Chapter 145 Disorders of Cardiac Rhythm
Cardiac arrhythmias include disorders of cardiac impulse formation, conduction, rate, and regularity. Terms such as dysrhythmia, ectopia, and ectopy also are used to identify arrhythmias. Cardiac arrhythmias can be benign and clinically insignificant, or they can cause clinical signs. They can even progress to malignant arrhythmias that lead to heart failure, syncope, or sudden death.
Causes of cardiac arrhythmias include heart disease and disorders involving the autonomic nervous system, endocrine system, electrolytes, and other body systems. Anesthetic agents and other drugs can precipitate rhythm disturbances. Cardiac arrhythmias are diagnosed and classified electrocardiographically; see Chapter 144 for additional pertinent information regarding electrocardiography. A summary of the clinical pharmacology of drugs used in the treatment of congestive heart failure (CHF) is found in Chapter 146.
ETIOLOGY
• Cardiac arrhythmias are classified in Table 145-1. They occur with congenital or acquired cardiac disease or systemic disorders (Table 145-2).
• Arrhythmia variation in animals with cardiac or systemic disorders may be explained by the complex interactions among cardiac cell transmembrane potentials, the autonomic nervous system, and body fluids.
Table 145-1 CLASSIFICATION OF CARDIAC ARRHYTHMIAS
Table 145-2 CAUSES OF CARDIAC ARRHYTHMIAS
Adapted from Miller MS, Tilley LP: Treatment of arrhythmias and conduction disturbances. In Miller MS, Tilley LP, eds.: Manual of Canine and Feline Cardiology. Philadelphia: WB Saunders, 1995, with permission.
Cardiac Causes in Dogs
Heredity (genetics not documented in all cases)
Atrial and/or ventricular arrhythmias
MECHANISMS
• The normal cardiac impulse is generated automatically in the sinus node and is spread through the atria rapidly and sequentially via the His bundle, the bundle branches, and the intraventricular conduction system to the ventricular myocardium.
• The normal atrioventricular (AV) node serves as a bridge between the atria and the ventricles and slows the cardiac impulse prior to rapid impulse conduction through the ventricles.
• Enhanced automaticity in sinus node or subsidiary pacemaker cells can generate tachycardias or ectopic rhythms. Such activity may be influenced by sympathetic activity.
• Triggered activities are common causes of ectopic rhythms and tachycardias. Early or late afterdepolarizations follow a previously driven (sinus) depolarization. The premature impulses occur when the cell spontaneously depolarizes during or just after repolarization.
• Reentry, a common arrhythmia mechanism, typically is caused by functional dissociation of cardiac tissue, a unidirectional block in one pathway, and slowed conduction in the other pathway. The impulse then returns to the origination point by retrograde conduction through the unidirectionally blocked pathway.
• Electrophysiologic mechanisms, arrhythmia manifestations and accompanying clinical signs and symptoms may vary widely among dogs with specific inherited cardiac diseases. Arrhythmogenic mechanisms can be modified (for better or for worse) by autonomic activity, heart rate, and many cardiac and non-cardiac drugs.
DIAGNOSTIC APPROACH
Systematic Evaluation of the Electrocardiographic Strip
• Are P waves present?
• Yes. Do the P (atria) waves occur at regular or irregular intervals? What are the height, width, and direction?
• Do the QRS (ventricular) complexes occur with regularity and uniformity? What is their morphology? If wide and bizarre, is this due to a ventricular arrhythmia or caused by a premature atrial impulse that is aberrantly conducted, or is bundle branch block evident?
• What is the relationship between the P waves and the QRS complexes? Is the relationship consistent?
SUPRAVENTRICULAR RHYTHMS
Sinus Arrhythmia
Definition
• A wandering pacemaker (a change in the morphology of the P wave due to a change in pacemaker location or conduction) is often present.
Etiology and Clinical Significance
• Sinus arrhythmia is a normal rhythm variation in the resting dog, often correlated with varying levels of sinus node vagal tone, which changes with respiration (decreased vagal tone and increased heart rate during inspiration).
Sinus Bradycardia
Etiology and Clinical Significance
• Sinus bradycardia may be a normal physiologic rhythm variation resulting from high levels of resting vagal tone.
• Hypothyroidism, sinus node disease (sick sinus syndrome), elevated cerebrospinal fluid pressure, and hypothermia are among the pathologic causes of sinus bradycardia.
• Drugs that can cause a sinus bradycardia include acepromazine, xylazine, other alpha2-agonists (e.g., medetomidine), narcotics, digoxin, beta-blockers, diltiazem, pilocarpine, and general anesthetics.
Treatment
• When correlated with signs of weakness or syncope, an atropine response test should be performed (0.04 mg/kg IM) followed by an electrocardiogram (ECG) in 15 to 30 minutes.
• If there is an increase in the cardiac rate following atropine administration, the animal may benefit from oral anticholinergic agents (Table 145-3).
• A poor clinical response to atropine suggests the need for a temporary or permanent cardiac pacemaker in symptomatic animals.
Sinus Block and/or Sinus Arrest (Fig. 145-1)
Definition
• A primary disorder of the sinus node resulting in lack of generation of the cardiac impulse or its poor propagation across surrounding tissue.
• It is not possible to distinguish between sinus block and sinus arrest in dogs because of the normal variation in the R-R interval (sinus arrhythmia).
• There is a normal P wave for each QRS complex with a pause equal to or greater than 2 times the normal R-R interval.
Etiology and Clinical Significance
• Sinus arrest may be consistent with an increase in vagal tone (e.g., ocular pressure, irritation of the vagus nerve, brachycephalic breeds, or respiratory disease).
• Diseases of the atria (including fibrosis, cardiomyopathy, and neoplasia) and drug toxicity (e.g., digitalis, propranolol, quinidine, xylazine, and acepro-mazine) may result in sinus arrest.
Sinus Tachycardia
Etiology and Clinical Significance
• Sinus tachycardia may be a normal physiologic rhythm resulting from high sympathetic tone occurring with exercise or excitement.
• Sinus tachycardia may also occur with conditions such as stress, anxiety, pain, shock, fever, anemia, CHF, hyperthyroidism, and pheochromocytoma.
Electrocardiographic Differentials
• Other supraventricular tachyarrhythmias confused with sinus tachycardia include paroxysmal (atrial or AV junctional) tachycardia, atrial flutter with 2:1 AV block, and ventricular tachycardia when sinus tachycardia is associated with wide QRS complexes.
Atrial Premature Complexes (Fig. 145-2)
Definition
• There is usually an abnormal P’ wave (premature P wave) followed by a normal QRS complex. The P’-R interval of the APC may vary from the sinus rhythm P-R interval. The P’ wave may have various morphologies and may be fused with the T wave of the preceding beat.
• The P′ wave may occur so early in the cardiac cycle that the AV conduction system will be refractory and the impulse will not be conducted to the ventricles (e.g., APC with physiologic AV block).
• The pause following the APC is often less than fully compensatory because of premature depolarization and resetting of the sinus node. Full compensatory pause occurs when the R wave-to-R wave interval surrounding the APC is equal to two normal R-R intervals.
• The QRS complex is usually normal, but the intraventricular conduction system may be, in a relative or absolute refractory period, causing a bizarre (abnormal shape or direction) QRS complex. This abnormality is termed an APC with aberrant ventricular conduction.
Etiology and Clinical Significance
• APCs often indicate underlying cardiac disease (e.g., chronic valvular fibrosis, cardiomyopathy, congenital defect, or cor pulmonale) resulting in atrial enlargement.
Electrocardiographic Differentials
• Sinus rhythm with APCs may be confused with marked sinus arrhythmia and ventricular premature complexes during auscultation, and with ventricular premature complexes on the ECG, when APCs are conducted with aberrant ventricular conduction.
Atrial Tachycardia (Figs. 145-3 and 145-4)
Definition
• Atrial tachycardia indicates rapid, abnormal impulses originating from an atrial site other than the sinus node.
• The atrium and/or AV junctional areas may be involved in a reentrant circuit that allows the impulse to restimulate the atrium, as well as to pass to the ventricles. (A vagal maneuver may abolish this arrhythmia.)
• An abnormal automatic focus in the atrium may also be responsible for this arrhythmia. (A vagal maneuver will cause AV block but not abolish the atrial tachycardia.)
• The heart rate is >140 to 180 bpm in dogs and >240 bpm in cats, in which it often approaches 300 bpm.
• There is a P′ wave for each QRS complex, although the P′ wave is usually of different morphology than the sinus P wave. The P-R interval is constant.
• The P′ wave may not be evident because it may be fused with the preceding T wave or occur simultaneously with the preceding QRS complex.
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