Symposium on Cardiology Diagnosis and Treatment of Cardiac Arrhythmias Sheila M. McGuirk, D.V.M., M.S.,* and William W. Muir, D.V.M., Ph.D.* Cardiac arrhythmias are more common in horses than in other domestic animal species.!° The prevalence of cardiac arrhythmias without any other signs of heart disease may be greater than 25 per cent.25.16 When accompanied by other cardiac problems, such as a loud cardiac murmur, the prevalence of arrhythmias may be as high as 40 per cent.?5"5 Unlike most other domestic animal species, the horse may have arrhythmias at rest that are considered benign or functional.!2".7 Tt is important, therefore, to distinguish patho- logic from benign or physiologic arrhythmias. In addition, a distin tion should be made between primary and secondary cardiac arrhyth- mias. The treatment of arrhythmias that have arisen from pathologie conditions of the heart such as myocarditis, valvular disease, con- duction system abnormalities, and pericarditis (primary arrhythmias) will be considerably different than treatment instituted for arrhyth- mias due to vagal tone, excitement, fever, electrolyte imbalances, or toxemia (secondary arrhythmias). In this article, the diagnosis and treatment of cardiac arrhythmias (including conduction system disorders) of horses are reviewed; a clinical approach to the problem of cardiac arrhythmia is taken. The authors consider information obtained from the history and findings of the physical examination that are pertinent to this problem and emphasize the diagnosis of arrhythmias based on auscultation. Infor- mation that can be used to distinguish physiologic from pathologie and primary from secondary arrhythmias is discussed as well as the effects of exercise. Distinctive electrocardiographic features of each arrhythmia are presenced, but the reader is encouraged to refer to * Diplomate, American College of Veterinary Intemal Medicine; Assistant Professor, De- partment of Medical Sciences, University of Wisconsin School of Veterinary Medi- cine, Madison, Wisconsin + Diplomate, American College of Veterinary Anesthesiologist: of Veterinary Clinical Sei Medicine, Columbus, Ohio Chairman, Department ices, The Ohio State University College of Veterinary Veterinary Clinker of North America: Equine PructicoVul. {, No. 2. August 1985. 353,354 Suwa M. MeGuine anp Winuias, W. Moin the references for an in-depth electrocardiographic description of each condition 2°-'!-1427 Criteria for treatment of cardiac arrhyth- mias in the horse are offered and appropriate drugs are suggested for instances in which therapy is appropriate. The reader is also referred to the article “Equine Heart Di: An Overview” for an overall perspective of cardiac arrhythmias. HISTORY The information obtained from a good history may be yery im- portant in establishing a diagnosis when a cardiac arrhythmia is present. The use of the horse and the frequency and duration of exercise must be ascertained. The duration of the problem and the etiologic relationship between onset of signs and associated changes in feed, environment, exercise, performance, attitude, or recent ill- ness are important. Some cardiac arrhythmias are paroxysmal, so it should be determined if signs are constant or intermittent. If signs are intermittent, it is helpful to establish if there is any relationship between the onset of signs and exercise, excitement, or rest. As with most clinical problems involving horses, the owner should be ques- tioned about recent wormings and vaccinations. The most common complaints that accompany cardiac arrh: mias are poor performance and exercise intolerance.*5°!.!>!6 Horses with lameness or respiratory disease may present with similar histories, but if severe signs of incoordination, weakness, collapse, or fainting have been noted, one should consider cardiac arrhythmias. Exertional dyspnea, cough, respiratory tract infections, and epistaxis can accompany cardiac arrhythmias. Signs of congestive heart failure, such as subcutaneous edema and jugular venous distention, may also be presenting complaints in horses with cardiac arrhythm 26 PHYSICAL EXAMINATION Successful diagnosis and treatment of cardiac arrhythmias are dependent on a complete physical examination. Emphasis is naturally placed on the cardiovascular examination, but the distinction be- tween primary versus secondary and the physiologic versus patho- logic arrhythmias may rest on evaluation of other body systems. Prior to handling of the horse, inspection from a distance can yield valuable information about the patient. One should note the level of anxiety, excitement, sweating, dyspnea and presence of a jugular venous pulse. Rectal temperature, respiratory rate, and heart and pulse rates should be obtained with a minimum amount of han- dling or restraint of the horse. Color of the mucous membranes, capillary refill time, and hydration status should be evaluated. Ar- rhythmias are occasionally observed in dehydrated or toxic horsesCanpiac ARRUYTIMIAS 355 that have electrolyte or acid base abnormalities associated with esx- tracardiac dise: processes, The pectoral and ventral abdominal areas should be palpated for the presence of subcutaneous edema. When arrhythmias accompany valvular heart disease, signs of conges- tive heart failure are more common. Both sides of the thorax should be palpated in order to locate and determine the strength of the cardiac impulse. The impulse should be strongest in the fifth intercostal space at the level of the costochondral junction on the left side and between the third and fourth intercostal spaces just above the level of the sternal border on the right side. When cardiac arrhythmias are associated with cardiac enlargement, the cardiac impulse may be displaced caudally. Abdom- inal ascites may push the cardiac impulse forward in severe conges tive heart failure. The strength of cardiac impulse will be increased with excitement, exercise, and with the first heart heat after a pause dropped beat, or extrasystole. The arterial pulse should be evaluated. Simultaneous ausculta- tion and palpation are helpful to determine heart rate cardiac rhythm. The transverse facial and submaxillary arte: a most accessible to palpation. For simultancous auscultation and pal- pation, the median or posterior digital arteries may be more conve- nient. The strength of the arterial pulse is influenced by stroke yolume and peripheral vascular resistance. Cardiac arrhythmias char- acterized by a fast rate (usually greater than 50 beats per minute) and reduced stroke volume may be associated with a weak arterial pulse.*" Bradyarrhythmias are often associated with an arterial pulse of increased strength. Arterial pulse strength will vary with irregular rhythms such as atrial fibrillation, sinus arrhythmia, and second-de- gree atrioventricular (AV) block. Long diastolic pauses are generally followed by an arterial pulse of increased strength. Very rapid heart rates, such as those encountered with congestive heart failure, ven- tricular tachycardia, or atrial fibrillation, may be associated with a pulse deficit. Physical examination of the horse with a cardiac arrhythmia should also include close scrutiny of the jugular venous pulse, A detailed description of the venous pulse waves has been provided in other publications*” and in the article “Evaluation of the Equine Cardiovascular System.” Arrhythmias that are atrial in origin will most likely be manifested as abnormal jugular venous “a” waves, which occur late in diastole and can be Visualized just before palpa tion of the cardiac apex beat. Cannon “a” waves may be evident with third-degree AV block, ventricular tachycardia, nonconducted atrial extrasystoles, and occasionally with second-degree AV block. Giant “a” waves may be seen if right ventricular extrasystoles are associated with a thickened myocardium such as with chronic obstructive pul- monary disease. The absence of atrial waves is a feature of atrial fibrillation. Abnormal jugular vein filling may be found with arrhyth- mias characterized by long diastolic periods such as second-degree AV block, sinus block, or sinus arrest.356 Suma M. McGurk ano W Auscultation reful ause The detection of cardiac arrhythmia is based on c: tation of the thoracic cavity with a quality stethoscope in an environ- ment that allows undistracted listening. It is important to note heart rate (slow, normal, or fast), b: rhythm (regular or irregular), the heart sounds that are heard, and split sounds if present. The presence of extra sounds and abnormal pauses should be noted. The normal heart rate for the horse is 26 to 50 beats per minute.'*!° Four heart sounds may be audible in the normal horse under ideal listening conditions. The first (S,) and second (S,) heart sounds are more easily identified than the third (S,) and fourth (S,) heart sounds, and should be identified in all horses. The first heart sound is generated at the onset of systole (onset of the QRS complex) by AV valve (tricuspid and mitral) closure. The second heart sound is attributed primarily to the closing of the semilunar valves and a small component may be due to the opening of the AV valves and occurs near the end of the T wave. Splitting of S) is relatively common in the horse and is usually associated with the respiratory cycle. Both inspiratory and expiratory splitting have been reported and either the aortic or pulmonic valye can close first in normal horses.*:!"* The third heart sound is a low-intensity sound that occurs shortly after Sy in early diastole and is associated with rapid ventricular filling. The fourth heart sound occurs late in diastole after the P wave and just prior to S$, and is due to atrial contraction. For a detailed review of the origin of heart sounds, the reader should consult other sources." 1° The first heart sound is a low-intensity sound heard best over the mitral valve area. Either an increase or variability in the intensity of S, ure identifying features of some cardiac arrhythmias. The inten- sity of S, is increased in pree such as the Wolff Parkinson-White syndrome.™!' y of S, is also increased immediately after ventricular extrasystoles and with atrial extrasys- toles that are followed closely by or superimposed on the next ven- tricular contraction. The intensity of S$; may be extremely variable with atrial fibrillation (Fig. 1) because of the inconstant time interval for ventri + Figure 1. Base-apex electrocardiogram recorded from « horse with atrial brillation. Note the irregular interval between QRS complexes, which accounts for the irregular rhythm and variable intensity of S,. There are no P waves present, which is the reason that S, is not heard on auscultation. Heart rate is 40 to 50 beats per minute. Paper speed is 25 mm per second.Canoiac Annnyriytias 357 rate may allow insufficient time for ventricular filling, thereby di- minishing the intensity of S, and producing a pulse deficit. The second heart sound (S;) is louder than S, and is heard best at the heart base. The S,-S) interval is constant in normal horses. The cardiac arrhythmias that have normal S,-S, intensities and timing but that are characterized by slow rates (less than 26 beats per minute) are sinus bradycardia (Fig. 2A) and third-degree AV block (Table 1). A normal §,-S, relationship associated with a fast heart rate (more than 50 beats per minute) could be either sinus, ventricular, (Fig. 3) or supraventricular tachycardia (Fig. 2B). The diagnosis can be made by electrocardiogram. The cardiac arrhythmias in which S; and S, are evident but the S,-S, intervals are irregular are listed in Table 2. The irregular rhythms that are slow (less than 26 beats per minute) are most com- monly sinus arrhythmia (Fig. 4), sinus arrest, sinus block, or second- degree AV block (Fig. 5). The irregular cardiac rhythms that are more commonly associated with normal or fast heart rates are atrial fibril- lation (see Fig. 1), atrial premature beats (Fig. 6), and ventricular premature beats (Fig. 7). Although S, and S, are more difficult sounds to distinguish by auscultation, information about them may help to establish the di- agnosis of some cardiac arrhythmias. Atrial fibrillation is character- ized by an irregular rhythm and heart sounds of variable intensity (S, and Sq). It can be distinguished from other irregular rhythms that are supraventricular in origin because there is no atrial contraction and, therefore, no S, (see Fig, 1). Auscultation of an isolated § , during Gece n Figure 2. Base-apex electrocardiogram recorded from two different horses. A, Sinus bradyeaydia (heart rate 16 beats per minute) in « horse with a late systolic cardiac murmur and no other signs of heart disease. $, (atrial contraction) and S, (ventricular filling) were clearly audible because of the slow rate, B, Sinus tachycardia (heart rate 100 beats per mi i a horse with septic shock. There was a loud diastolic heart sound 1 Summation) in this horse owing to the fast heart rate, Paper speed is 25358 Sueica M, McGuing ann Wittian W, Mun Table 1. Cardiac Arrhythmias of Horses Classified According to the Effect on Heart Rate suow NonMAL rast (Less THAN 26 apa) (26-50 west) (MORE THAN 50 xs) Sinus bradycardia Sinus arrhythmia Atrial fibrillation Sinus arrhythmia Atrial fibrillation Supraventricular Sinus block First-degree AV block tachyeardia Sinus arrest Second-degree AV block Ventricular Second-degree AV block Atrial premature beats tachycardia ‘Third-degree AV block Ventricular premature beats Atrial fibrillation Idioventricular tachycardia Preexcitation Wandering pacemaker Bundle branch block a pause in the normal cardiac rhythm is characteristic of second- degree AV block in which atrial contractions are not always conducted to the ventricles. Variation in the $,-5, interval may be found with sinus arrhythmia and third-degree AV block, a cardiac arrhythmia that is relatively rare in the horse. Increased intensity of S, is difficult to distinguish from normal in the horse but may be associated with ventricular arrhythmias in horses with myocarditis or ventricular failure. Summation of §, and S, (summation gallop) produces a loud diastolic sound that may be louder than either $, or $, and can be heard with cardiac arrhythmias during elevated atrial rates caused by supraventricular tachycardia, or AV dissociation. Variations in the normal heart sounds (S, and $,) may also alert one to a class of cardiac arrhythmia associated with changes in the conduction system (wandering pacemaker, first-degree AV block, bundle branch block, and preexcitation syndromes), the diagnosis of which is made by electrocardiography. Auscultation of a late atrial sound (S,') may suggest that first-degree AV block is present. Patho- logic splitting of either S, or Sy may be associated with bundle branch block, an arrhythmia that is extremely rare in the horse. Increased intensity of S, occurs owing to the short PR interval in sinus tachy- cardia and with preexcitation syndromes. Figure3. Base-apes clectrocardiogram recorded from a horse with ventricular tachy- cardia, Heart rate is 100 beats per minute. Only $, and $; could be heard when this horse was auscultated. Paper speed is 25 mm per second.Canpiac ARRHYTHMIAS 359 Table 2, Cardiac Arrhythmias Characterized by an Irregular Rhythm RUVTHM WITH OSDERLYING KEGULARITY TRULY IRREGULAR BEYTHSI Sinus bradycardia (with escape beats) Sinus arrhythmia Second-degree AV block Sinus arrest Sinus block Atrial fibrillation Atrial premature beats Ventricular premature beats The cardiac arrhythmias that are characterized by auscultation of extra sounds are listed in Table 3. Premature beats (see Figs. 6 and 7) occur earlier than expected, may produce a loud diastolic summation sound, have variable intensity $,, and are followed by a pause in the otherwise regular rhythm. Escape beats occur after a pause in the normal rhythm and are usually junctional or ventricular in origin, so only S, and S, are auscultated with escape beats. The effect of exercise in cardiac arrhythmias is a useful diagnostic tool. 16 The benign or physiologic arrhythmias that are thought to be attributable to vagal tone should disappear with exercise. When sinus arrhythmia, sinus arrest, sinus block, sinus bradycardia, wan- dering pacemaker, first-degree AV block, and second-degree AV block persist immediately after vigorous exercise, excitement, or ad- Figure 4, Base-apex electrocardiogram recorded from a horse with sinus ar thythmia. Two different appearing P waves as present, indicating the presence of a wan- dering pacemaker. This rhythm was slightly irregular snd S,-S, and S, could be identified on auscultation Figure 5. Base-apex electrocardiogram recorded from a horse with second-degree atrioventricular block. The underlying thythms are sinus arrhythmia and a wandering pacemaker, The heart rate is irregular and 30 beats per minute, During the pause be- tween the fourth and fifth QRS-T complex, an isolated $, could be heard. Paper speed is 25 mm per second.360 Sueia M. McGurk avo Wituiaw W. Mui Figure 6, Base-ancx electrocardiogram recorded from a horse with a premature atrial depolarization (third QRS complex fiom the left). The pause is not compensatory following the premature beat. Paper speed is 25 mm per second. owes SPOOR ee ees tt Figure 7. Base-apex electrocardiogram recorded from a horse with ventricular pre- mature depolarizations (VPD), At times (A). the VPD is interpolated between two normal sinus beats. At other times (B), the VPD is followed by a compensatory pause. Paper speed is 25 mm per second. ministration of atropine, they are usually considered abnormal. Cer- tain arrhythmias become worse during or immediately after exercise; these are pathologic. Atrial and ventricular extrasystoles, for ex- ample, may become more frequent with exercise. Atrial fibrillation and ventricular tachycardia are often exacerbated by exercise; the heart rate becomes abnormally fast, with rates exceeding 200 beats per minute. DIAGNOSIS Electrocardiography The diagnosis of many cardiac arrhythmias in the horse can be made with some degree of assuredness by auscultation, as discussed in the preceding section. Furthermore, the effect of exercise oftenCanpiac Agniyrinias 361 Table 3. Cardiac Arrhythmias of Horses Characterized by Auscultation of Long Pauses or Additional Sounds ADDITIONAL SOUNDS LoNe pauses Atrial premature beats Sinus arrest Ventricular premature beats Sinus block Sinus bradveardia (with eseape heats) Ventricular premature beats can be used to distinguish arrhythmias like sinus arrhythmia, which are due to vagal tone, from pathologic arrhythmias. The electrocar- diogram (ECG) is necessary to confirm the clinical diagnosis of the cardiac arrhythmia, however. Many cardiac arrhythmias with similar auscultatory findings cannot be readily distinguished without the aid of an ECG. For example, premature beats that are followed by a compensatory pause may be supraventricular or ventricular in origin Atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia are difficult to distinguish by auscultation alone. The ECG is the only way one can make a diagnosis of wandering pace- maker, first-degree AV block, preexcitation syndrome, bundle branch block, or other cardiac dysrhythmias that are a result of conduction system abnormalities. The ECG is employed in making therapeutic decisions. It is necessary to know the frequency and location of extrasystoles in the cardiae cycle and to assess conduction abnormalities by the ECG before one chooses therapy. An important use for the ECG is mon- itoring of the patient during drug therapy for arrhythmias. The ECG can be used to determine toxicity during repeated doses of antiar- rhythmic drugs. The ECG can be obtained using a standard limb lead system.!' Small changes in the position of the limbs, shivering, and shifting of weight will decrease the quality of the tracing obtained. For this reason, a simple monitor lead is more frequently employed for the assessment of cardiac arrhythmias.!!--'5'5 One such monitor lead is referred to as the base-apex lead and is recorded with the right arm electrode attached to the skin over the jugular furrow two thirds of the way down the neck. The left arm electrode is applied just behind the left elbow, where the apex beat of the heart is palpable. The ground electrode can be attached at any body surface site remote from the heart. The advantages of this monitor lead are its ease of application and the inscription of large wave forms that are relatively immune to changes in limb position. The ECG diagnosis of arrhythmias originating in the sinus node is relatively simple, for a P wave (atrial activation), QRS complex (ventricular activation), and T wave (ventricular repolarization) will be present for every beat. Sinus bradycardia and tachycardia (see Fig. 2) are characterized by normal wave forms, regular P-P and R-R intervals, and heart rates of less than 26 or faster than 50 beats per min, respectively. Sinus arrhythmia is characterized by a slow to normal rate, normal P-QRS-T relationships, variable P-P and R-R362 Suena M, McGuirk aso Wittiam W. Mont intervals, and cyclic variation in the heart rate that may or may not be associated with changes in the respiratory cycle (see Fig. 4). Both sinus block and sinus arrest have slow to normal rates and normal P-QRS-T complexes. Both arrhythmias exhibit long, pauses during which no P waves are present but junctional or ventricular escape beats may occur. The P-P and R-R intervals may be normal (or progressively decrease) prior to the pauses, or the underlying rhythm may be a sinus arrhythmia or wandering pacemaker, which produces variability in these intervals. The pauses in sinus block are equal to two of the previous P-P intervals, whereas the pauses in sinus arrest are greater than two P-P intervals. Wandering pacemaker is a diagnosis made by inspection of the ECG. A diagnosis of wandering pacemaker is made when the P waye has a variable configuration, and minor changes are noted in the P- R interval (see Fig. 4). There is a high prevalence of this arrhythmia in horses.*!0445.1527 Jt is generally considered to be normal. Ventricular preexcitation, by itself, may be a benign arrhythmia. This diagnosis is made when a “markedly shortened P-R interval is present with either normal or abnormal ventricular activation. Al- though somewhat variable with different horse breeds, a P-R interval of Jess than 0.22 seconds is characteristic for preexcitation. The QRS configuration depends on the location of the accessory pathway, the intra-atrial impulse conduction time, the accessory pathway conduc- tion time, and the AV conduction time.*!'*! The QRS complex can be abnormally widened and slurred by the presence of a delta wave (Wolff-Parkinson-White syndrome), of normal duration with an ab- normal activation pattern, or normally activated (Lown-Ganong- Levine syndrome).*"*#! The significance of this arrhythmia in horses has not been established when paroxysmal supraventricular tachy- cardia is not a feature.257%10182129 Atrial arrhythmias are characterized electrocardiographically by premature, undetectable, or variable P waves, flutter, or fibrillation waves. In general, the appearance of the QRS and T waves are rel- atively normal. The ST-T wave may be slightly altered by superim- posed (buried) P waves. The ECG findings with atrial or junctional (supraventricular) premature depolarizations are a normal underlying rhythm with abrupt interruptions of the normal R-R interval by pre- mature complexes that have normal-appearing QRS complexes. (see Fig, 6). There usually is an ectopic P wave (positive or negative) ed with the premature beat, but it may be buried in the previous QRS, T wave, or ST-T segment and, therefore, may be difficult to detect. If the sinus node is penetrated and reset by the premature impulse, a less than compensatory pause will follow. Supraventricular tachycardia occurs either as a sustained or par- oxysmal arrhythmia. The ECG characteristics are a rapid heart rate (short R-R intervals), with regular R-R intervals and normal QRS-T complexes. If there is aberrant ventricular conduction, the QRS-T complexes might be bizarre in shape and slightly longer in duration,Canpiac Arnnyrrivias 363 resembling complexes of ventricular origin. The P waves, when they can be detected, may be positive, negative, or a combination of both. The ECG diagnosis of atrial fibrillation is easily made from the distinctive combination of features of irregular R-R intervals, absence of P waves, appearance of fibrillation waves (f waves) in place of P waves, and slight variability in QRS-T configuration from beat to beat (see Fig. 1). The QRS-T complexes, although variable in appeara are supraventricular in origin. After long pauses between ventricul beats, the Q-T interval and T-wave amplitude may be reduced. The appearance and frequency of f waves are variable in horses and, de- pending on the ECG lead used, may be difficult to detect.*! When the baseline undulations are coarse and regular, the ratio of flutter waves to QRS complexes may be consistent, and the arrhythmia is referred to as atrial flutter.5!” Variations of impulse conduction through the atrioventric- ular node are the most frequently diagnosed arrhythmias in horses. 25162" First-degree AV block is an ECG diagnosis, the cri- teria for which are somewhat variable depending on the breed of horse and the person determining the criteria. '"''?" The ECG fea- tures are a normal heart rate and normal P-QRS-T configuration and relationships, In general, a P-R interval greater than 0.44 seconds a horse with regular sinus rhythm is considered first-degree AY block."”""7 Second-degree AV block with a slow or normal heart rate is the most commonly reported rhythm disturbance of normal horses. being present in 12 to 18 per cent of horses.!25!!S The P-QRS-T complexes are normal in appearance and, except during the pauses of blocked conduction, their relationship is normal. The basic rhythm is almost always sinus arrhythmia, so the R-R intery ariable even when blocked be: re not present. Mobitz type I (Wenckebach) second-degree AV block is more common in horses than is Mobitz type I] block.!!4:'527 The relationship between the gradually in- creasing R-R interval and the dropped beat is variable in type 1 block, but usually the longest P-R interval precedes the dropped beat." © The increment in the P-R interval may be greatest in the second postblock beat, which may produce a paradoxic shortening of the R- R interval prior to the dropped beat. In some horses, the P-R interval progressively shortens until the P wave is blocked. The distinguishing feature of either type of second-degree AV block is the presence of pauses in the established rhythm: conducted P waves are visualized during these pauses. This rhythm is considered pathologic if a large number of P waves are not conducted (high-grade block) or if the P- R interval is consistently greater than 0.6 seconds. Third-degree AV block is a pathologic arrhythmia. In some the block may be temporary owing to interference with a faster nodal or ventricular pacemaker rather than conduction system dis~ ease. The ventricular rate with anatomic disruption of the atrioven- tricular conduction system is usually slow, the QRS-T configuration is normal (idionodal pacemaker) or widened (idioventricular pace-364 Sema M. McGuirk ayo Wittiam W. Muti maker), and the R-R interval is regular. The P waves are normal but nonconducted. The P wave rate is usually more rapid than the ven- tricular rate, the P-P interval is usually regular, but there is no con- sistent relationship between the P and QRS-T complexes. Ventricular arrhythmias of the horse are less common than su- prayentricular arrhythm and, in general, are more indicative of cardiac disease. Ventricular premature depolarizations. escape beats, and parasystolic rhythms are characterized by QRS-T complexes that are abnormal in appearance. The QRS complexes originating from the ventricles are generally widened and bizarre, and the T wave is wide and oriented in a direction opposite the QRS complex, P waves may be present but are not conducted through the ventricle during the ventricular rhythm, The timing of the ectopic depolarization is late (more than an R-R interval) in ventricular escape rhythms and early (less than an R-R interval) with ventricular premature depolar- izations. Ventricular premature depolarizations usually demonstrate a fixed coupling interval to the previous QRS complex even if they are multiform, and this feature is used to distinguish extrasystoles from ventricular parasystole.* Ventricular premature depola are usually followed by a compensatory pause. The first normal beat following a compensatory pause may have a shorter P-R and Q-T interval and a decreased T-wave amplitude compared to the previous normal beats. Ventricular tachycardia is an arrhythmia characterized by the presence of four or more ventricular premature depolarizations that are linked together (see Fig. 3). Idioventricular rhythms (rhythms of ventricular origin) exhibit a normal or near normal heart rate. Ac- celerated idioventricular rhythms are termed idioventricular tachy- cardia or ventricular tachycardia. Ventricular tachycardia is chat terized by a faster than normal rate, and P waves, which occur at a slower rate than the ventricular pacemaker, are present but not eon- ducted. Ectopic ventricular depolarizations may be coupled to the previous normal beats. Some P waves may be partially or incom- pletely conducted when the ventricular pacemaker is dominant, re~ sulting in fusion or capture beats. During paroxysmal (intermittent or nonsustained) ventricular tachycardia, fusion and capture beats may be present during the transition to normal-appearing P-QRS-T complexes Ventricular flutter and fibrillation are arrhythmias that are in- compatible with life and are characterized by a lack of recognizable QRS-T complexes. Ventricular fibrillation is distinguishable from flutter by the pattern of ventricular electrical activity, which is highly disorganized h fibrillation. Bundle branch block is a cardiac arrhythmia that requires an ECG for diagnosis. The prevalence of this arrhythmia is low in horses; therefore, the significance is not established.*!°*7 Right bundle branch block as well as other nonspecific intraventricular conduction have been reported." The ECG criteria are prolongation of the QRS complex for greater than 0.17 seconds, slurring of the ventricular complex, and an abnormal T wave.Canbiac Agniytisias 365 Other Diagnostic Tests The possibility that cardiac arrhythmias can oceur in normal horses, in horses with illness not associated with the primary cardio- vascular system, or in horses with primary cardiovascular disorders necessitates further laboratory testing. Horses may have vagally in- duced wandering pacemaker, sinus arrhythmia, sinus arrest, sinus block, sinus bradycardia, first-degree AV block, or second-degree AV block present at rest. Such horses should develop normal sinus rhythm or sinus tachycardia following exercise, excitement, admin- istration of atropine or glycopyrrolate. Such horses are considered normal and are excluded from further testing unless there are indi- cations for such tests Toxemia, septic shock, anemia, metabolic disorders, renal, he- patic, respiratory, endocrine, or neurologic disease, and drug therapy with compounds such as xylazine, aminophylline, or digoxin are but a few of the conditions that cause cardiac dysrhythmias without de- tectable heart disease. The diagnosis of these conditions is often ob- vious from clinical history, but laboratory tests may aid in the diag- nosis, prognosis, and assessment of therapeutic interventions. A com- plete blood count and serum chemistry profile are considered the minimum data base for horses with cardiac arrhythmias. The com- plete blood count may indicate sepsis, toxemia, or anemia conditions that can be associated with arrhythmias like sinus tachycardia or ex- trasystoles. The serum chemistry profile is used to assess electrolyte concentrations, the most important of which are potassium and cal- cium. Changes suggestive of renal and liver disease are often present on a routine chemistry profile. Renal disease may be indirectly re- sponsible for cardiac arrhythmias because of electrolyte changes. Ic- terus secondary to liver disease or anorexia has been associated with sinus bradycardia.* The assessment of the acid base status and venous blood gases are helpful in ruling out metabolic causes of cardiac ar- rhythmias. Laboratory testing of horses with cardiac arrhythmias depends on clinical assessment of the patient. Endocrinologic diseases such s hyperadrenocorticism, thyroid dysfunction, and catecholamine-se- creting tumors can be responsible for an arrhythmia and must be ruled out when indicated. Respiratory disease may be indirectly re- sponsible for a mumber of cardiac arrhythmias because of hypoxia, pulmonary hypertension, autonomic imbalance, or secondary right heart disease. Diagnostic tests used to assess the respiratory system, such as percussion, radiography, tracheal fluid cytology, endoscopy, and arterial blood gases, may be helpful. Cerebrospinal fluid analysis may be needed to exclude the possibility of a neurologic cause of eardiac arrhythmias, particularly when there is a history of central nervous system disease or when signs of inereased cranial pressure or brainstem disease are present. Laboratory assessment of some horses may include submission of blood or plasma for drug analysis. The most notable example is the evaluation of digoxin level | in plasma from the horse who later develops cardiac arrhythmias.366 Sema M. McGutnk ano Wittiay We Moin Arrhythmias may be caused by valvular, myocardial, or pericar- dial diseases (see the article “Acquired Cardiovascular Disease”). The primary condition may require therapy before antiarrhythmic therapy is given, This is particularly true in horses with endocarditis or congestive heart failure. Echocardiography, radiography, and in- direct blood pressure measurement are the most commonly used noninvasive tools for a ing organic heart disease. Cardiac cathe- terization and pericardiocentesis are also valuable diagnostic tools in selected cases. THERAPY With the completion of the physical examination and diagnostic tests, including assessment of the patient after exercise, the veteri narian can usually establish the diagnosis as well as the significance of the cardiac arrhythmia. Arrhythmias due to vagal tone (wandering pacemaker, sinus arrhythmia, sinus block, sinus arrest, sinus brady- cardia, first degree AV block, and second-degree AV block) are usu- ally normal and seldom require treatment. Arrhythmias due to non- cardiac disorders may require specific therapy if hemodynamic pa- rameters such as cardiac output and arterial blood pressure are severely reduced or if the potential for the development of a more life-threatening arrhythmia, such as ventricular tachycardia, is great For the most part, arrhythmias that are not caused by organie heart disease respond well to therapy for the underlying condition, such as correction of hypoxia, acid base imbalance. electrolyte disorders, or septicemia. Notable exceptions to this rule are atrial fibrillation and ventricular tachycardia. These arrhythmias may persist despite resolution of the primary disease problem and may require specific therapy, which will be discussed in the following sections, Arrhyth- mias due to organic heart disease may improve with management of underlying myocarditis, vegetative endocarditis, congestive heart failure, or pericarditis. Some arrhythmias are never treated because of the poor prognosis associated with the primary condition. Specific antiarrhythmic treatment of cardiac arrhythmias is based on. cert! Cardiac arrhythmias resulting in hemodynamic or associated with clinical signs of exercise intolerance, poor performance, heart failure, dyspnea, or syncope are treated. Arrhythmias that worsen with exercise or result in heart rates during exercise that exceed 200 beats per minute are treated. One should also be familiar with electrocardiographie criteria for cardiovascular drug therapy. Rapid arrhythmias (heart rate greater than 120 beats per minute) at rest are treated because of the depression of cardiac output associated with short diastolic filling periods. Arrhythmias characterized by extrasystoles are treated if the ectopic beats are frequent or originate from more than one focus (multiform). Arrhyth- mias of ventricular origin are generally considered to have more po-Carpiae ARRIYTIMIAS 367 tential for hemodynamic compromise than atrial arrhythmias; there- fore, they are more likely to be treated. There are few antiarrhythmic drugs for which pha data are established in the horse. The most frequently used antiar- rhythmic drugs are digoxin, quinidine, anticholinergies, and oc sionally lidocaine and propranolol. Arrhythmias induced by vagal tone are eliminated by anticholinergic drugs such as atropine (0.01 ing per kg, intravenously) and glycopyrrokate (0,003 mg per kg, in- travenously), These drugs are usually administered for diagnostic, rather than therapeutic, purposes because of their relatively short duration of action, lack of therapeutic indication, and gastrointestinal side effects. The cardiac arrhythmias that are thought to be due to inereased vagal tone and that are not corrected by excitement, ex- ercise, or anticholinergics may require therapy if the heart rate is less than 20 beats per minute or the horse exhibits signs of weakne: or syncope. Intravenous isoproterenol (0.05 to 0.1 wg per kg, intr venously), or dopamine (3 to 5 wg per kg per minute, intravenously provides an immediate, but short-lived, increase in heart rate.*!?? Sinus tachyeardia, which may be caused by pain, fear, excite- ment, feyer, shock, hemorrhage, colic, catecholamine administration, hyperthyroidism, and electrolyte abnormalities does not usually re~ quire antiarrhythmic therapy. Treatment of the primary disturbance usually results in a return to normal sinus rhythm. If circulatory failure is a result of the rapid heart rate, treatment for shock or heart failure or therapy as described in the following section for supraven- tricular tachycardia is given. Cardiac conditions such as preexcitation syndrome, atrial en- largement, myocarditis, or drug toxicosis from therapy with quinidine or digoxin way result in development of supraventricular tachycardia (SVT). When possible, the primary condition is treated prior to an- tiarrhythmic therapy. Digoxin is the initial treatment of choice if the heart rate is markedly elevated or associated with congestive heart failure or hypotension. Loading doses of digoxin given intravenously (6 to 10 pg per kg per day) or orally (40 to 70 xg per kg per day) have been recommended.*® An intravenous dose (8 to 5 wg per kg per day) or an oral dose (15 to 35 px per ky per day) of digoxin is then administered for maintenance.*°* Quinidine can be used to effectively treat SVT. Oral quinidine therapy is safest, but several hours may pass before the arrhythmia is abolished when this route of therapy is chosen, Quinidine sulfate in water is administered by nasogastric tube at a dose of 20 mg per kg (approximately 10 g ina 1000-[b horse) every 2 hours until correction of the arrhythmia or a total of six to eight doses have been administered. The first oral dose is used as a test dose. If no adverse reactions have been noted by 2 hours after administration of the first dose, therapy is continued. Quinidine can also be administered by the intravenous route when the severity of arrhythmia does not allow the time needed for oral therapy. The intravenous quinidine dose of 4 to 6 mg per kg is given macokinetic368 Sena M, McGumx axe Wiis W. Muir as an infusion over 1 hour or at a rate of 0.5 mg per kg every 10 minutes until the total dose has been administered.°°* Intravenous fluid administration is recommended as supportive therapy because of the hypotensive effect of quinidine. Propranolol is a third choice for treatment of SVT. Intravenous administration of 0.05 mg per k of propranolol has been yecommended.'* Propranolol is not very et fective when administered orally because of a large first-pass effect by the liver, but doses of 175 to 350 mg, given three times a day, have been used for horses.!> Vagal maneuvers can be effective in other species for conversion of SVT to normal sinus rhythm, Pressure applied to the eyes, carotid artery pressure. or application of a nose twitch might be effective in some horses, but has not been studied. Treatment of frequent atrial premature depolarizations or atrial fibrillation is similar to that described above for SVT. Horses that are used for work (racing, endurance, or show) that do not have evidence of organic heart disease should be treated. The chances for conversion to normal sinus rhythm and the prognosis for return to normal func- tion are good.® Horses that have had atrial fibrillation for a prolonged period of time, loud cardiac murmurs, or cardiac enlargement have a more guarded prognosis for conversion and return to successful work. Although these horses may respond to therapy by converting to normal sinus rhythm and the prognosis for return to normal func- tion again, Horses with a rapid ventricular response at rest (more than 90 beats per minute) or congestive heart failure have a guarded to poor prognosis and are either not treated with quinidine or are first stabilized by treatment with digoxin and furosemide prior to attempting conversion to sinus rhythm with quinidine. Quinidine is the drug of choice for treatment of frequent atrial premature depolarizations and atrial fibrillation, Oral administration of quinidine is preferred using the dosage schedule described in the preceding section. Chronic maintenance therapy with quinidine is not recommended because of the increased risk of toxicity and the impracticality of long-term administration. Digoxin is the drug of choice for more chronic treatment of frequent atrial premature de- polarizations or refractory atrial fibrillation in pets or breeding ani- mals with concurrent heart failure. Digoxin (and furosemide) may successfully control edema and maintain a more normal ventricular rate. The dose for digoxin has been described in a previous section. Propranolol may also be employed, on a short-term basis, for treat- ment of these arrhythmias when the heart rate is elevated. Neither digoxin nor propranolol are used as the sole therapy to convert atrial fibrillation to normal sinus rhythm. These drugs are used to slow the ventricular response rate so that hemodynamic stability is main- tained. There is no effective drug therapy for treatment of third-degree AV block. The installation of a cardiac pacemaker has been reported in horses.* Administration of isoproterenol or dopamine may provide temporary relief from syncopal episodes but it is not practical for long-term maintenance therapy,Cynprac Agnnyti Mas 369 Quinidine is the most effective drug for the treatment of ven- tricular arrhythmias in the horse. Lidocaine can also be used at a dose of 0.5 mg per kg, intravenously, for acute control of severe yen- tricular arrythmias, but continuous intravenous infusion is not pra tical for long-term control. Corticosteriods may be helpful in cases of myocarditis associated with recurrent ventricular arrhythmia SUMMARY Cardiac arrhythmias are probably more common in horses than in any other domestic animal species, The most frequent clinical complaint associated with cardiac arrhythmias is exercise intolerance. Physical examination is characterized by auscultation abnormalities such as fast or slow heart rate, irregular rhythm, extra sounds, long pauses, or abnormal heart sounds. The electrocardiogram is used to make a definitive diagnosis of the dysrhythmia. Other laboratory and cardiac function tests are employed to determine the etiology and to assess the significance of the arrhythmia. Antiarrhythmic therapy is given when clinical signs specifically related to the arrhythmia are present, when hemodynamic parameters are compromised by the arrhythmia, or when the ECG reveals abnormalities that put the patient at risk for development of more severe arrhythmias. The cardiovascular drugs most frequently used are digoxin and quinidine. Digoxin is most commonly used for supraventricular arrhythmias, especially arrhythmias characterized by fast heart rates. Quinidine is very effective for short-term treatment of ventricular and supraven- tricular arrhythmias but must be used with caution because of the potential for toxic side effects. The cardiac arrhythmias due to vagal tone (sinus arrhythmia, sinus block, sinus arrest, sinus bradyeardia, wandering pacemaker, first-degree AV block, and second-degree AV block) that are found in resting horses are generally considered to be normal and generally do not require therapy. REFERENCES 1. Blood, D. C,, Redostits, O, M., and Henderson, J. A.: Diseases of the cardiovascular system, In Blood, D, C., Radostits, O. M.. and Henderson, J. A. (eds. Veterinary Medicine: A Texthook of Diseases of Cattle, Sheep. Pigs, Goats, and Horses, Edi tion 6. London, Bailliere Tindall, 1983, pp, 270-30) Brooijmans, A. W. M.: Electrocardiography in horses and cattle, Collected papers from Laboratory of Veterinary Physiology. State University of Utrecht, Nether lands, 1957. 3. Button, C.. Scrutchfield, W. L., Clark, R. G., et al.: Multiple atrial dysrhythmias in a horse. J. Am, Vet. Med. Assoc., 177-714-719, 1980, 4. Button, C., Gross, D.R., Jolmiston, J. T., et al.: Digoxin. pharmacokinetics, bie- availability, efficacy, and dosage regimens in the horse. Am. J. Vet, Res,. #1-1385- 1395, L980. 5. Cooper, 5. A.: Ventricular preexcitation (WollEParkinson-White syndrome) ina horse. Vet. Ree 330. 1962,370 Snema M. MeGuirk axo Wittiase We Mui 6. 1g. 16. 17. 18. 19, 20. 25. 26. 27. 2B. 29, Deem, D. A., and Fregin, G. F: Atrial fibrillation in horses: 4 review of 106 clinical cases, with consideration of prevalence, clinical signs, and prognosis. J. Am. Vet Med. Assoc, 180:261-265, 1982 Delahanty, D. D., and Glusier, D, Bei The Woli-Parkinson-White (atrioventricular conduction) syndrome in a horse. fr. Vet, J.. £3:203-207, 1959. Detweiler, D. K., and Patterson, D, By The cardiovascular system. I Catcott B,J. and Smitheors. J. F, (eds): Equine Medicine and Surgery. Edition 2. Santa Bar bara, California, American Veterinary Publications, Ine. 1972. pp. 2 Franchet, B. and Schatemann, HL. J.: Pharmacological experiinents as a basis fr the administration of digoxin in the horse. Res. Vet. Sci, 20:84-89, 1976. Fregia, G. Fi: The cardiovascular system, Zn Mannsmann, B. A., and Mcallister E. S. (eds.): Equine Medicine and Surgery. Edition 3. Volume 1. Santa Barbara California, American Veterinary Publications, Ine., 1982, pp. 645-704. . Fregin, G. F: The equine electrocardiogram with standardized body and limb po- sitions. Cornell Vet., 72:304—324, 1982. Gallagher, J. J., Pritchett, E. L, C,, Sealy, W. C., et al.: The preexcitation syu- dromes. Prog. Cardiovasc. Dise., 20:285-327, 1978. . Hamlin, R. L., Himes, J, A., Guttridge, H., et al: P wave in the electrocardiogram of the horse. Am. J, Vet. Res., 31-1027—1031, 1970, Hilwig, R. W.; Cardiac arrhythmias in the horse. J. Am. Vet. Med. Assoc., 170:1 163, 197 . Hilwig, R. W.: Cardiac arrhythmias. In Robinson, N. 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M.: Hemodynamics before and alter conversion of atrial fibrillation to normal sinus rhythm in horses, J. Am. Vet. Med. Assoc. 184:965-970, 1984. Muir, W.W., and Sams, R. A.+ Clinical pharmacodynamics and pharmacokinetics of beta-adrenoceptor blocking drugs in veterinary medicine, Compend. Contin. Ed. Pract. Vet. 6:156-167, 1954. Pedersoli, W. M., Ravis, W. R., Belmonte, A. A., et al.; Pharmacokinetics of a single, orally administered dose of digoxin in the horse. Res. Vet. Sei., 20:84—89, 1976 Power, H. T-: Atrial fibrillation in a horse. Compend. Contin. Ed. Pract. Vet,, ASA46-S448, 1982. Steel, J. D.: Studies of the eleetrocardiogram of the racehorse. Sydney, Australia, Australasian Medical Publishing Co. Ltd., 1963. Welker, F. H.: An investigation of the second heart sound in the horse. Columbus, The Ohio State University, 1984. White, N. A.: ECG of the month, J. Am. Vet. Med. Assoe., 171:1236~1238, 1977. M - Thesis. 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