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Prospective study of cardiac arrhythmias--a survey of 20,000 canines.

Introduction

Cardiac arrhythmias are defined as abnormality in the rate, rhythm, site of origin or conduction of cardiac impulse (Silber and Katz, 1975). Their prevalence in dog population has been studied in many countries abroad (Patterson et al., 1961; Spaulding and Tilley, 1976). In India, no such large scale surveys seem to have been conducted barring aside a few studies (Changkija, 2007) and sporadic reports (Varshney and Dey, 2000; Varshney and Tiwari, 2002a and b; Kumar and Varshney, 2004; Varshney and Kumar, 2004; Varshney et al., 2011). Some of these are associated with severe clinical signs warranting their immediate management with anti-arrhythmic drugs. The present investigation was therefore undertaken to study the prevalence of arrhythmias in dogs along with their management approach.

Materials and Methods

Twenty thousand new canine cases, brought at the hospital during last 4 years formed the population for studying prevalence of arrhythmias. Dogs with unexplained weakness, exertion, irregular heartbeat, dyspnoea or history of syncope were subjected to thorough cardiovascular examination including electrocardiography (1 cm= 1mv; 25 mm/second speed, 6 leads with crocodile clips, filter off, right lateral recumbency). Arrhythmic dogs were further subjected to detailed clinical examination, chest radiography, serum chemistry and blood examination for ascertaining probable cause. Data were analyzed for studying the prevalence.

After ascertaining the nature of arrhythmias, prompt measure with anti arrhythmic drugs along with supportive electrolyte fluid as per the merit of the case were undertaken. Sinus tachycardia associated with severe excitement was treated with Diazepam (5 mg PO BID) or Phenytoin (100 mg PO TID). Other cases associated with hyperpyrexia or severe anemia were treated for primary diseases. Cases of symptomatic bradycardia were treated with ocular pressure, chest thumping or Glycopyrolate (0.005 mg/kg i.m till heart rate improved). Sinus arrhythmia and wandering pacemaker were not treated. Treatment of atrial fibrillation /flutter was initiated with Quinidine (6.0 mg/kg PO BID) for 72 hours. Unresponsive dogs were treated with Digoxin (0.06 mg/kg PO BID) for 2-4 days and failures were switched on to Verapamil (2mg/kg PO TID). Therapy was continued for 6-8 months. Atrial premature complex, atrial tachycardia and A-V junctional arrhythmias were attended with Digoxin (0.06 mg/ kg PO BID. Dogs with ventricular premature complex and ventricular tachycardia were attended immediately with 2% Xylocaine given intravenously @ 2mg/kg as bolus over 2 minutes followed by a maintenance of 50|jg/kg/minutes in 5% Dextrose solution intravenously subject to a maximum of 8 mg in 6 hours. From 2nd day onwards the dogs were given Propranolol @ 0.5 mg/kg PO TID with Frusemide @ 2mg/ kg PO for 2-3 days. Dogs with ventricular fibrillation/flutter were also given Sodium bicarbonate solution intravenously. Nothing substantial could be done in dogs with ventricular asystole except attempting with intravenous calcium chloride. Symptomatic dogs with A-V Block or Sinus arrest were treated with in the same manner as dogs with bradycardias. Dogs with atrial stand still were treated with Glycopyrrolate @ 0.01 mg/kg b.wt. intramuscularly and fluid (saline solution and sodium bicarbonate solution) therapy.

Results and Discussion

The diagnosis of cardiac arrhythmias was based on history, signs, chest auscultation and electrocardiography. The frequency of arrhythmias is summarized in Table 1. Of 20,000 dog's population examined, 608 dogs revealed conduction disturbances or arrhythmias of different nature making the prevalence as 3.04%. Prevalence of cardiac arrhythmias has varied widely from 2.5 to 43.22% (Patterson et al., 1961; Tilley 1985; Changkija, 2007) in different surveys. Cardiac arrhythmias have also been recorded in association with babesiosis caused by Babesia canis (Dvir, 2001) or B. gibsoni (Chaudhari, 2006); or with Ehrlichiosis caused by Ehrlichia canis (Varshney and Kumar, 2006). Although, cardiac arrhythmias and conduction disturbances may occur with primary heart disease or diseases primarily affecting the vagal activity, their frequent occurrence in the absence of detectable heart diseases is an important factor in majority of cases. These extra cardiac causes include hypoxia, electrolyte imbalance, acid-base disturbances, neurological disorders, hyperthyroidism, gastric torsion, renal failure or pancreatitis (Rush and Atkins, 1991). The arrhythmias were grouped into three categories as sinus arrhythmia, abnormalities of impulse formation and abnormalities of impulse conduction (Tilley, 1985). Their prevalence was recorded as 1.295, 1.415 and 0.33% respectively. Amongst arrhythmias (608 cases) the prevalence of abnormalities of impulse formation was higher (46.54%), followed by sinus arrhythmia (42.59%), and abnormalities of impulse conduction (10.85%).

The group of sinus arrhythmia included Sinus Bradycardia, Sinus Tachycardia, Sinus Arrhythmias and Wandering pacemaker and their prevalence was 3.12 (19/608), 27.13 (165/608), 11.34(69/608), 0.98% (6/608) amongst arrhythmic dogs (Table 1). Sinus bradycardia was characterized by heart rate slower than 60 bpm without change in 'R-R' interval (Fig. 1). Sinus bradycardia with syncope and sudden death is generally reported in cardiomyopathies (Calvert et al., 1996). Bradyarrythmias can have a negative clinical impact even with moderate physical activity owing to cerebral hypoxia (Rishnew and Thomas, 2000). Bradycardia has also been reported in dogs with increased parasympathetic stimulation owing to gastrointestinal disturbances, respiratory diseases, increased intracranial pressure, hypothermia or hyperkalemia. In the present study cases of bradycardia were associated mostly with hypothermia. Sinus tachycardia was the most common amongst sinus arrhythmias and was characterized by heart rate higher than 160 in large breeds and 180 bpm in small breeds with regular 'R-R' interval (Fig. 2). These cases were found associated with nervousness, excitement, pain, hyperthermia, infection, severe anaemia or hypoxia (Bolton, 1975; Varshney, 2005; Changkija et al., 2006a and b). Sinus arrhythmia with second highest prevalence was characterized by irregular 'R-R' interval and rhythm originating in sino-atrial node (Fig. 3). Such arrhythmia are generally innocuous because of dominant parasympathetic tone (Detweiler, 1997). Wandering pacemaker was characterized by 'P' wave of varying amplitude and morphology (Fig. 4). It is a common nonpathological condition in dog.

Abnormalities of impulse formation accounted for 46.54% (283/608 dogs) cases of arrhythmias. Of which, 212 (34.06%) and 71(11.67%) were atrial and ventricular origin suggesting that arrhythmias of atrial origin were more common. Atrial arrhythmias included atrial flutter, atrial fibrillation, atrial tachycardia, atrial premature complex and AV junctional disturbances. It was observed that atrial flutter/fibrillation were more common clinically significant arrhythmias in dogs (Ettinger et al., 2000) and were electrocardiographically characterized by rapid and regular atrial rhythm in chaotic manner. In atrial flutter 'P' wave was replaced by saw tooth wave (Fig. 5) while in fibrillations saw tooth wave was difficult to appreciate and was replaced by 'f' wave oscillations (Fig. 6). Unattended atrial fibrillations/ flutter may lead to congestive heart failure because of reduced cardiac output. Atrial fibrillations were more common in dogs of large breed (German shepherd, Labradors, Mastiffs, Boxers, Doberman, Great dane) but also observed in Cocker spaniel, Pomeranians and in nondescript dogs (Bonagura and Ware, 1986; Tidholm and Johnsson, 1996; Meur et al. (2001); Varsheny et al., 2011). Atrial flutter/ fibrillation have been reported with conditions producing atrial enlargement, chronic valvular insufficiency, dilated cardiomyopathy, patent ductus areriosus, myocardial infarction, tricuspid valve dysplasia, pulmonic stenosis and ventricular septal defects (Liu and Tilley,1975; Edward and Tilley, 1981); heartworm disease; cardiac trauma or supraventricular arrhythmias (Morgan, 1992) or even without cardiomyopathy. Prevalence of atrial flutter/fibrillations was higher in the present study as compared to other studies Tilley, 1985; Changkija, 2007). Male dogs were more predisposed to atrial fibrillations. Atrial premature complexes (Fig. 7) arise from ectopic foci in the atrium. The complexes varied from isolated, couplets to triplets. They can lead to atrial flutter, atrial fibrillation or atrial tachycardia. In aged dogs isolated atrial premature complexes are considered normal variations (Tilley,1985). Electrocardiographically heart rate is generally normal but rhythm is irregular due to premature 'P' wave which is different in configuration (Fig. 7). Atrial tachycardia is caused by rapid discharge of an abnormal atrial focus or by re-entry. It is characterized by rapid atrial rate usually higher (>260 bpm) with an atrial: ventricular ratio of 2:1 or 3:1 (Fig. 8). Atrial tachycardias were of paroxysmal or substantial type. A-V junctional premature complex (Fig. 9)/tachycardia (Fig. 10) occur when ectopic foci in the A-V junction acts as a primary pacemaker other than SA node. Characteristic features of A-V junctional arrhythmia/tachycardias are heart rate faster than 40-60 beats per minutes with a regular rhythm and a negative 'P' wave in lead II (Fig. 9 and 10).

Prevalence of Ventricular arrhythmias was lower than that of atrial arrhythmias. This group of consisted of ventricular flutter (Fig.11), ventricular fibrillation (Fig.12), ventricular premature complexes (Fig.13), ventricular tachycardia (Fig. 14) and ventricular asystole (Fig. 15) with a prevalence rate of 0.65, 0.98, 6.41, 2.76 and 0.65% respectively. Ventricular premature complexes or ventricular escape rhythm are impulses arising from an ectopic focus in the ventricle and are characterized by normal heart rate but irregular rhythm. Amongst ventricular arrhythmias, ventricular premature complexe is more frequent and its incidence has been reported as high as 26% (Tilley,1985) to 45% (Patterson et al.,1961).Ventricular premature complexes have been found associated with congestive heart failure, myocardial infraction, neoplasia, pericarditis, cardiomyopathy and traumatic myocarditis (Ettinger, 1983); hypoxia, anaemia, uraemia, pyometra, gastric dilatation-volvulus, pancreatitis, parvovirus infection (Carpenter et al., 1980); anaesthesia, digitalis intoxication or atropine intoxication (Muir, 1978). These complexes have also been observed with normal heart rate with no apparent cause (Ettinger, 1983). Ventricular tachycardia was next in order of prevalence amongst ventricular arrhythmias. It was characterized by a continuous series of ventricular premature complexes (Fig. 14) resulting from stimulation of an ectopic ventricular focus. It is one of the most serious arrhythmias owing to its association with serious heart disease. Ventricular flutter or fibrillations were recorded in 4 and 6 dogs respectively. These are considered serious and fatal leading to arrest. These arrhythmias were electrocardiographically characterized by deformed deflections with rapid and irregular heart rate in chaotic manner without recognition of 'P' wave. Ventricular asystole was characterized by the absence of QRS and presence of 'P' waves of normal configuration (Fig.15).Ventricular asystole is a serious arrhythmia with a grave prognosis.

Abnormalities of impulse conduction were comprised of A-V Blocks, SA Blocks (Fig. 19), Atrial standstill (Fig. 20) and sick sinus syndrome (Fig. 20) and were observed in 45 (7.4%), 12 (1.97%), 3 (0.49%) and 06 (0.98%) dogs respectively. In this category A.V blocks were common conduction disturbances. These are defined as delay or stoppage of conduction and may be transient or permanent between atria and ventricle (Ettinger et al., 2000). Of these first degree blocks were more common followed by second degree (Table 1). The first degree blocks were characterized by normal heart rate and rhythm, normal QRS but a prolonged P-R interval of > 0.13 seconds (Fig.16). Second degree A-V blocks are intermittent failure of AV conduction and were characterized by absence of QRS-T complex following one or more 'P' waves (Fig. 17). These blocks were more common in older dogs (>7 years). Third degree AV blocks were characterized by slower ventricular rate than atrial with the predominance of 'p' wave with out QRS complex. P waves were of almost normal configuration (Fig. 18). There seems no conduction between atrium and ventricles, hence there was no constant relationship of 'P' to QRS complex. Sinus arrest or sino-atrial blocks were observed in 1.97 dogs (11/608) and were characterized by irregular rhythm and pauses were equal or greater than twice the normal R-R interval (Fig. 19). It seems to be a failure of SA nodal impulse formation caused by depressed automaticity. Intermittent sinus arrest may be normal in brachycephalic breeds owing to reflex increase in vagal tone. Bolton (1975) reported that sinus arrest may not have much clinical significance. Nevertheless occasional prolonged pauses may lead to bradycardia. Persistent atrial standstill is a rare clinical condition reported in English springer spaniels (Tilley, 1985). Silent atrium has also been reported in German shepherd, Great dane and Doberman dogs (Kumar and Varshney, 2005; Chingkija, 2007). In present study, three cases of atrial standstill were observed in nondescript (1); German shepherd (1) and Doberman (1) dogs suffering from hyperkalemia. The conduction disturbance was characterized by total absence of atrial depolarizatioin despite normal impulse formation in the SA node (Ettinger et al., 2000) and was reflected by the absence of 'P' wave in electrocardiogram (Fig. 20). These dogs were not on digitalization indicating that it was a transient silent atrium possibly due to hyperkalemia. Sick sinus syndrome (Fig. 21) seems a complex disturbance of conduction tissues of heart producing simultaneous defect in SA activity, AV conduction and disturbance in supraventricular and ventricular activity (Ettinger et al., 2000).

Dogs with arrhythmias were clinically characterized by muscular weakness, dullness, posterior paresis or ataxia, exercise intolerance, dyspnoea or syncope of short duration and heart failure in cases of sustained tachyarrhythmias. Dogs with ventricular tachycardia or asystole invariably showed heart failure leading to death. Signs of congestive heart failure were also evidenced in dogs with severe atrial fibrillation/ flutter/tachycardias.

Sinus tachycardia associated with fear, pain, excitement were not treated with antiarrhythmic drugs. Nevertheless dogs showing sinus tachycardia associated with severe excitement responded well to diazepam or phenytoin. Ocular pressure and chest thumping failed to improve heart rate therefore glycopyrolate, an anticholinergic drug, was given in the bradycardic dogs. Response to glycopyrolate was quite satisfactory and heart rate improved substantially in all cases. This favourable response to glycopyrolate suggested the role of excessive vagal tone in the development of bradycardia in these dogs. Varshney and Dey (2000) have reported encouraging results with atropine sulphate and propanthelene bromide, an oral anti-cholinergic drug (Smith et al., 1994), in the management of brady-arrhythmia in an adult Pomeranian dog. Treatment response in cases of atrial fibrillation/flutter is complicated owing to dilatation of atria in most of the cases. Though quinidine is the drug of first choice in the management of atrial flutters/fibrillations, a sizeable number of dogs did not responded well to quinidine and therefore were switched to digoxin and most of the dogs responded well except 13 dogs. These unresponding dogs responded well to verapamil as reported earlier (Varshney et al., 2011). Therapy for atrial flutter/ fibrillation continued for 6-8 months and eight dogs could not survive more than 60-80 days. Therefore prognosis of the cases with atrial flutter/fibrillation seems guarded as many dogs may succumb. Atrial premature complex and, atrial tachycardia were attended with digoxin. A-V junctional premature complexes were treated with in the same manner as atrial premature complexes. Dogs with ventricular premature complex and ventricular tachycardia were attended immediately with 2% xylocaine and from 2nd day onwards propranolol with frusemide were added. Dogs with ventricular fibrillation/flutter were also given sodium bicarbonate solution intravenously. Response to treatment in cases of ventricular arrhythmias was poor as many fatalities occurred within a period of 3-4 days. Nothing substantial could be done in dogs with ventricular asystole except attempting with intravenous calcium chloride. Symptomatic dogs with A-V Block or Sinus arrest were treated with in the same manner as dogs with bradycardias. Saline/sodium bi carbonate fluid was intended to lower blood potassium level and glycopyrrolate to improve heart rate in cases of atrial standstill.

Acknowledgements

The authors are thankful to the Chairman, Managing trustees and Board of trustees for providing necessary facilities at the hospital. Authors are also thankful to the owners for cooperating in the study.

References

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Varshney, J.P., Deshmukh, V.V. and Chaudhary, P.S. (2011). Atrial fibrillation/ flutters in dogs and its management. Intas Polivet 12 : 271-73.

J. P. Varshney (1), Prajwalita Sutaria (2), V.V. Deshmukh (3) and P. S. Chaudhary (4)

Shree Surat Panjarapole Prerit

Nandini Veterinary Hospital

Ghod-Dod Road

Surat--395007 (Gujarat)

(1.) Medicine Consultant and Corresponding Author

E-mail:dr_jpvarshney@rediffmail.com

(2.) Assistant Professor, Department of Surgery, SDAU, Dantiwada

(3.) Veterinary Pathologist

(4.) Veterinary Surgeon

Table 1 : Prevalence of arrhythmias in dogs.

Types of Arrhythmias        No. of       Prevalence     Prevalence of
                           cases of       amongst        Arrhythmias
                         Arrhythmias    Arrhythmias        amongst
                                        % (n = 608)    population (%)

1. Sinus arrhythmias         259           42.59            1.295
Sinus Bradycardia             19            3.12
Sinus Tachycardia            165           27.13
Sinus Arrhythmias             69           11.34
Wandering pacemaker           06            0.98

2. Abnormalities of          283           46.54            1.415
impulse formation

(a) Atrial Arrhythmias       212           34.86
Atrial flutter                08            1.31
Atrial fibrillation          129           21.21
Atrial premature              13            2.13
  complex
Atrial Tachycardia            51            8.38
A.V junctional                06            0.98
  premature complex
A.V junctional                05            0.82
  Tachycardia

(b) Ventricular               71           11.67
  arrhythmias
Ventricular flutter           04            0.65
Ventricular                   06            0.98
  fibrillation
Ventricular escape            39            6.41
  rhythm (VPC)
Ventricular                   18            2.96
  Tachycardia
Ventricular Asystole          04            0.65

3. Abnormaities of            66           10.85            0.330
impulse conduction

(a) A-V Block                 45            7.40
1st degree                    27            4.46
2nd degree                    14            2.30
3rd degree                    04            0.65

(b) S.A Block                 12            1.97

(c) Atrial Stand Still        03            0.49

(d) Sick Sinus                06            0.98
  Syndrome
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Title Annotation:Clinical Article
Author:Varshney, J.P.; Sutaria, Prajwalita; Deshmukh, V.V.; Chaudhary, P.S.
Publication:Intas Polivet
Article Type:Report
Geographic Code:9INDI
Date:Jan 1, 2013
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