ECG of the Month

Vinícius B. Costa Silva 1Department of Veterinary Medicine, Federal University of Paraná, Curitiba, PR, 80035-050, Brazil.

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Marcela Wolf 1Department of Veterinary Medicine, Federal University of Paraná, Curitiba, PR, 80035-050, Brazil.

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Marlos G. Sousa 1Department of Veterinary Medicine, Federal University of Paraná, Curitiba, PR, 80035-050, Brazil.
1Department of Veterinary Medicine, Federal University of Paraná, Curitiba, PR, 80035-050, Brazil.

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A 9-year-old 16.2-kg (35.6-lb) neutered female Chow Chow was referred to a veterinary teaching hospital for investigation of inappetence, progressive weight loss, and diarrhea during the preceding month as well as vomiting for 7 days. The dog had been treated with antimicrobials by the referring veterinarian, but no change in clinical status was reported.

On physical examination, the dog was alert and responsive, had a body condition score of 3/9 and rectal temperature of 38.9°C (102.0°F), and was minimally dehydrated (approx 6%). However, the dog's mucous membranes were still pink and moist, and the capillary refill time was < 1 second. There was abdominal distension, and the result of a fluid wave test was positive. Thoracic auscultation revealed increased bronchovesicular sounds with a respiratory rate of 32 breaths/min. No cardiac murmur was heard, but a regular rapid heart rate (240 beats/min) was documented. Femoral pulses were weak but regular.

Blood samples were submitted for hematologic and plasma biochemical analysis. Mild neutrophilic leukocytosis and normocytic normochromic anemia were detected. Plasma biochemical analysis revealed high activities of alanine aminotransferase (283 U/L; reference interval, 21 to 102 U/L) and alkaline phosphatase (184 U/L; reference interval, 20 to 156 U/L), hypoproteinemia (4 g/dL; reference interval, 5.4 to 7.1 g/dL), hypoalbuminemia (1.6 g/dL; reference interval, 2.6 to 3.3 g/dL), hypocalcemia (total calcium concentration, 7.6 mg/dL; reference interval, 9 to 11.3 mg/dL), and hypomagnesemia (1.4 mg/dL; reference interval, 1.8 to 11.3 mg/dL). The result of a pancreatic lipase immunoreactivity test was positive. Abdominal ultrasonography revealed diffusely reduced liver echogenicity with mildly congested vessels. There was evidence of diffuse peritonitis, and the echogenicity of the mesentery around the pancreas was increased. These findings confirmed the initial suspicion of pancreatitis.

The dog was hospitalized for treatment. In brief, isotonic fluids were administered IV (maintenance rate), and ondansetron hydrochloride (0.22 mg/kg [0.1 mg/lb], IV, q 8 h), metronidazole (15 mg/kg [6.82 mg/lb], IV, q 12 h), amoxicillin–clavulanic acid (20 mg/kg [9.1 mg/lb], SC, q 12 h), and tramadol hydrochloride (5 mg/kg [2.3 mg/lb], SC, q 8 h) were prescribed. That same day, the dog was referred to the cardiology section for further investigation of the tachyarrhythmia auscultated during physical examination. Electrocardiography and echocardiography were performed. The most remarkable findings in the echocardiogram were thickened mitral and tricuspid valve leaflets, which caused minimal insufficiency. The sizes of the cardiac chambers were considered normal.

ECG interpretation

On a 10-lead ECG recording, sustained supraventricular tachycardia was evident and low-amplitude R waves (0.45 mV; reference interval, 0.5 to 3.0 mV) were detectable in the lead II tracing (Figure 1). The dog's heart rate was ≤ 350 beats/min. The precise mechanism that generated the supraventricular tachycardia could not be determined because P waves were not visible. The cardiac axis was in the range of +60° to +90°.

Figure 1—
Figure 1—

Lead I, II, and III tracings of an initial 10-lead ECG recording obtained from a Chow Chow that was referred for investigation of inappetence, progressive weight loss, and diarrhea during the preceding month as well as vomiting for 7 days. On the basis of clinical findings, a diagnosis of pancreatitis was made. At the time of this ECG examination, the dog had sustained supraventricular tachycardia, with a heart rate of ≤ 350 beats/min. Notice the low-amplitude R waves in lead II. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 254, 12; 10.2460/javma.254.12.1397

To differentiate atrial and sinus tachycardia, the carotid sinus was vigorously massaged to produce a parasympathetic stimulus. This procedure resulted in prompt restoration of sinus rhythm (90 beats/min) with only 2 supraventricular premature beats and a single ectopic depolarization recorded (Figure 2). On the basis of the ectopic beat's morphology in the lead II tracing, that ectopic beat originated within the left ventricular myocardium. Unfortunately, the sinus rhythm was short-lived, and the supraventricular tachycardia recommenced as soon as the parasympathetic stimulus was discontinued.

Figure 2—
Figure 2—

Lead I, II, and III tracings of a 10-lead ECG recording obtained from the dog in Figure 1 during carotid sinus massage. The massage procedure restored the sinus rhythm, although 2 supraventricular premature beats (asterisk) and a single premature depolarization (hash) are evident in the lead II tracing. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 254, 12; 10.2460/javma.254.12.1397

Antiarrhythmic treatment with diltiazem (0.5 mg/kg [0.23 mg/lb], PO, q 12 h) was recommended with the expectation of normalizing the dog's cardiac rhythm. Four days later, the ECG examination was repeated. At this time, the cardiac rhythm was regular with visible P waves followed by narrow QRS complexes (Figure 3). The dog's heart rate had decreased to approximately 130 beats/min. The ECG findings were compatible with sinus rhythm. Moreover, the dog's clinical condition was also dramatically improved, compared with its status at the initial evaluation.

Figure 3—
Figure 3—

Lead I, II, and III tracings of a 10-lead ECG recording obtained from the dog in Figure 1 four days after initiation of treatment with diltiazem. At this time, sinus rhythm has resumed, and the dog's heart rate is 130 beats/min. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 254, 12; 10.2460/javma.254.12.1397

Discussion

Supraventricular tachyarrhythmias are fast cardiac rhythms either originating above the bifurcation of the atrioventricular node or produced by electrical circuits close to this location. Because electrical impulses originating in the atria are usually conducted normally to the ventricles through the atrioventricular node, QRS complexes are likely to have a normal narrow configuration during episodes of supraventricular tachycardia.1 For atrial tachycardia to develop, a series of atrial extra-systoles must occur more rapidly than do the normal sinus beats. Atrial tachycardia can be either continuous (sustained) or intermittent (paroxysmal).2

In the dog of the present report, 10-lead ECG was performed to identify the supraventricular tachycardia. In people, 12-lead ECG is normally required to differentiate supraventricular tachycardias. Several ECG features including P-wave localization in relation to the QRS complexes during the tachycardia episode, P-wave axis on both the frontal and horizontal planes, duration of the PR interval, and evidence of QRS alternans and abnormal repolarizations are good discriminators for the various types of supraventricular tachycardia.3 However, in a study4 that evaluated a 3-lead ECG device, high sensitivity and specificity for the detection of 1 type of supraventricular tachyarrhythmia—atrial fibrillation—were identified.

In a retrospective study5 intended to evaluate the clinical and prognostic factors among 65 dogs with supraventricular tachycardia, 40 (62 %) dogs were male, with a high proportion of Labrador Retrievers and Boxers. Among the 65 dogs, mean age was 9 years and mean heart rate was 270 beats/min. The most frequent clinical sign was syncope (20/65 [31%]), but 15 of 65 (23%) dogs had no clinical signs. The dog of the present report had signs attributable only to pancreatitis.

In dogs, supraventricular tachycardias are usually a consequence of complicated cardiac disease.6 However, for the dog of the present report, it was likely that tachycardia was the result of the pancreatic inflammatory process. For people with pancreatitis, several ECG abnormalities including atrial fibrillation, atrial flutter, supraventricular tachycardia, prolonged PR interval, QT-interval aberrations, and torsades de pointes have been described.7 The latter is a type of polymorphic ventricular tachycardia in humans, which is characterized by a gradual change in amplitude and twisting of the QRS complexes around an isoelectric line on an ECG tracing.8

On initial evaluation, the dog of the present report had hypocalcemia and hypomagnesemia. Electrolyte imbalances are common in dogs with pancreatitis and might interfere with cardiac physiologic functions; for example, hypocalcemia is known to have a detrimental effect on myocardial contractility and cardiac rhythm.7,9

Baroreceptors function as a measure of autonomic efferent activity, and the baroreceptor reflex may be activated by either mechanical stimulation of the carotid bodies or administration of drugs that alter arterial blood pressure, thereby changing heart rate.10 Hence, as in the case described in the present report, massaging the carotid sinus can cause resumption of sinus rhythm and reduced heart rate. The augmented parasympathetic tone should reduce both the abnormal automaticity and the velocity of electrical conduction, which eventually allows the sinus node to take control of cardiac pacing.11

Diltiazem is a calcium channel blocker used in people and dogs to treat supraventricular arrhythmias.12 It is known to depress atrioventricular conductibility and sinus node excitability, with the former being more effective in patients with high heart rates; it can also cause relaxation of vascular smooth muscle.13 In the dog of the present report, there was a notable heart rate reduction and restoration of sinus rhythm following administration of diltiazem twice daily at a low dose. The dog's clinical status improved dramatically following the start of treatment. Whether the normalization of heart rhythm was a consequence of diltiazem treatment or spontaneous remission could not be determined, but it was unlikely that treatment adversely affected systolic function.

Four days after treatment was initiated, the dog of the present report had signs of remarkable clinical improvement and was discharged from the hospital. Home treatment included administration of amoxicillin–clavulanic acid (20 mg/kg, PO, q 12 h) and diltiazem (0.5 mg/kg, PO, q 12 h). It was also recommended that the dog be fed a low-fat prescription diet. At a recheck examination 1 week later, the owner reported that the dog appeared clinically normal. Recheck ECG revealed only sinus tachycardia (169 beats/min).

References

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