Tachyarrhythmia in a St Bernard dog

Journal of Veterinary Cardiology, Vol. I , No. 2, December 1999

Tachyarrhythrnia in a St Bernard dog Ruth Willis BVM&S Cert VC MRCVS',

Dr. Paul R. Wotton BVSc DVC PhD MRCVS', Dr. Chris I+ 1, Little BVMS Cert SAC PhD MRCVS2

A young St Bernard dog was referred on three separate occasions for investigation of dyspnea and exercise intolerance. Electrocardiography was performed on each occasion and showed various forms of supraventricular tachycardia with aberrant conduction. Echocardiography showed a progressive decrease in systolic function and thoracic radiographs showed progressive cardiomegaly. The arrhythmia responded rapidly to treatment with propanolol.

I

Case History

A 7 month old, entire male Saint Bernard dog weighing 52kg was presented to the referring veterinary surgeon with sudden onset lethargy, anorexia, tachycardia and tachypnea which responded to treatment with furosemide 250mg i/v and enalapril 20mg PO. The dog's exercise tolerance had always been poor and a littermate had reportedly died of a congenital heart defect. The dog was referred to Glasgow Univer- sity Veterinary School the following day for further investigation.

On examination the dog was subdued, the heart rate was 120bpm, the rhythm was regular, femoral pulses were weak but there was no pulse deficit. The mucous membranes, capillary refill time, jugular veins, precordial impulse, rectal temperature and chest percussion were normal. There was mild bilateral otitis externa and bilateral epiphora due to entropion. Auscultation was difficult as the dog was panting but the heart rhythm was regular and no murmur was detected.

Hematology and plasma biochemistry were unremarkable.

Electrocardiography (Fig 1) lead I1 measurements were as follows (reference ranges for giant breeds in parathesis'):

Heart rate Predominant rhythm Ectopics P wave duration P wave amplitude PR interval QS duration QS voltage S-T segment

QT interval T waves Mean electrical axis

185bpm sinus none seen 0.06s 0.4mV 0.14s 0.08s -1.2mV, notched coving present

0.22s wide and tall -60°

(60-140bpm)

(<0.05s) (<0.4mV)

(<0.06s) (0.06-0.13s)

(elevation <0.15mV, de- pression <0.2mV) (0.15-0.25s)

(+40"- +loo")

These findings were suggestive of left atrial enlargement and a ventricular conduction disturbance possibly right bundle branch block with left anterior fascic- ular block2. A thoracic radiograph (Fig 2) showed that the heart was enlarged with a vertebral heart score of 11.5. The radiograph was blurred due to movement artefact but the pulmonary veins were more than 3/4 the width of the cranial third of the fourth rib suggesting that they were enlarged and the cranial lung lobe arteries were also prominent. The great vessels and pleural space appeared normal. The xiphoid cartilage was displaced slightly dorsally into the chest. Echocar- diography showed left atrial enlargement (4.9 cm from a right parasternal long axis view) and the fractional shortening was 25%. Spectral Doppler echocardiography showed insignificant mitral and tricuspid incompetence.

These findings were suggestive of a sinus tachycardia associated with a ventricular conduction disturbance of unknown etiology and the dog was pre- scribed digoxin 0.25mg PO q12h, furosemide 80mg PO q12h and enalapril20mg PO q24h.

One week later the dog was presented for re-examination. His exercise tolerance and appetite had im-

Small Animal Clinic, University of Glasgow Veterinary School, Bearsden Road, Bearsden, Glasgow G61 1QH. Tel: 0141 330 5700. E-mail: [email protected]. *Wits' End, 63 St Leonards Road, Deal, Kent, CT14 9AY.

27

Ruth Willis, Paul R. Wotton, Chris J. L. Little

proved, the heart rate was 120bpm, there was no pulse deficit, pulse strength was moderate and the rhythm was regular. A digoxin assay showed the level to be l.lnmol/l 8 hours post-pill. The treatment regime was continued unchanged for six weeks and then the furosemide was stopped.

Ten months later the dog (now 17 months old) suddenly deteriorated and was found collapsed and dyspneic. The referring veterinary surgeon increased the dose of enalapril to 30mg PO q24h and digoxin to 0.375mg PO q12h and a partial improvement occurred. The dog was again referred to Glasgow University Veterinary School the following day.

O n examination the heart rate was 130bpm, the rhythm was irregularly irregular, mucous membranes were pink with a capillary refill time of 2 seconds, femoral pulses were weak and the pulse rate was 60bpm. O n auscultation lung sounds were normal, heart sounds were quiet and no murmur was detected. The dog now weighed 70.5kg. Hematology and plasma biochemistry showed only an eosinophilia (2.2 x 1 09/1) and urine analysis was unremarkable.

Electrocardiography (Fig 3) lead I1 measurements were:

Heart rate Rhythm Bizarre complexes

P wave QRS duration

QS amplitude

S-T segment ($:::rval

MEA

160bpm irre larly irregular, bigeminal in laces

pensatory ause none visibL 0.06s upright complexes, 0.1s bizarre complexes upright complexes tI.OmV, notched bizarre complexes -1.OmV slurnng present 0.2s wide and tall after bizarre complexes t120"

mu ? tiple or single, some followe B by a com-

The bizarre complexes occurred singly or in pairs and some were followed by a compensatory pause. The rhythm was thought to be atrial fibrillation with ventricular premature complexes, but an alternative ex- planation, especially in view of the findings the previous year, is atrial fibrillation with intermittent aberrant conduction.

The dog was cage rested, an intravenous catheter was placed in case of emergency and the enalapril and digoxin were continued at the same doses. The follow-

ing day thoracic radiographs (Figs 4 and 5) showed the vertebral heart score was unchanged (1 1.5). The pleural space, great vessels and lung pattern appeared normal, but the pulmonary vessels again appeared enlarged. The diagonal shadow seen in the cranial thorax on the lateral view was assumed to be due to superimposition of the triceps muscle.

Echocardiography showed that the fractional shortening had decreased to 20%, the dimensions of the left ventricle were normal (LVIDd 5cm, LVIDs 4cm), the EPSS was increased to Icm and the left atrium was enlarged (7cm from the same view as in the previous examination. Spectral Doppler echocardiography showed mild mitral valve incompetence. The rhythm changed briefly to sinus during the examination.

The following day the dog's heart rate was 80bpm, the rhythm was regular and there was no pulse deficit. Electrocardiography (Fig 6) showed that the QRS morphology was similar to the trace obtained 11 months previously i.e. sinus rhythm with a conduction deficit. The dog was discharged two days later on digoxin 0.375mg PO q12h and enalapril 30mg PO q24h. The owner was advised to restrict the dog's exercise and to worm the dog regularly in view of the eosinophilia. A digoxin assay taken five days later showed that the level 8 hours post-pill was 1.3nmol/l. The referring veterinary surgeon monitored the dog's digoxin levels every 3 months.

Fourteen months later the dog (now 2 years and 7 months old) was presented due to sudden onset dyspnea, lethargy and tachycardia of two days duration. O n examination the dog was very depressed, the heart rate was 24Obpm, femoral pulses were weak, there was a marked pulse deficit (80bpm), mucous membranes were pale with a capillary refill time of 2 seconds. O n auscultation there were inspiratory and expiratory crackles, the heart sounds were quiet and no murmur was detected.

Electrocardiography (Fig 7) lead I1 measurements were:

2'0bf

$;TinErval 0.2s

Heart rate Predominant rhythm regu ar P wave none visible QRS duration 0.08s R wave 0.6mV S-T segment slurring present

0.3mV MEA -60"

28

Journal of Veterinary Cardiology, Vol. 1, No. 2, December 1999

These findings were suggestive of ventricular tachycardia or supraventricular tachycardia with aberrant conduction but, in view of the previous findings, the latter was thought more likely.

A lateral thoracic radiograph (Fig 8) showed that the vertebral heart score had increased to 13, there was increased sternal contact, straightening of the caudal border of the heart, tracheal elevation, loss of the caudal cardiac waist and splitting of the mainstem bronchi. The pulmonary vessels were enlarged and there was a mixed lung pattern - in the peripheral lung field there were fine, reticular markings characteristic of an inter- stitial pattern; in the perihilar area there were prominent bronchial markings and air bronchograms sugges-

tive of a mixed bronchial and alveolar pattern possibly due to peri-bronchial oedema. The great vessels and pleural space appeared normal.

Treatment involved cage rest, furosemide 200mg i/v q12h, enalapril 30mg PO q24h, digoxin 0.375mg PO q12h and an intravenous catheter was placed in case of emergency.

Hematology and biochemistry showed a mild ma- ture neutrophilia (12.15 x I09/l; reference range 3.0- 11.8 x 109/1), mild eosinophilia (1.3 x 109/l; 0.1 - 1.25 x 109/1), elevated urea (15mmol/1; 2.5 - 8.5mmol/l) and normal creatinine (148pmol/l; 45 - 155mmob'l).

The following day echocardiography showed marked left atrial enlargement (9 crn diameter from the same view as previously), the fractional shortening was 25%, EPSS was 1.1 cm and there was sub-endocardial hyperechogenicity. The rhythm converted briefly to sinus during this procedure but there was no response to a vagal maneuvre (oculo-cardiac reflex). Spectral Doppler echocardiography showed increased duration of the jet of mitral valve incompetence.

The dog was treated with propanolol2dmg tid and the digoxin and enalapril were continued at the same doses. Twelve hours later the dog's heart rate was 100bpm, the rhythm was regular and there was no pulse deficit. Electrocardiography (Fig 9) showed sinus rhythm and the QRS complexes were slightly pro- longed (0.08s) but the morphology of the complexes was otherwise normal.

The dog was discharged two days later on digoxin 0.375mg PO q12h, enalapril 30mg q24h and

29

Ruth Willis, Paul R. Wotton, Chris J. L. Little

propanolol 2Omg PO qUh. A digoxin assay, taken 5 days later, showed that the

level 8 hours post-pill was 3.9nmo1/1 and, although the dog was not showing signs of toxicity, the dose was reduced to 0.25mg PO q12h. Biochemistry was repeated two weeks later and showed that the urea level was within the normal range.

At the time of writing, 11 months later, the dog is reported to be asymptomatic and the medication has been continued at the same doses.

Discussion

This case is an example of a complex arrhythmia. Unanswered questions include the etiology of the arrhythmia, whether it was ventricular or supraventricular with aberrancy in origin, and whether it would have reverted to sinus without treatment. It is reported that right bundle branch block and left anterior fascicle block can progress to second or third degree atrioventricular block and therefore may require pacemaker in- sertion2.

The atrioventricular valve regurgitation seen in this case was of short duration (protosystolic) and therefore was not considered to be clinically significant; whether it was congenital or acquired (secondary to cardiomegaly) is unknown.

The enlarged pulmonary veins and the prominent pulmonary arteries seen radiographically in this case could have been the result of high cardiac output associated with the tachycardia. In figures 4 and 5 atrial fibrillation could account for an increase in pulmonary venous pressure resulting in pulmonary venous distension.

No P waves were seen on figure 3 (due to paroxysmal atrial fibrillation), or Figure 7 but this can occur in supraventricular tachyarrhythmias (SVT) and ventricular tachyarrhythmias (VT). If the arrhythmia was supraventricular in origin then it was associated with a conduction disturbance. Supraventricular tachyarrhythmias can be classified into automatic and re- entrant tachycardias. Re-entrant pathways can be mi- croreentrant (within the atrioventricular node) o r macroreentrant (via an accessory pathway) but which mechanism was involved in this case is unknown. Fig- ure 3 showed periods of a bigeminal rhythm with a constant coupling interval suggesting that re-entry

could be causing ventricular premature complexes (VPCs). The wide bizarre complexes were followed by a compensatory pause therefore it is possible that these complexes were left ventricular in origin and the pre- ceding upright complexes were conducted atrial beats. The arrhythmia in this case appeared to be paroxysmal and a Holter monitor could have been used to record the duration of the paroxysms. Paroxysmal tachyarrhythmias are usually caused by re-entry whereas autonomic tachyarrhythmias tend to be non-paroxys- ma1 with a warm-up phase. Lone atrial fibrillation is reported in giant breeds, but should not be associated with cardiomegaly and therefore was not considered in this case.

A precordial thump will sometimes stop tachyarrhythmias because the shock to the myocardium may cause a VPC which may break a re-entrant circuit, however this procedure may worsen some tachyarrhythmias and was not attempted in this case. Atri- oventricular node and sinus node re-entrant rhythms will often respond to vagal maneuvres, however the arrhythmia seen in this case did not respond to gentle digital pressure on the eyes. This procedure may not work if there is excessive sympathetic tone due to the patient being nervous or if this procedure causes dis- comfort. Alternatively, esmolol could have been ad- ministered (to attentuate the effects of sympathetic stimulation) before repeating the oculo-cardiac reflex.

Intravenous verapamil o r diltiazem could have been used to reduce the heart rate if treatment was required urgently3. Chronic treatment of SVT usually in- volves the use of digoxin, a p blocker or a calcium channel blocker. The latter two are thought to be preferable as digoxin may worsen macroreentrant arrhythmias. Both calcium channel blockers and p blockers are negative inotropes and therefore should be used cautiously in cases of myocardial failure. In this case the fractional shortening has decreased over the years (although a fractional shortening of 20% is probably within normal limits for the giant breeds) and, with the benefit of hindsight, this case should have been treated sooner with an negative chronotrope as myocardial damage resulting in reduced contractili- ty could be associated with the tachycardia.

Class la anti-arrhythmics can be used in unresponsive cases or if the SVT is thought to be due to an automatic rather than re-entrant rhythm4. Other possible treatments for supraventicular tachyarrhythmias include propafenone, flecainide and encainide5.

30

Journal of Veterinary Cardiology, Vol. 1, No. 2, December 1999

Propafenone can be given by intravenous or oral routes and it is reported that a high proportion of dogs showed partial or complete elimination of the arrhythmia and minimal side effects5. Amiodarone and flecain- inde are used frequently in human medicine in the treatment of paroxysmal atrial fibrillation. Radiofre- quency ablation of concealed accessory pathways has been described in humans and dogs6. At present this case appears to be stable on medical therapy but, if the dog becomes unresponsive in the future, then such in- terventions may be indicated.

Key Words

Supraventricular tachydysrhythmia, supraventricular tachyarrhythmid, conduction deficit.

Acknowledgements

The authors gratefully acknowledge the assistance of several colleagues at the Ghsgow University Veteri- nary School who dealt with this patient on occasion, and also the refemng veterinary surgeon.

References

1. Martin M & Corcoran B. Electrocardiography. In Martin and Corcoran. Cardiorespiratory diseases of the dog and cat. Oxford: Blackwell Science; 1997: 41

2. Tilley LP. Interpretation of QRS deflections. In Tilley LP, ed. Essentials of Canine and Feline Elec- trocardiography. Philadelphia, PA: Lea & Febiger;

3 . Kittleson M, Keene B, Pion P, et a1 Verapamil admin- istration for acute termination of supraventricular tachycardia in dogs. Journal of American Medical As- sociation 1988; 193: 1525 - 1529

4. Wright, K.N., Clarke, E.A. & Kanter, M.D Supraven- tricular tachycardia in four young dogs. Journal of the American Medical Association 1993; 208: 75-80

5. Kittleson, M.D. & Kienle, R.D. Diagnosis and treatment of arrhythmias (dysrhythmias). In Kittleson and Kienle. Small animal cardiovascular medicine. St Louis: Mosby Inc; 1998: 474

6. Scherlag, B.J., Wang, X., Nakagawa, H. et a1 Ra- diofrequency ablation of a concealed accessory pathway as a treatment for incessant supraventricular tachycardia in a dog. Journal of the American Veteri- nary Medical Association 1993; 203: 1147-1 152

1992: 80-81

he defacto recognition period for cardiology has been T closed now for more than one

year. This means that the only way of becoming a diplomate of the ECVIM-CA (Cardiology) is either by passing the ECVIM-CA examination, or the ACVIM examination. Euro- peans that are ACVIM diplomates can become ECVIM-CA diplomate if they fulfill the European requirements for publications. These requirements are slightly different in Europe, in that we usually require one extra publication. In October 1999 the Examination Committee and the Credential Com- mittee were appointed. It is planned that the first examination in Cardiolo- gy will be held in September 2001. Candidates will have until March Ist, 2001 to submit their application. Requirements for candidates are published in the Information Brochure which can be found on the ECVIM-CA web site; http://www .agri.huji.ac.il/ecvim/.

This brochure as well as the examination application form can be down- loaded from the web site. Although one of the requirements for taking the examination is having completed a formal recognised residency programme, this requirement cannot be enforced for the next cou- ple of years as the first formal pro- grammes still have to be recognised. Therefore, each candidate’s training will be evaluated individually by the Credentials Committee to determine if it is equivalent to a formal residency training. As it is anticipated that until now not all candidates will have kept an accurate patient log, some flexibility on this issue will be consid-

ered. However, documented and signed statements from the supervi- sor will be required that should indi- cate the number and type of patients were personally handled by the candidate during the training period. Starting from January 2000, all candidates will be required to keep an accurate and detailed case log, so that after 2002 only applications with three years detailed case logs will be accepted. In addition, potential candidates should fulfill all other requirements mentioned in the Information Brochure. Those colleagues that would like to do an internship and residency in cardiology should contact the secre- tary of the ECVIM-CA for addresses. If the candidate wants to do an alternative programme rather than a formal programme, the details of this programme should be submitted in writing to the Education Committee

Erik Teske Cardiology.

President ECVIM-CA

31

Tachyarrhythmia in a St Bernard dog

Documents

Transcript of Tachyarrhythmia in a St Bernard dog