A7-month-old 10-kg (22-lb) sexually intact male Boston Terrier was referred to the North Carolina State University College of Veterinary Medicine for evaluation of a systolic murmur that had been present since birth. The dog had no clinical signs until 4 days prior to referral, when the owner noticed abdominal distention and lethargy. The referring veterinarian had prescribed furosemide (2.5 mg/kg [1.2 mg/lb], PO, q 24 h) and enalapril (0.5 mg/kg [0.23 mg/lb], PO, q 24 h) for this dog; there was a history of multiple littermate deaths attributed to presumed cardiac causes.
At the initial evaluation at the hospital, the dog was quiet but alert. The respiratory rate was 50 breaths/ min, and rectal temperature was 34.4°C (94°F); mucous membranes were pale, and thus, assessment of capillary refill time was difficult. The heart rate was 220 beats/ min, and the rhythm sounded regular. Femoral pulses were regular and symmetrical, but weak. A grade 5/6 ejection-quality murmur was associated with the region of the left heart base; a loud systolic murmur was also heard over the right hemithorax.
Initial diagnostic evaluations included Doppler systemic blood pressure measurement, a CBC, serum biochemical analyses, echocardiography, and thoracic radiography. Abnormalities detected included azotemia (BUN concentration, 165 mg/dL [reference range, 8 to 27 mg/dL]; serum creatinine concentration, 2.2 mg/dL [reference range, 0.5 to 1.6 mg/dL]), hyperphosphatemia (12.6 mg/dL; reference range, 2.0 to 6.7 mg/dL), hyponatremia (123 mmol/L; reference range, 147 to 154 mmol/L), hyperkalemia (5.5 mmol/L; reference range, 3.9 to 5.2 mmol/L), and arterial hypotension (systolic blood pressure, 60 mm Hg [reference range, 90 to 140 mm Hg]). Thoracic radiography revealed marked cardiomegaly with minimal pleural and abdominal effusions. Echocardiography revealed a large right atrium secondary to a complex congenital heart defect consisting of an infundibular fibrous ridge in the right ventricle that was causing marked subvalvular pulmonic stenosis and tricuspid valve dysplasia with severe resultant tricuspid valve insufficiency. Electrocardiography was performed.
ECG Interpretation
A 6-lead ECG revealed rapid supraventricular tachycardia with a ventricular rate of approximately 210 depolarizations/min (Figure 1). Atrial flutter was suspected on the basis of the regularity of the rhythm and apparent flutter (F) waves in lead I. A clinical diagnosis of heart failure (cardiogenic shock) secondary to complex right-sided congenital heart disease and complicated by atrial flutter with a rapid ventricular response rate was made.
Six-lead ECG tracings obtained from a 7-month-old Boston Terrier that was evaluated because of a systolic murmur that had been present since birth and a 4-day history of abdominal distention and lethargy. The ventricular rate is 215 depolarizations/min. The QRS complex duration is normal, and the rhythm is regular with no consistently identifiable P wave for each QRS complex. These findings are consistent with a supraventricular tachycardia, and atrial flutter was suspected on the basis of saw-toothed baseline flutter (F) waves that were consistently identifiable in the lead I tracing. The F waves are difficult to identify in the other lead tracings. The conduction ratio appears to be 3:1 (ie, 3 F waves for each QRS complex), and the atrial rate is approximately 645 depolarizations/min. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 231, 2; 10.2460/javma.231.2.209
In light of the recent and sudden onset of clinical signs, it seemed possible that the arrhythmia was playing an important role in the pathogenesis of the dog's heart failure. The dog was admitted to the intensive care unit with a treatment plan of arrhythmia management and, if possible, cardiac catheterization and pulmonic balloon valvuloplasty. One dose of diltiazem (0.05 mg/kg [0.023 mg/lb]) was administered IV, followed 5 hours later by another dose of diltiazem (0.5 mg/kg) that was administered orally. Seven hours after the oral administration of diltiazem, a continuous rate infusion of diltiazem was administered (2 μg/kg/min [0.91 μg/lb/min] over a 4-hour period) in an attempt to pharmacologically manage the arrhythmia and improve cardiac output and blood pressure prior to anesthesia. The dog's ventricular response slowed to 115 beats/min, but the conversion to sinus rhythm was not achieved. Electrical cardioversion was attempted in an effort to restore sinus rhythm prior to cardiac catheterization.
Following routine induction of anesthesia, the dog was placed in sternal recumbency and the apex beat was located via palpation. The defibrillator output was synchronized to the dog's R wave (Figure 2). A monophasic 50-J shock (5 J/kg [2.27 J/lb]) was delivered transthoracically at the level of the apex beat via pediatric defibrillator paddles (Figure 3). Cardioversion was successful, and the dog remained in sinus rhythm following the procedure. The attempted valvuloplasty had no measurable effect on the pressure gradient across the right ventricular outflow tract; despite this failure, the dog's postoperative clinical improvement was immediate and dramatic. Systolic blood pressure increased to 135 mm Hg, and azotemia (BUN concentration, 27 mg/dL; creatinine concentration, 0.5 mg/dL) resolved; overall, the dog's clinical status improved considerably. At the time of discharge from the hospital (the day after the procedure), the dog had a sinus rhythm. At home, the dog's condition remained stable for 1 month following the procedure. Follow-up ECGs could not be obtained, and the dog was euthanized by the referring veterinarian because of clinical deterioration despite medical management of heart failure.
Lead II ECG obtained from the dog in Figure 1 after induction of anesthesia. The dog was administered diltiazem at 2 μg/kg/ min (0.91 μg/lb/min) for 4 hours prior to and during this procedure. The rhythm appears regular with an atrial-to-ventricular conduction ratio of 6:1; the atrial rate is 720 depolarizations/min, and the ventricular rate is 120 depolarizations/min. The normal isoelectric baseline and P waves are replaced by uniform F waves. The inverted triangles superimposed on the QRS complexes confirm the cardioverter's synchronization with the QRS complex and its ability to appropriately discharge the electrical impulse during ventricular depolarization, thereby minimizing the risk of inducing ventricular fibrillation. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 231, 2; 10.2460/javma.231.2.209
Lead II ECG obtained from the dog in Figure 1 before and immediately after administration of a monophasic direct current electrical impulse (50 J). The inverted triangles mark each QRS complex, indicating that the machine appropriately identified the R wave and would deliver the cardioverting electrical shock during ventricular depolarization. The shock was applied during the time period denoted by the vertical dotted lines and resulted in an immediate and stable return to normal sinus rhythm. Following the shock, noble P waves (0.5 mV) in sinus rhythm are thought to indicate right atrial enlargement (P pulmonale). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 231, 2; 10.2460/javma.231.2.209
Discussion
Atrial flutter is a relatively uncommon cause of supraventricular tachyarrhythmia in dogs. The rhythm is a result of a macroreentrant loop (a single large circuit) that repetitively depolarizes the atria, traveling around either anatomic or functional boundaries.1,2 Reentrant loops are promoted by dispersion of refractoriness between myocytes, a condition that can occur with stretch, fibrosis, scarring from previous surgeries, or other anatomic or functional barriers to conduction.2 In instances of atrial flutter, anatomic boundaries are thought to include the tricuspid valve, cristae terminalis, and caudal vena cava.1 Atrial flutter is characterized by replacement of P waves that originate from the sinus node, with distinct F waves that are identical to each other with respect to complex morphology, cycle length, and polarity.1 There is no identifiable isoelectric shelf between each F wave, indicating continual reentrant electrical activity in the atria.2 The atrial rate generally varies from 300 to 600 depolarizations/min (375 to 750 depolarizations/min in the dog of this report). Conduction of these reentrant waves of atrial depolarization to the ventricles depends on the relative refractoriness of the atrioventricular (AV) node.1
To treat sustained atrial flutter, conversion to sinus rhythm or control of the ventricular response rate by slowing conduction through the AV node (if cardio-version is not possible) is attempted. Conduction through the AV node can be slowed effectively by the use of calcium channel blockers, although administration of β-adrenergic receptor blockers or digoxin might be considered under some circumstances. Conversion to sinus rhythm can be achieved via administration of anti-arrhythmic agents, direct current electrical cardio-version, rapid atrial pacing, or catheter ablation.2 In humans, pharmacologic interventions that are reported to convert atrial flutter to sinus rhythm include class III antiarrhythmics (eg, amiodarone, sotalol, and ibutilide), class Ia or Ic antiarrhythmics (eg, propafenone and flecainide), and calcium channel blockers.1,2
Direct current cardioversion uses electricity to depolarize all vulnerable cardiac myocytes simultaneously. This strategy is most successful with reentrant arrhythmias, including atrial flutter, atrial fibrillation, AV nodal reentrant tachycardia, ventricular flutter, ventricular fibrillation, and tachycardia associated with Wolf-Parkinson-White syndrome.2 The electrical current disrupts the reentrant loop and may prolong the refractory period.2 The result, if successful, is the reestablishment of electrical homogeneity. It is essential to emphasize that the application of transthoracic electrical current must be synchronized with the QRS complex (except in animals with ventricular fibrillation) to avoid the possibility of stimulating the myocardium during the ST segment or T wave, which can promote ventricular fibrillation and flutter.2 The most effective dose of electrical energy (measured in joules) for this purpose is not well characterized. Animals requiring this treatment must be completely anesthetized and intubated prior to receiving a transthoracic electrical shock.
Potential complications of electrical cardioversion include arrhythmogenesis, myocardial injury, dermal injury, and transient mechanical myocardial dysfunction (stunning). These complications are generally dose dependent, and more complications develop with repeated or high-dose electrical shock.3 In humans, embolic events are among the most commonly reported complications following cardioversion of atrial flutter.4 This is presumably a result of expulsion and subsequent embolization of thrombi that have formed within the atria or as a result of atrial stunning (transient mechanical impairment of the atria and subsequent stasis of atrial blood) following conversion to sinus rhythm.5 Complications involving embolic events following cardioversion of atrial flutter have not been reported in dogs, to the authors' knowledge. Arrhythmogenesis can result from inadequate synchronization of the electrical stimulus and the QRS complex, whereby the stimulus occurs during the ST segment or T wave of the ECG.2 Results of studies3,6,7 in humans suggest that biphasic electrical shocks accomplish cardioversion more effectively than monophasic shocks and do so at a lower electrical energy level. Low electrical doses decrease the incidence of postshock dermal injury and also, presumably, decrease the incidence of myocardial injury and stunning.3,6
In the dog of this report, deterioration of the sinus rhythm to atrial flutter may well have been responsible for at least part of the acute clinical decompensation that became apparent 4 days prior to evaluation. Impaired cardiac output associated with atrial flutter may reflect a lack of diastolic filling time, as well as the loss of appropriately timed atrial contractions. If allowed to continue at rapid ventricular response rates, atrial flutter can also cause pacing-induced cardiomyopathy.8,9 In the dog of this report, successful cardioversion was associated with dramatic and sustained clinical improvement.
References
- 1↑
Moïse NS. Diagnosis and management of canine arrhythmias. In:Fox PR, Sisson D, Moïse NS, ed.Textbook of canine and feline cardiology. 2nd ed. Philadelphia: WB Saunders Co, 1999;331–385.
- 2↑
Olgin JE, Zipes DP. Specific arrhythmias: diagnosis and treatment. In:Zipes DP, Libby P, Bonow RO, et al, eds. Braunwald's heart disease: a textbook of cardiovascular medicine. 7th ed. Philadelphia: Saunders, 2005;803–863.
- 3↑
Page RL, Kerber RE & Russell JK, et al. Biphasic versus monophasic shock waveform for conversion of atrial fibrillation. The results of an international randomized double-blind multicenter trial. J Am Coll Cardiol 2002;39:1956–1963.
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Ghali WA, Wasil BI & Brant R, et al. Atrial flutter and the risk of thromboembolism: a systematic review and meta-analysis. Am J Med 2005;118:101–107.
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Deakin CD, Ambler JJS. Post-shock myocardial stunning: a prospective randomized double-blind comparison of monophasic and biphasic waveforms. Resuscitation 2006;68:329–333.
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Mittal S, Ayati S & Stein KM, et al. Transthoracic cardioversion of atrial fibrillation. Comparison of rectilinear biphasic versus damped sine wave monophasic shocks. Circulation 2000;101:1282–1287.
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Luchsinger JA, Steinberg JS. Resolution of cardiomyopathy after ablation of atrial flutter. J Am Coll Cardiol 1998;32:205–210.
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Umana E, Solares CA, Alpert MA. Tachycardia-induced cardiomyopathy. Am J Med 2003;114:51–55.
