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Camden M. Rouben Department of Clinical Sciences, College of Veterinary Medicine, University of Florida, Gainesville, FL 32608.

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Geri Lake-Bakaar PULSE Veterinary Cardiology, 701 Pine Ridge Rd #5, Golden, CO 80403.

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A 10-year-old 30.2-kg (66.4-lb) spayed female Doberman Pinscher was referred for evaluation of suspected congestive heart failure. The dog was reported to have a 2- to 3-day history of a progressive, nonproductive dry cough with no other pertinent medical history.

On examination, the dog was quiet, alert, and responsive. Rectal temperature was 38.1°C (100.7°F). Thoracic auscultation revealed a heart rate of 140 beats/min with a grade 2/6 left apical systolic murmur. The femoral pulses were fair in quality and synchronous with the heartbeat. Mucous membranes were pink and slightly tacky, with a capillary refill time of 1 to 2 seconds. The dog was tachypneic with a respiratory rate of 50 breaths/min and dyspnea. Lung auscultation revealed bronchovesicular sounds with mild diffuse inspiratory crackles bilaterally.

A blood sample was collected for serum biochemical analysis. All results were within reference ranges. Thoracic radiography revealed a severe interstitial, coalescing to alveolar lung pattern in the dorsal aspects of the right and left caudal lung lobes and in the perihilar region. The margins of the cardiac silhouette could not be clearly delineated, although cardiomegaly was suspected. Pulmonary vasculature was obscured by interstitial infiltrates. The remaining mediastinal and soft tissue structures appeared to be normal.

Because of the dog's clinical status, an abbreviated echocardiographic examination was performed. Findings were consistent with dilated cardiomyopathy (DCM); there was moderate eccentric hypertrophy of the left ventricle with decreased systolic function, severe left atrial enlargement, subjective eccentric hypertrophy of the right ventricle with poor systolic function, and subjective mild enlargement of the right atrium. The mitral valve apparatus and tricuspid valve appeared morphologically normal with mild amounts of centrally directed tricuspid valve regurgitation detected via color Doppler ultrasonography. The dog was hospitalized overnight and was administered furosemide (2 mg/kg [0.9 mg/lb], IV, q 4 h), oxygen supplementation, and dobutamine hydrochloride (5 μg/kg/min [2.27 μg/lb/min], continuous rate IV infusion for 8 hours).

Twenty-four hours after the initial evaluation, results of repeated serum biochemical analysis were all within reference intervals, and repeated thoracic radiography revealed a dramatic decrease in the amount of pulmonary interstitial infiltrate, a more prominent and mildly enlarged cardiac silhouette, and persistent infiltrate in the right and left caudal lung lobes as well as mild persistent venous distension of the cranial lobar vein. Doppler ultrasonographic assessment of systolic blood pressure (right forelimb; 4-cm cuff) was 108 mm Hg.

A repeated echocardiographic examination revealed little change from the previous day, and findings remained consistent with the previous diagnosis of severe DCM. Electrocardiography was performed (Figure 1).

Figure 1—
Figure 1—

Initial 6-lead ECG recording obtained from a Doberman Pinscher that was evaluated for suspected congestive heart failure. A normal sinus rhythm intermixed with periods of ventricular bigeminy with ventricular premature complexes of right bundle branch morphology is evident. Notice the notched P waves of lead II, III, and aVF, which are consistent with left atrium dilation. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 251, 3; 10.2460/javma.251.3.285

ECG Interpretation

With the dog in right lateral recumbency, a 6-lead ECG examination (Figure 1) was performed. The ECG revealed a sinus rhythm (heart rate ranged from 100 to 150 beats/min) intermixed with periods of ventricular bigeminy with premature ventricular complexes (PVCs) of right bundle branch morphology (left ventricular origin). The PVCs were also of varied morphology (Figure 2). As the ECG examination continued, a couplet (Figure 3) at a rate of 300 beats/min with R-on-T morphology was identified.

Figure 2—
Figure 2—

Lead II ECG trace obtained from the dog in Figure 1 at the same time as the initial ECG examination. Notice the varied morphology of the premature ventricular complexes (A and B). There are continuous J waves following each sinus QRS complex (arrow) consistent with delayed activation of the right ventricle. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 251, 3; 10.2460/javma.251.3.285

Figure 3—
Figure 3—

A continuation of the initial 6-lead ECG recording obtained from the dog in Figure 1. Notice the couplet (C) with R-on-T morphology. Paper speed = 50 mm/s; 1 cm = 1 mV.

Citation: Journal of the American Veterinary Medical Association 251, 3; 10.2460/javma.251.3.285

In all tracings, the sinus P waves were consistently notched, a feature that is associated with left atrial enlargement or slowed conduction. The sinus P waves had prolonged duration (0.05 seconds; reference range,1 0.037 to 0.043 seconds) and elevated amplitude (0.4 mV; reference range,1 0.139 to 0.283 mV). The morphology, duration, and amplitude of the QRS complexes were evaluated. There was a deep Q wave present, which is considered a physiologic finding in deep-chested dogs.2 The sinus R waves had normal amplitude (1.5 mV; reference range,1 1.10 to 2.22 mV); the sinus QRS complexes were of normal duration (duration, 0.02 seconds; reference range,1 0.043 to 0.54 seconds) and were followed by J waves. The calculated mean electrical axis was > 50°. The plotted measurement of the vectors revealed an initial depolarization cranially and to the right, with a terminal depolarization caudally and to the left.

Discussion

The term ventricular bigeminy refers to the coupling of PVCs with sinus beats. A PVC is an example of an ectopic rhythm, originating from an area distal to the atrioventricular nodal (junctional) tissue. A PVC is characterized by the premature occurrence of 1 or more QRS complexes that are abnormal in morphology and have a duration that usually exceeds 20 milliseconds (ie, the complexes are described as wide and bizarre). The slow myocyte-to-myocyte transmission gives rise to the QRS complexes' wide morphology, and their shape usually reflects the site of origin. For example, left ventricle–originated beats arrive last at the right ventricle, thereby giving the QRS complexes a right bundle branch black morphology because of delayed right ventricular activation. The converse usually applies to right ventricle–originated beats; right ventricle–originated beats arrive last at the left ventricle, thereby giving the QRS complexes a left bundle branch black morphology because of delayed left ventricular activation. The T waves of these complexes are large and usually of opposite polarity to that of the QRS complexes. With these large T waves, large J waves are consistently present. Those PVCs that have different contours and variable coupling intervals are often referred to as multiform (or multifocal).2

For the dog of the present report, the ventricular bigeminy had 2 degrees of fixed coupling. Specifically, when the Q-T interval was shorter, the QRS complex amplitude was greater (Figures 1 and 2). Therefore, there was fixed coupling but it varied according to the reentrant path, emphasizing that reentrant or triggered activity without true fixed coupling can occur.

A notched P wave (bifid or biphasic) has been associated with left atrial enlargement or dilation and occurs as a result of asynchronous depolarization of the atria. A notched P wave is detected when a dilated left atrium depolarizes fractionally later than does the right atrium.3

There are several common ECG findings in dogs with DCM that were not identified in the dog of the present report. Among the ECG findings for this case, there was no R wave of increased amplitude in lead II, which would have been suggestive of left ventricular enlargement. The other notable finding that was not detected was a slow or so-called sloppy, sometimes notched, descending limb of the R wave in the lead II tracing.4

AJ wave (or Osborn wave) is an ECG finding at the R-ST junction (J-point). This wave can be partially or completely buried in the QRS complex and is detected in 2% to 5% of humans. Although there is controversy regarding the terminology and pathogenesis of J waves in human and veterinary medicine, these waves are believed to represent waves of early repolarization.5,6 Several conditions are associated with the presence of J waves including hypothermia, hypercalcemia, brain injury, Brugada syndrome, sepsis, acute myocardial ischemia, and left ventricular hypertrophy. In a study6 evaluating J waves in geriatric dogs, J waves constituted a normal finding in approximately 30% to 40% of 34 study dogs. In 4 healthy dogs in that study,6 the mean ± SD J-wave amplitude was 0.19 ± 0.017 mV and J-wave duration was 28 ± 2.54 milliseconds.

Retrograde transmission to the atria from a PVC can occur, although evidence of this (a retrograde P wave) on ECG tracings is often obscured by the wide QRS complex and T wave. More commonly, the atria and sinus node do not prematurely discharge owing to the collision of impulses that occurs at the atrioventricular node. The collision occurs between an anterograde impulse from the sinus node and a retrograde impulse from the PVC, and can result in a noncompensatory pause following a PVC (Figure 2). The PVC may not generate any pause and therefore may be interpolated. Whether a compensatory or noncompensatory pause occurs is merely a function of how the atrioventricular junction conducts and the timing of the events taking place.7

For the dog of the present report, the second R wave in the single couplet was just after (and before the completion of) the preceding T wave. This is called the R-on-T phenomenon and indicates that the depolarization of the ventricle is coincident with the end of the previous repolarization. The ventricle is considered vulnerable to fibrillation, flutter, or tachycardia when this occurs, especially in a patient with an ischemic, fibrotic, or metabolically deprived myocardium.

It is interesting to note that the dog of the present report, despite its underlying disease, had no evident gallop sounds (specifically an S3) on cardiac auscultation. An S3 gallop is a low-frequency diastolic sound that occurs when the stiffness of the ventricle terminates filling. An S3 gallop can be ausculted in animals with DCM, congestive heart failure, and advanced valvular disease.8

In Doberman Pinschers with DCM, ventricular arrhythmias are common findings on 24-hour ECG (Holter) recordings. Dilated cardiomyopathy is characterized as an adult-onset disease of the myocardium, which is associated with ventricular chamber dilation and impaired systolic function.9 In dogs, it primarily affects large and giant breeds, and the Doberman Pinscher is one of the breeds most frequently affected.10 The frequency of development of DCM among Doberman Pinschers in North America is estimated at 41% for males and 31% for females.11 The mean age of onset of DCM in Doberman Pinschers is 7.3 years in males and 8.6 years in females. Although dogs of other breeds that have occult disease can have an extended survival time of up to 4 years, overt DCM in Doberman Pinschers is rapidly progressive.12

Treatment of DCM in dogs is focused toward modulating preload, afterload, contractility, and ventricular arrhythmia through medicinal intervention. Treatment involves administration of angiotensin-converting enzyme inhibitors, positive inotropes, diuretics, vasodilators, and antiarrhythmic agents, if necessary. There is also evidence that screening of individuals for preclinical DCM enables early pimobendan treatment of Doberman Pinschers that have systolic dysfunction, which can increase the time to development of congestive heart failure.13

Whether administration of an antiarrhythmic drug is appropriate should be based on various considerations, such as the patient's degree of hemodynamic or functional impairment, history of clinical signs (eg, syncope or episodic weakness), other concurrent conditions, potential for adverse drug interactions with currently administered medications, assurance that the drug can be administered correctly, and frequency or complexity of the arrhythmia. To the authors' knowledge, there are no published data to confirm that the use of antiarrhythmic drugs leads to increased survival times in dogs with DCM.14

The dog of the present report was discharged from the hospital 13 hours after the referral evaluation. While the dog was receiving oxygen supplementation, its respiratory rate decreased after initiation of diuretic treatment and was normal (28 to 32 breaths/min without oxygen supplementation) on reevaluation the following morning (approx 8 hours after the initial evaluation). The owner was instructed to administer furosemide (2 mg/kg) orally 3 times daily for 4 days followed by twice-daily dosing if the dog's resting respiratory rate remained normal, pimobendan (0.25 mg/kg) orally 2 times daily, and mexiletine hydrochloride (5 mg/kg) orally 3 times daily. One week after the initial evaluation, a recheck examination revealed that the dog had been doing well at home. Its respiratory rate and effort had remained normal (approx 20 breaths/min at rest), so the owner had lowered the furosemide dosing frequency to twice a day. In addition, the owner had elected to discontinue administration of mexiletine because he perceived that the dog had a decreased appetite when taking the medication. A serum biochemical analysis performed at the time of recheck examination revealed moderate hypokalemia (2.6 mmol/L; reference range, 3.5 to 5.8 mmol/L); therefore, spironolactone (37.5 mg [17.05 mg/lb], PO, q 12 h) was added to the treatment regimen. Financial limitations of the client did not permit further evaluation of the dog.

Acknowledgments

The authors thank Mallory Leake for technical assistance.

References

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