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Standards of Care April 2003 (Vol 5, No 3)

Canine Bradyarrhythmias

by Barret J. Bulmer, DVM, DACVIM (Cardiology)


    Normal cardiac impulses originate within the sinoatrial (SA) node, traverse the atria, and conduct through the atrioventricular (AV) node and His-Purkinje system to ultimately depolarize the ventricles. If the stimulating impulse fails to form or if the conduction pathway of the impulse is delayed or blocked, a bradyarrhythmia develops. Because the product of heart rate and forward stroke volume determines cardiac output, bradycardia may result in weakness, exercise intolerance, congestive heart failure, or syncope.

    The most commonly encountered canine bradyarrhythmias that require treatment include sinus bradycardia, high-grade second-degree and third-degree AV block, sick sinus syndrome (SSS), and persistent atrial standstill. These arrhythmias occur secondary to a variety of physiologic, pharmacologic, and pathologic disease conditions; therefore, a thorough evaluation is vital to appropriately diagnose and manage these patients.

    Diagnostic Criteria

    Historical Information

    Gender Predisposition: Females appear predisposed to the development of SSS; there is no pronounced gender predisposition for the other bradyarrhythmias.

    Age Predisposition: SSS most frequently occurs in middle- to old-aged dogs; second-degree and third-degree AV blocks occur in old-aged dogs; persistent atrial standstill and sinus bradycardia may occur in any age.

    Breed Predisposition: Schnauzers, West Highland white terriers, and cocker spaniels appear to most frequently develop SSS, while German shepherds and large-breed dogs most frequently develop AV block. English springer spaniels and Old English sheepdogs may be predisposed to the development of persistent atrial standstill, while dogs with high resting vagal tone (e.g., brachycephalic breeds) frequently display sinus bradycardia.

    Owner Observations: Owners may identify weakness, exercise intolerance, syncope, abdominal distension, coughing, or tachypnea. Because these arrhythmias frequently occur in older dogs, some owners mistakenly recognize these signs as “old-age changes.”

    Physical Examination Findings

    • Dogs with sinus bradycardia, high-grade second-degree or third-degree AV block, and persistent atrial standstill generally display a slow (less than 70 bpm for adult dogs, 60 bpm for giant breeds), regular heart rhythm despite the stress of a hospital setting. Dogs with SSS may display bradycardia, tachycardia, or a normal rate.
    • The femoral pulse quality is normal to strong in most bradycardic dogs.
    • Jugular pulses may be identified in dogs with third-degree AV block as the atria contract against a closed (tricuspid) valve.
    • Jugular distension may be present in association with right-sided heart failure (hepatomegaly, ascites), or pulmonary edema may be present with left-sided heart failure. Three out of 154 patients (2%) in a recent review of artificial cardiac pacing presented with heart failure second to bradycardia. An additional 12 patients (8%) had heart failure associated with bradycardia and another form of heart disease (5 with valvular disease, 3 with dilated cardiomyopathy, 3 were unspecified, and 1 with endocarditis).
    • Rapid, low-pitched fourth heart sounds that occur subsequent to atrial contraction may be ausculted in dogs with third-degree AV block.
    • Systolic murmurs of mitral or tricuspid insufficiency may be ausculted if the patient displays concurrent myxomatous valvular disease (e.g., SSS dogs) or if eccentric ventricular hypertrophy/dilation of the valve annulus has developed.
    • Systolic, aortic ejection murmurs may occur because of the large ventricular stroke volume.

    Laboratory Findings

    • Most bradycardic dogs have normal routine laboratory tests (complete blood count, chemistry profile, and urinalysis).
    • A mild elevation in alkaline phosphatase (ALP) may be identified in bradycardic dogs, presumably from hepatic congestion/cholestasis.
    • Dogs with hypoadrenocorticism or urethral obstruction may have significant hyperkalemia and present with sinus bradycardia or a “sinoventricular” rhythm that looks identical to atrial standstill.

    Other Diagnostic Findings

    Electrocardiogram (See Figure 1)

    • Sinus bradycardia: Slow and regular rhythm, P wave present for every QRS–T complex, QRS–T complexes are supraventricular, P–R interval is consistent.
    • High-grade second-degree AV block: Slow and variable rhythm, P waves are associated with one another but there are numerous P waves that are “blocked” and fail to produce a ventricular impulse. The impulses that are able to propagate across the AV node are associated with a supraventricular (tall, upright and narrow) QRS–T complex. This rhythm is frequently named based on the ratio of P waves to QRS–T complexes, whereby a 3:1 ratio would indicate one conducted QRS–T complex for every 3 P waves.
    • Third-degree AV block: Slow and regular rhythm, P waves are associated with one another and QRS–T complexes are associated with one another, but there is no association between the P and QRS–T complexes; QRS–T complexes may be junctional (tall, upright, and narrow) or ventricular (wide and bizarre) in origin.
    • SSS: Variable rate and rhythm, represents a constellation of conduction abnormalities that may include prolonged periods of sinus arrest, sinus bradycardia sinoatrial block, supraventricular tachycardia, and/or AV block.
    • Atrial standstill: Slow and regular rhythm, no P waves present, QRS–T complexes are frequently junctional but may be ventricular in origin, hyperkalemia may be associated with tall, tented T waves or a prolonged QRS duration.

    Thoracic Radiographs
    Thoracic radiographs from bradycardic dogs are in some instances normal, while others may display significant cardiomegaly. Pulmonary venous congestion or caudal vena caval engorgement may be present along with pulmonary edema, ascites, and/or hepatomegaly if congestive heart failure developed.

    Eccentric ventricular hypertrophy with hyperdynamic contractility is frequently identified in the face of bradycardia. AV valve insufficiency may be present secondary to eccentric hypertrophy/dilation of the valve annulus or secondary to concurrent myxomatous valvular disease.

    Atropine Response Test
    Sinus bradycardia, episodes of sinus arrest, or AV block may be secondary to conditions that increase vagal tone (e.g., gastrointestinal disease, central nervous system disorders, or respiratory disease). An atropine response test involves recording a baseline electrocardiogram (ECG) followed by a second ECG recording obtained approximately 15 to 20 minutes after atropine administration (0.02 to 0.04 mg/kg IM or IV). Depending on the baseline rate, atropine should result in a 50% to 100% increase in the heart rate, or achievement of a rate above 150 bpm, if an autonomic imbalance is responsible for the bradycardia.

    Holter ECG Recorder
    A 24-hour Holter ECG recorder or an event monitor may be required to document an intermittent bradyarrhythmia, especially in dogs with SSS.

    Summary of Diagnostic Criteria

    • Clinical signs may include:
      – Weakness
      – Exercise intolerance
      – Syncope
      – Abdominal distension
      – Coughing
      – Tachypnea
    • Physical examination findings may range from normal (especially in dogs with SSS) to pronounced bradycardia, normal to strong femoral pulses, jugular distension, ascites, hepatomegaly, and coughing with audible crackles over the lung fields.
    • Cardiac auscultation may identify rapid, low-pitched fourth heart sounds, an aortic ejection murmur subsequent to a large stroke volume, or an apical systolic murmur of AV valve insufficiency.
    • The electrocardiogram will distinguish between the common bradyarrhythmias although it alone cannot differentiate intrinsic conduction/automaticity defects from electrolyte, pharmacologic, or parasympathetic influences.
    • Thoracic radiographs and echocardiography are required to identify the presence of congestive heart failure and determine the suitability of the patient for pacemaker implantation; however, these modalities are not required to diagnose the bradyarrhythmia.
    • Hyperkalemia subsequent to hypoadrenocorticism or urethral obstruction may cause any of these bradyarrhythmias.
    • Routine blood work is usually normal, although mild elevations in cholestatic enzymes may be present subsequent to hepatic congestion.
    • In the unusual case of an unstable bradyarrhythmia, low cardiac output and decreased water intake may contribute to azotemia, while prolonged periods of ventricular asystole may contribute to syncope or death.

    Differential Diagnoses

    • It is important to identify if the bradyarrhythmia is subsequent to physiologic, pharmacologic, or pathologic disease conditions.
    • Physiologic conditions, including athleticism and sleep, or pathologic conditions including hypothermia, severe hypothyroidism, gastrointestinal, central nervous system, or respiratory disorders, may increase vagal tone and contribute to bradyarrhythmias. Atropine should be administered (0.02 to 0.04 mg/kg IM or IV) and the ECG rechecked in 15 to 20 minutes to identify if the bradycardia is atropine responsive
    • Administration of sedative or anesthetic agents, beta-blockers, calcium channel blockers, or digoxin may contribute to bradyarrhythmias and should be discontinued.
    • Conditions resulting in hyperkalemia (e.g., hypoadrenocorticism, urethral obstruction) may produce atrial standstill, sinus bradycardia, sinus arrest, or AV block. A chemistry profile should identify the hyperkalemia while an ACTH stimulation test may document the presence of hypoadrenocorticism.
    • Infiltrative neoplasms, inflammatory or immune-mediated disease conditions, infectious disease agents (e.g., Lyme disease, bacterial endocarditis), or ventricular septal defects may disrupt the normal cardiac conduction system or atrial myocardium. Although echocardiography may identify some of these abnormalities, the cause for most cases of third-degree AV block, SSS, and persistent atrial standstill remains uncertain (presumably ischemia and fibrosis).

    Treatment Recommendations

    Initial Treatment

    • An atropine response test (0.02 to 0.04 mg/kg IM or IV) and repeat ECG, 15 to 20 minutes after atropine administration, should be performed to assess the influence of the parasympathetic nervous system on the bradyarrhythmia. $
    • Asymptomatic dogs with physiologic sinus bradycardia rarely require treatment. More often, the treatment should be aimed at the underlying disease condition that is contributing to the excessive vagotonia.
    • In cases where hyperkalemia has induced the bradyarrhythmia, therapy should be aimed at reducing the potassium level (IV fluids, sodium bicarbonate, dextrose, and insulin therapy) and treating the underlying disease condition (hypoadrenocorticism, urethral obstruction). $$–$$$$
    • Pharmacologic therapy that may be contributing to the bradycardia (beta-blockers, calcium channel blockers, digoxin, sedative/anesthetic agents) should be discontinued.
    • Oral sympathomimetics (theophylline, 10 mg/kg PO tid or sustained-release theophylline, 20 mg/kg PO bid) and/or oral anticholinergics (propantheline, 0.5 to 1.0 mg/kg PO tid) may be attempted in cases of symptomatic sinus bradycardia or SSS. Unfortunately, these agents are often ineffective at alleviating the clinical signs and use may result in significant tachyphylaxis. $
    • Symptomatic dogs that present with prolonged episodes of sinus arrest or ventricular asystole require isoproterenol (0.04 to 0.08 µg/kg/min constant rate IV infusion, to effect) to increase the discharge rate of the escape rhythm or placement of a temporary pacemaker until a permanent pacemaker can be placed. $–$$
    • Ultimately, most dogs with symptomatic bradyarrhythmias require placement of an artificial cardiac pacemaker. $$$$

    Supportive Treatment

    Exercise restriction and cage rest serve to eliminate exertional syncopal episodes and decrease the body’s cardiac output demands.

    Patient Monitoring/ Home Management

    Medical Therapy
    Dogs that are initially responsive to sympathomimetics or anticholinergics often develop tolerance to their administration, side effects (anorexia, nervousness, and agitation), or progression of their underlying disease with redevelopment of clinical signs. Periodic ECGs, every 2 to 3 months, and careful client observations are important to determine if artificial cardiac pacing is indicated.

    Pacemaker Therapy

    • Antibiotics (cephalexin, 22 mg/kg PO bid to tid) are administered for 1 week postoperatively.
    • Dogs should be cage rested and severely exercise restricted for the first month postoperatively in an effort to prevent pacemaker lead dislodgement.
    • A thoracic radiograph and ECG are performed 1 month postoperatively to evaluate the integrity and performance of the pacemaker system.
    • Thoracic radiographs and electrocardiograms are performed every 6 months to evaluate the stability of the pacemaker system and monitor for progressive cardiac enlargement that may accompany artificial cardiac pacing.
    • Owners are instructed to take their dog’s heart rate once monthly to make certain it does not drop below the lower rate limit of the pacemaker.

    Milestones/Recovery Time Frames

    • Medical therapy alone may decrease the frequency of syncope to an acceptable owner level, although it rarely abolishes the fainting episodes completely.
    • Alleviation of symptomatic bradycardia by artificial pacing should quickly resolve congestive heart failure and syncope. Most owners identify a marked increase in exercise tolerance and quality of life.
    • Dogs tend to recover from transvenous pacemaker placement quickly and are typically discharged from the hospital the day following surgery. Within a week many owners find it is difficult to maintain the 1-month postoperative, strict exercise restrictions.

    On The News Front: Canine Bradyarrhythmias

    Treatment Contraindications

    • Under no circumstance should agents be used that may suppress junctional or ventricular escape beats (lidocaine, procainamide, quinidine, atenolol). It is imperative these complexes are recognized as escape beats (complexes that occur following a pause) rather than ventricular premature contractions (complexes that occur prematurely, thereby creating a shorter R–R interval than the underlying rhythm).
    • In dogs with SSS displaying both bradycardia and tachycardia, antiarrhythmic, sympathomimetic, or anticholinergic drugs should not be used prior to artificial pacemaker implantation. Antiarrhythmic agents may exacerbate the bradycardia or suppress escape beats while theophylline or propantheline may worsen the tachycardic episodes.


    • 1-year, 2-year, and 3-year survival rates following pacemaker implantation have been reported at 70%, 57%, and 45%, respectively. The average age of dogs requiring pacemaker implantation in the referenced study was 8.5 ± 3.7 years. This population of dogs may be more susceptible to developing concurrent systemic diseases, and in the author’s experience, it appears many dogs requiring pacemaker implantation eventually succumb to noncardiac diseases. The development of systemic disease processes unrelated to the original conduction defect may unfavorably alter the reported survival time.
    • Postoperatively, many owners report their dog’s activity level and quality of life are enhanced compared to the months preceding surgery.

    Unfavorable Criteria

    • Advanced age.
    • Preexisting congestive heart failure.
    • Persistent atrial standstill. Artificial cardiac pacing provides temporary improvement but the myocardial fibrosis often progresses into the ventricular myocardium, leading to systolic dysfunction and/or failure of pacemaker capture within 12 to 18 months.

    Garrod L, Rush JE: Transvenous pacing, in Bonagura JD (ed): Kirk’s Current Veterinary Therapy XIII. Philadelphia, WB Saunders, 2000, pp 197–200.

    Miller MS, Tilley LP, Smith FW, Fox PR: Electrocardiography, in Fox PR, Sisson DD, Moise NS (eds): Textbook of Canine and Feline Cardiology, ed 2. Philadelphia, WB Saunders, 1999, pp 67–105.

    Moise NS: Diagnosis and management of canine arrhythmias, in Fox PR, Sisson DD, Moise NS (eds): Textbook of Canine and Feline Cardiology, ed 2. Philadelphia, WB Saunders, 1999, pp 371–375.

    Oyama MA, Sisson DD, Lehmkuhl LB: Practices and outcome of artificial cardiac pacing in 154 dogs. J Vet Intern Med 15(3):229–39, 2001.

    Rishniw M, Thomas WP: Bradyarrhythmias, in Bonagura JD (ed): Kirk’s Current Veterinary Therapy XIII. Philadelphia, WB Saunders, 2000, pp 719–725.

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