A 13-year-old 7.4-kg (16.3-lb) spayed female Miniature Schnauzer underwent a routine recheck evaluation. The dog had had a transvenous permanent pacemaker implanted 3.5 years earlier because of sick sinus syndrome. Depletion of the generator battery necessitated a generator battery change 10 months prior to the recheck evaluation, which was performed with no complications. The pacemaker mode was programmed for ventricular demand rate-responsive pacing (VVIR) with a base rate of 40 beats/min and a maximum rate of 160 beats/min. Previous medical history included American College of Veterinary Internal Medicine classification1 stage B1 degenerative mitral and tricuspid valve disease, a gallbladder mucocele that was medically managed with ursodiol (11.4 mg/kg [5.2 mg/lb], PO, q 24 h), recurrent urinary tract infections, and a transient vestibular episode that occurred 6 months prior to the recheck evaluation.
On physical examination, the dog was quiet, alert, and responsive. Rectal temperature was 38.0°C (100.4°F). Mucous membranes were pink and moist, with a capillary refill time of < 2 seconds. An irregularly irregular rhythm was ausculted, with no detectable murmurs or abnormal heart sounds; the heart rate was 120 beats/min. Bronchovesicular sounds were considered normal, and respiratory rate was 24 breaths/min. Femoral arterial pulse quality was mildly hypokinetic but synchronous with the heartbeat. Signs of mild pain were elicited during palpation of the cranial portion of the abdomen, although no changes in the dog's appetite or bowel movements had been noted by the owner.
Abdominal ultrasonography revealed persistent biliary debris within the gallbladder, resolution of the gallbladder mucocele, a right nephrolith and mild pyelectasia, and changes consistent with historical or current focal pancreatitis. Echocardiography revealed stable mild degenerative mitral and tricuspid valve disease with normal cardiac chamber sizes and function (American College of Veterinary Internal Medicine classification stage B1). The pacemaker lead could be visualized within the right atrium and right ventricle without any visible thrombus formation; mild tricuspid valve regurgitation was detected. Results of pacemaker interrogation were consistent with appropriate pacemaker function, and no program settings were altered. Electrocardiography was performed to further evaluate the arrhythmia.
ECG Interpretation
A 6-lead ECG examination was performed (Figure 1). No distinct P waves could be seen in any of the lead tracings; instead, a sawtooth baseline was present with flutter waves occurring at a rate of approximately 500 depolarizations/min. Narrow QRS complexes were conducted with an irregularly irregular rhythm that was consistent with a supraventricular arrhythmia. The calculated mean ventricular rate was 125 beats/min. An ECG diagnosis was made of atrial flutter with a conduction ratio that varied from 2:1 to 6:1 (Figure 2) A lidocaine bolus (2 mg/kg [0.9 mg/lb]) was given IV, which successfully terminated the atrial flutter, resulting in a brief period of sinus arrest with appropriate ventricular pacing at 40 beats/min (Figure 3) The dog was discharged from the hospital; no further episodes of atrial flutter were noted at any subsequent recheck evaluations. The dog was lost to follow-up 2 years later.
Six-lead ECG tracing obtained from a 13-year-old Miniature Schnauzer during a routine recheck evaluation. The dog had had a transvenous permanent pacemaker implanted 3.5 years earlier because of sick sinus syndrome. During the recheck evaluation, an irregularly irregular heart rhythm had been detected. On the ECG tracings, notice that a sawtooth baseline is present with tall and narrow QRS complexes consistent with atrial flutter. Every fourth flutter wave is conducted across the atrioventricular node to cause ventricular depolarization. Paper speed = 50 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 7; 10.2460/javma.255.7.793
Another portion of the lead II ECG tracing from the same dog as in Figure 1. Atrial flutter with a conduction ratio of 2:1 to 6:1 is present. The calculated mean ventricular rate is 135 beats/min. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 7; 10.2460/javma.255.7.793
Another portion of the lead II ECG tracing from the same dog as in Figure 1. Atrial flutter is present with variable conduction across the atrioventricular node. After IV administration of a lidocaine bolus, the atrial flutter is terminated, resulting in a brief period of sinus arrest and a ventricular paced rhythm at 40 beats/min. Small ventricular pacing spikes (asterisks) preceding the last 2 QRS complexes are evident. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 255, 7; 10.2460/javma.255.7.793
Discussion
Atrial flutter is an uncommon supraventricular arrhythmia in dogs, which involves a macroreentrant circuit that creates a single large loop of electrical conduction within the atria that causes repetitive depolarizations around an anatomic or functional barrier.2 The most common anatomic barrier in humans involves the cavotricuspid isthmus, an area of the right atrium bounded by the caudal vena cava, Eustachian ridge, and tricuspid valve annulus; the cavotricuspid isthmus has also been implicated in atrial flutter in dogs.3 Characteristic ECG findings include sawtooth undulations (flutter waves) of the baseline in place of P waves; in dogs, this commonly results in an atrial rate of > 300 depolarizations/min. A variable ventricular rate is present depending on the degree of conduction block across the atrioventricular node.2
Two forms of atrial flutter involving the cavotricuspid isthmus have been identified. With typical atrial flutter, the activation wave front rotates counterclockwise around the tricuspid valve annulus, whereas the activation wave front rotates clockwise with reverse typical atrial flutter.4 Factors that predispose individuals to develop atrial flutter include enlarged atria and atrial stretch, which can result in changes in the effective refractory period and an increased heterogeneity of repolarization within the atrial tissue. Changes in autonomic tone can also increase the likelihood for initiation of arrhythmias because increased vagal tone causes unequal shortening of the action potential duration in atrial tissue, which results in increased heterogeneity of repolarization.2
In humans, the use of single-chamber pacemakers is associated with an increased risk of atrial arrhythmias, such as atrial fibrillation, compared with the use of dual-chamber pacemakers that maintain atrioventricular synchrony.5 Single-chamber pacemakers consist of 1 lead implanted in the right ventricle, whereas dual-chamber pacemakers have an additional lead implanted in the right atrium. The 2 leads allow sensing of native P waves to maximize synchronous contraction between the atria and ventricles. In contrast, single-chamber pacemakers pace the ventricle without atrial sensing and, therefore, without synchronous atrioventricular contraction. In humans, the difference in the risk of atrial fibrillation between the 2 pacemaker systems is thought to be secondary to electrical remodeling that occurs with loss of atrioventricular synchrony because the use of single-chamber pacemakers results in prolongation of the atrial effective refractory period, P-wave duration, and sinus node recovery time.6 Changes in these variables can subsequently increase the heterogeneity of repolarization and predispose pacemaker recipients to the development of atrial fibrillation. In a study7 involving 10 dogs, placement of a single-lead pacemaker that maximized atrioventricular synchrony significantly reduced left atrial size and left ventricular end-systolic dimension, increased cardiac output, and reduced plasma N-terminal proatrial natriuretic peptide concentration, compared with findings after placement of a single-lead pacemaker that did not attempt to conserve atrioventricular synchrony. It is possible that similar electrical remodeling could occur in dogs as a result of loss of atrioventricular synchrony, which may increase the risk of development of arrhythmias such as atrial fibrillation and atrial flutter; however, data to support this association are lacking.
Lidocaine is a class I antiarrhythmic agent, the administration of which has previously been shown to successfully convert vagally mediated atrial fibrillation in dogs.8,9 One potential mechanism involves the difference in sodium channel characteristics between atrial and ventricular myocardial tissues. Sodium channel blockers, such as lidocaine and ranolazine, are able to exploit this difference to cause selective sodium channel blockade in the atria, leading to decreased excitability and a prolonged postrepolarization refractory period, which ultimately favors suppression of atrial fibrillation and conversion to sinus rhythm.10 Although ranolazine's effects on the atrial myocardium are much more pronounced than those of lidocaine, lidocaine also has direct antagonistic effects on muscarinic receptors, and its success in conversion of vagally mediated atrial fibrillation may relate in part to its ability to decrease the effect of acetylcholine.11,12
The cause of atrial flutter in the dog of this report was unclear. Echocardiography revealed mild degenerative valve disease without any evidence of atrial enlargement. Although this dog had undergone implantation of a single-chamber pacemaker, it is unknown how much electric remodeling secondary to loss of atrioventricular synchrony contributed to increased heterogeneity of repolarization and the initiation of atrial flutter because the electrophysiologic effects of single-chamber pacing in dogs have not been extensively studied. The relatively low ventricular rate and conversion with lidocaine administration implicated increased vagal tone as a cause of atrial flutter. At the time of the recheck evaluation, the dog had signs of pain in the cranial aspect of the abdomen and abdominal ultrasonographic findings were consistent with possible pancreatitis; this could have played a role in the initiation of atrial flutter in this patient since gastrointestinal tract disease is known to cause increases in vagal tone. Although lidocaine has been associated with successful conversion of vagally mediated atrial fibrillation, it may also be effective in conversion of atrial flutter when increased vagal tone is suspected as a causative factor.
References
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