioversion of supraventricular tachycardia using lidocaine in five dogs. J Vet Intern Med 2006;20:272276.

    • Search Google Scholar
    • Export Citation
  • Figure 1—

    Lead II ECG trace obtained from a dog that was evaluated because of chronic renal failure during an episode of tachycardia. A supraventricular tachycardia is present with a heart rate of approximately 270 beats/min; p waves cannot be identified. Paper speed = 50 mm/s; 1 cm = 1 mV.

  • Figure 2—

    Lead II ECG trace obtained from the dog in Figure 1 following IV administration of diltiazem (0.1 mg/kg [0.05 mg/lb], IV). Notice negative pa waves (arrows) are visible during the SVT with block of the pa waves just before the rhythm is terminated. Once the SVT terminates, the sinus node begins to fire slowly again and then eventually recovers to a normal rate. This was likely attributable to overdrive suppression by the arrhythmia on the sinus node. A period of AV block is then followed by a ventricular escape complex, then recovery of the AV node and normal conduction, followed by another period of AV block. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • Figure 3—

    Lead II ECG trace obtained from the dog in Figure 1 after 3 days of treatment with diltiazem (3 mg/kg [1.36 mg/lb], PO, q 12 h). Paroxysmal nonsustained SVT is again identified (heart rate, 270 beats/min), followed by a long period (4.8 seconds) of AV block and then gradual recovery of the sinus node. The block is again followed by a ventricular escape beat and then normal sinus rhythm (heart rate, 120 beats/min). During this tachycardia, negative pa waves are again identified (arrows) with a long RP interval. Just prior to termination of the arrhythmia, there is 2:1 block; thus, this is most likely an atrial tachycardia. Paper speed = 25 mm/s; 1 cm = 1 mV.

  • 1

    Wright KN. Assessment and treatment of supraventricular tachycardias. In: Bonagura JD, ed. Kirk's current veterinary therapy XIII. Philadelphia: WB Saunders Co, 2000;726733.

    • Search Google Scholar
    • Export Citation
  • 2

    Kittleson MD. Diagnosis and treatment of arrhythmias (dysrhythmias). In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;449494.

    • Search Google Scholar
    • Export Citation
  • 3

    DiMarco JP, Gersh BJ, Opie LH. Antiarrhythmic drugs and strategies. In: Opie LH, Gersh BJ, eds. Drugs for the heart. 6th ed. Philadelphia: WB Saunders Co, 2005;218274.

    • Search Google Scholar
    • Export Citation
  • 4

    Kittleson MD. Drugs used in treatment of cardiac arrhythmias. In: Kittleson MD, Kienle RD, eds. Small animal cardiovascular medicine. St Louis: CV Mosby Co, 1998;502524.

    • Search Google Scholar
    • Export Citation
  • 5

    Talajic M, Nattel S. Frequency-dependent effects of calcium antagonists on atrioventricular conduction and refractoriness: demonstration and characterization in anesthetized dogs. Circulation 1986;74:11561167.

    • Search Google Scholar
    • Export Citation
  • 6

    Johnson MS, Martin M, Smith P. Cardioversion of supraventricular tachycardia using lidocaine in five dogs. J Vet Intern Med 2006;20:272276.

    • Search Google Scholar
    • Export Citation

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