Bradycardia

By | 2013-08-04

Symptomatic bradycardia results from problems of impulse generation in the sinus node and / or its conduction from the atria to the ventricles. Both of these processes are influenced by the autonomic nervous system with the parasympathetic system slowing and the sympathetic system accelerating impulse generation and conduction.

Non-cardiac causes of bradycardia

Sinus bradycardia is often a normal finding in athletic dogs (50 bpm or below) and is rarely associated with clinical signs. Even in dogs showing signs of vague illness, such as lethargy, which demonstrate mild sinus bradycardia, use of drugs which increase the heart rate (for example atropine) does not usually improve their behaviour. Profound symptomatic bradycardia may be caused by a number of factors which do not involve organic cardiac disease, some of which are shown in site. In many cases It is an alteration in the balance between parasympithetic and sympathetic tone to the heart which results in bradycardia so that therapy with antimuscarinic drugs (particularly where vagal tone is raised) or beta-adrenoceptor agonists is indicated to increase heart rate together with supportive therapy such as intravenous fluids and warmth. It is important to consider the underlying cause before using such symptomatic therapy as it may not always be indicated. For example, use of atropine to control bradycardia following the administration of an alpha2-adrenoceptor agonist may potentiate the transient hypertension which results after administration of such drugs to dogs and cats. Administration of beta-adrenoceptor agonists to increase the heart rate in a dog with bradycardia due to digoxin toxicity would increase the potential for ventricular tachycardia to develop. Thus, where possible, specific therapy should be administered based on the diagnosis of the underlying cause. These extrinsic factors should be considered before diagnosing the cause of symptomatic bradycardia as being due to organic disease of the sinoatrial node or of the conducting pathways in the heart.

Symptomatic bradycardia associated with organic cardiac disease

Sick sinus syndrome

This term is used to describe idiopathic disorders of the sinoatrial node, where the animals show signs of intermittent sinus arrest, sinoatrial block or sinus bradycardia. The subsidiary pacemakers fail to generate adequate escape rhythms. Some cases also show intermittent supraventricular tachyarrhythmias which may contribute to the clinical signs. This is a heterogeneous and imprecisely defined group of conditions rather than a single disease. Miniature schnauzers, pugs and dachshunds have been reported as presenting with this syndrome but it has also been seen in mixed breed dogs. In the management of this condition, it is important to manage the bradycardia first before treatment of the tachycardic episodes can be undertaken safely.

Persistent atrial standstill (silent atrium)

In persistent atrial standstill the sinus node fails to generate electrical impulses and the heart rate is governed by supraventricular, functional or ventricular escape beats. This condition is rare in dogs and cats and should be distinguished from the potentially reversible sinoventricular rhythm which accompanies severe and life-threatening hyperkalaemia.

Atrioventricular block

Failure or delay in the conduction of the sinoatrial impulse may be classified as first, second (Mobitz type I and II) or third degree atrioventricular block. In some cases, heart block can be intermittent and therefore more difficult to diagnose without the use of a continuous ambulatory ECG. First degree atrioventricular block and Mobitz type 1 seconddegree atrioventricular block are common in the dog and rarely signify intrinsic disease of the conducting system. They are easily abolished following exercise or atropine administration (0,02-0.04 mg kg-1 i.m. or i.v.). Atropine may cause an initial increase in the severity of the block (by a central action) but within 10-15 min sinus rhythm results. By contrast, in the cat even low-grade heart block is an abnormal finding and warrants further investigation.

Idiopathic persistent high-grade second-degree and complete (third degree) atrioventricular block occur in middle-aged or older dogs and are often associated with clinical signs. These may consist of weakness, exercise intolerance and syncope. Idiopathic third degree atrioventricular black has been reported in the dog in association with acquired myasthenia gravis. If obvious organic heart disease can be identified, the prognosis is much worse than for idiopathic cases where no obvious pathological process can be detected. Drug toxicity (calcium channel blockers, digoxin, beta-adrenoceptor antagonists) or electrolyte disturbances (hyperkalaemia) should be ruled out as possible causes of atrioventricular block.

Medical management of symptomatic bradycardia due to organic heart disease

Pacemaker implantation is the only long-term solution to animals exhibiting high-grade second-degree or complete atrioventricular block, persistent atrial standstill, and many cases of sick sinus syndrome. In an emergency, heart rate can be best increased by using beta-adrenoceptor agonists such as isoprenaline (10 ng kg-1 mm-1) or dopamine (2-10 μg kg-1 min-1), given by continuous intravenous infusion. An oral dose rare of isoprenaline has been described (5-10 mg three to four times daily) but there is less scope for the clinician to control the effects of the drug. Dopamine is the preferred choice since it lacks the profound peripheral vasodilatation in skeletal muscle which occurs following isoprenalinc administration. Although these drugs can be life-saving in severe cases before pacemaker implantation, their use can be associated with the occurrence of ventricular tachyarrhythmias. These should be controlled by stopping the infusion of the drug and not by the administration of drugs which suppress ventricular arrhythmias (for example lignocaine) since such drugs will suppress the escape rhythms which maintain some cardiac output in these animals.

Antimuscarinic drugs often fail to increase the heart rate in animals with heart block and atrial standstill since high vagal tone is not involved in the pathogenesis of these arrhythmias- Junctional escape rhythms may sometimes increase in rate when antimuscarinic drugs are used and some dogs with sick-sinus syndrome can be managed chronically with such drugs. Test doses of atropine will demonstrate those cases where such therapy may be worth trying. Oral preparations of antimuscarinic agents include propantheline bromide (7.5-15 mg three times daily for dogs). In dogs with both bradycardia and tachycardia, administration of antimuscarinic drugs may worsen the episodes of Tachycardia as these drugs increase conduction through the atrioventricular node. In these cases, the bradycardia should be managed by the use of a pacemaker and drugs which suppress the supraventricular tachycardia can then be safely employed. The use of pacemakers to treat symptomatic bradycardias has been extensively covered by others.