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Samuel J. Gabriel Filho Centro Avançado de Veterinária, Rua Nélio Guimarães 170, Ribeirão Preto, SP 14025-290, Brazil.

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César A. Ribeiro Emergěncia e Cuidados Intensivos, Endovet Centro Médico Veterinário, Rua João Ramalho 610, Ribeirão Preto, SP 14085-040, Brazil.

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A 5-year-old 39-kg (85.8-lb) sexually intact female Labrador Retriever was brought to the Veterinary Medical Center Soft Tissue Surgery Service for elective ovariohysterectomy. On initial evaluation, the dog was eupneic, bright, and alert. Cardiac auscultation revealed a right apical systolic heart murmur (grade 2/6); heart rate was 78 beats/min. The dog had no history of cough or collapse episodes. Results of a serum biochemical panel and CBC were unremarkable. The dog was anesthetized and underwent the planned procedure; recovery from anesthesia was uneventful. However, 4 hours later, the dog became prostrate. A physical examination revealed pale mucous membranes, increased capillary refill time, tachycardia, dyspnea, and weak femoral pulses. Results of a CBC performed at this time were indicative of moderate anemia. Abdominal ultrasonography revealed free fluid in the abdominal cavity. Echocardiography revealed the presence of mild tricuspid valve dysplasia, reduced cardiac function, and right ventricular enlargement. The dog underwent an exploratory laparotomy and concomitant whole blood transfusion; continuous ECG monitoring was performed during anesthesia (Figure 1).

Figure 1—
Figure 1—

Six-lead ECG tracings obtained from an anesthetized dog during exploratory laparotomy for the evaluation of free fluid in the abdominal cavity after an ovariohysterectomy. In these tracings, notice the atrioventricular dissociation due to ventricular tachycardia (heart rate, 210 beats/min) with a right bundle branch block pattern. There are 2 fusion beats that mark the conversion from focus 1 to focus 2. P waves are intermittent. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 241, 10; 10.2460/javma.241.10.1288

ECG Interpretation

The initial 6-lead ECG recording revealed tachycardia with wide QRS complexes (Figure 1). The QRS complex morphology alternated between right bundle branch block and left bundle branch block; heart rate was 210 beats/min. A vagal maneuver (gentle eye compression) was performed as the first attempt at parasympathetic stimulation but failed to reduce the heart rate or result in conversion to a sinus rhythm. Pharmacological cardioversion was performed initially via IV administration of lidocaine hydrochloride (2 mg/kg [0.91 mg/lb]), followed by diltiazem hydrochloride (0.25 mg/kg [0.11 mg/lb]); however, this technique also failed to achieve conversion to sinus rhythm. An attempt at rhythm conversion was made via administration of a constant-rate infusion of amiodarone hydrochloride (5 mg/kg/h [2.27 mg/lb/h], IV) during 1 hour. Following the infusion, dissociated P waves were observed in the late part of the ST segment (Figure 2), and the heart rate was 178 beats/min. At this time, the dog's condition appeared improved, and it was able to walk around the room and drink some water. The following day, the dog was discharged from the hospital; the owners were instructed to administer enalapril maleate (0.5 mg/kg [0.23 mg/lb], PO, q 12 h), furosemide (1.5 mg/kg [0.68 mg/lb], PO, q 12 h), digoxin (0.22 mg/m2, PO, q 12 h), and amiodarone (15 mg/kg [6.82 mg/lb], PO, q 12 h). The ECG performed before the dog was discharged from the hospital did not reveal any improvement. Three days later, the dog was brought to the clinic for the first follow-up examination. An ECG was performed and revealed a normal sinus rhythm; heart rate was 140 beats/min, and QRS complex width was 63 milliseconds (Figure 3). The diagnosis was multiform ventricular tachycardia.

Figure 2—
Figure 2—

Lead I, II, and aVF ECG tracings obtained from the dog in Figure 1 during constant rate infusion of amiodarone hydrochloride (5 mg/kg/h [2.27 mg/lb/h]). Notice the idioventricular accelerated rhythm (left bundle branch block pattern) with a heart rate of 178 beats/min or slow ventricular tachycardia, resulting in atrioventricular dissociation. P waves (arrows) are evident at beats 1, 4, and 6; between beats 7 and 8; and between beats 11 and 12. The R-wave variation is respiratory artifact. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 241, 10; 10.2460/javma.241.10.1288

Figure 3—
Figure 3—

Lead II ECG tracing obtained from the dog in Figure 1 after 3 days of oral treatment with amiodarone, digoxin, enalapril maleate, and furosemide. A sinus rhythm is present; heart rate is 140 beats/min, and QRS complex duration is 63 milliseconds. Paper speed = 25 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 241, 10; 10.2460/javma.241.10.1288

Discussion

Ventricular tachycardia can be caused by acute myocardial ischemia in humans with a structurally normal heart.1 In patients with chronic myocardial scarring, ventricular tachycardia is monomorphic, whereas in patients with acute myocardial ischemia, ventricular tachycardia is polymorphic and is reversible with coronary revascularization.1 In the dog of the present report, the hypotension caused by both the severe acute anemia and anesthesia predisposed the dog to develop a marked decrease in systemic blood pressure and coronary flow, which culminated in myocardial acute ischemia.

In general, within seconds after the onset of acute ischemia, there is rise in intracellular calcium and extracellular potassium concentrations.2 Continued influx of calcium into myocytes may generate after depolarizations, which are abnormal depolarizations of the cardiac myocytes that interrupt phase 2, phase 3, or phase 4 of the cardiac action potential in the electric conduction system of the heart and may lead to cardiac arrhythmias. An increase in extracellular potassium concentration results in shortening of the repolarization period of the myocytes, leading to slow conduction and ultimately to inexcitability. This response is more marked in the subepicardium than in the subendocardium and results in a prominent dispersion of repolarization across the myocardium during transmural ischemia. Human ventricular cardiac cells have long action potentials and thus long refractory periods, which can be considered as a safety mechanism by protecting the heart against excessively high rates. It has been known that the refractory period is not constant, but is dependent on the heart rate and also adapts gradually to an increase in heart rate. The difference in refractory period in adjacent areas could be responsible for the occurrence of arrhythmias. Spatial inhomogeneity of the repolarization phase of action potentials can be caused by different durations of the action potentials and also by some potentials appearing late because of slow conduction. Therefore, dispersion of refractoriness may be due to the presence of nonhomogeneous refractoriness, nonhomogeneous conduction, or both. The heterogeneity and increased dispersion of repolarization result in prolongation of QT dispersion in humans with ischemic heart disease.3 The QT dispersion is defined as the difference between the longest and shortest QT interval measured on 12-lead surface ECG tracings. It represents an index of electrical instability, which means the regional physiologic variation of the myocardium recovery of excitability. The QT dispersion interpretation is a feasible and noninvasive method to detect the heterogeneity of the ventricular repolarization in a myocardial ischemic environment.

Dispersion of conduction and refractoriness favor development of reentrant ventricular arrhythmias.4 The reentry mechanism is strongly associated with the development of cardiac arrhythmias.5,6 It has been reported that lidocaine and other class I antiarrhythmic drugs are rarely effective or even proarrhythmic in humans with polymorphic ventricular tachycardia and myocardial ischemia.7 Intravenous administration of amiodarone suppresses multiform and refractory ventricular tachycardia after myocardial ischemia.7–9 In the dog of the present report, treatment with lidocaine failed to achieve conversion to sinus rhythm. Amiodarone not only decreased the heart rate, but also failed to convert the dog to sinus rhythm. In humans with polymorphic ventricular tachycardia secondary to acute myocardial ischemia, revascularization therapy can be potentially curative, especially in those cases of refractory ventricular tachycardia or drug unresponsiveness.7 For the dog of this report, we hypothesized that the coronary spasms attributed to both moderate blood loss and anesthesia hypotension promoted acute myocardial ischemia. The acute myocardial ischemia caused drug-unresponsive polymorphic ventricular tachycardia. Rhythm conversion was achieved only after whole blood transfusion and fluid balance restoration, when the ischemia resolved and the dog recovered normal hemodynamic status and coronary blood flow.

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