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n 11-year-old 634-kg (1,395-lb) warmblood gelding was referred to the Equine Surgery Service at The Ohio State University Veterinary Medical Center for evaluation of chronic suspensory desmitis. The horse was not receiving any medication at the time of the initial evaluation. A hind limb plantar suspensory fasciotomy and neurectomy of the deep branch of the lateral plantar nerve were planned. During evaluation, the horse was bright, alert, and responsive. Rectal temperature was 37.6°C (99.7°F). Respiratory rate was 28 breaths/min, and lung sounds were considered normal. Heart rate was 36 beats/min; auscultation revealed no audible murmurs, but an irregular rhythm was detected. A serum electrolyte panel was performed, and serum cardiac troponin-I concentration was measured. Serum magnesium concentration was 1.01 mg/dL (reference range, 1.11 to 1.60 mg/dL); all other serum electrolyte concentrations were within reference ranges. Serum cardiac troponinI concentration was < 0.01 ng/mL (reference range, < 0.11 ng/mL). Transthoracic echocardiography was performed, and the results were considered normal. Electrocardiography was also performed (Figure 1). ECG Interpretation The initial ECG tracing (Figure 1) obtained when the horse was at rest during the referral evaluation revealed an underlying sinus rhythm with Mobitz type I second-degree atrioventricular (AV) block that was characterized by an incrementally increasing PR interval and blocked P waves. The PR interval of the conducted beats varied from 480 to 560 milliseconds. In addition, abnormal QRS complexes were apparent during pauses in the underlying sinus rhythm; the abnormal complexes occurred at a regular interval of 2,080 milliseconds, consistent with a ventricular escape rhythm at a rate of 29 beats/min. During the escape rhythm, short periods of isorhythmic AV dissociation were apparent. A Lewis (ladder) diagram of the rhythm was created to indicate the proposed origin of each QRS complex in the initial ECG tracing. To verify vagal mediation of the AV block, the horse was exercised and a second ECG examination was performed (Figure 1). After light exercise, a normal sinus rhythm was evident at a rate of 45 beats/min. Interestingly, the PR interval remained slightly prolonged at 520 milliseconds (reference range, < 500 milliseconds), consistent with first-degree AV block and 1:1 AV conduction. Over the next 2 to 3 minutes, the PR interval gradually increased until the second-degree AV block reappeared, with return of the intermittent ventricular escape rhythm. This report was submitted by Nicole M. Karrasch, DVM; Brian A. Scansen, DVM, MS, DACVIM; Turi K. Aarnes, DVM, MS, DACVAA; John A. Hubbell, DVM, MS, DACVAA; and John D. Bonagura, DVM, MS, DACVIM; from the Department of Veterinary Clinical Sciences, College of Veterinary Medicine, The Ohio State University, Columbus, OH 43210. Address correspondence to Dr. Karrasch ([email protected]). 1260

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Surgery was scheduled for the following day. Because the rhythm disturbance was not associated with clinical signs, the horse was assigned an American Society of Anesthesiologists physical status classification of II.1 On the day of surgery, the horse’s PCV was 33% (reference range, 32% to 52%) and the plasma concentration of total solids was 5.6 g/dL (reference range, 6.0 to 8.5 g/dL). The horse was premedicated with acepromazine maleate (0.03 mg/kg [0.014 mg/ lb], IM) administered 1 hour prior to anesthetic induction and detomidine hydrochloride (0.01 mg/kg [0.005 mg/lb], IM) administered 45 minutes prior to anesthetic induction. Immediately prior to anesthetic induction, the horse was sedated with detomidine hydrochloride (0.003 mg/kg [0.0014 mg/lb], IV). After premedication, second-degree AV block was again evident without the previously detected ventricular escape rhythm (Figure 1). At this time, the PR interval in the conducted beats remained consistent, although the sinus discharge interval varied from 1,400 to 1,800 milliseconds. Anesthesia was induced with guaifenesin (39.4 mg/kg [17.9 mg/lb], IV) and ketamine hydrochloride (2.05 mg/kg [0.93 mg/lb], IV). Orotracheal intubation was accomplished with a cuffed endotracheal tube (internal diameter, 26 mm), and the horse was positioned in dorsal recumbency. Anesthesia was maintained with isoflurane at a 2.5% to 3.0% vaporizer setting in oxygen with an out-of-circuit precision vaporizer through a standard large animal circle rebreathing system. During the procedure, the horse developed mild systemic hypotension with an invasive systolic arterial blood pressure recording of 78 mm Hg and diastolic arterial blood pressure recording of 43 mm Hg; mean arterial blood pressure was 55 mm Hg. Dobutamine (1 to 1.5 µg/kg/min [0.45 to 0.68 µg/lb/min]) was administered IV to maintain a mean arterial blood pressure > 70 mm Hg. A ventricular rhythm, also with isorhythmic AV dissociation, was observed during the dobutamine infusion (Figure 1). The rate of the ectopic focus at 25 beats/min (R-R interval, 2,400 milliseconds) was comparable to that previously recorded; however, the ventricular ectopy was initiated by a premature complex, as opposed to an escape complex. This suggested that either the mechanism of the ventricular rhythm observed during the dobutamine infusion was different than the escape rhythm observed at the initial evaluation or the electrophysiologic properties of the ectopic focus or surrounding tissues were altered by the effects of the catecholamine. Dobutamine administration was discontinued, and the horse returned to normal sinus rhythm with a heart rate between 35 and 45 beats/min for the remainder of the anesthetic period. The horse was given a dose of detomidine hydrochloride (0.002 mg/kg [0.001 mg/lb], IV) at the end of inhalation anesthesia, and recovery from anesthesia was uneventful. After standing, the horse’s heart rate was 40 to 45 beats/min and a normal sinus rhythm was evident; the PR interval was 360 milliseconds. JAVMA, Vol 243, No. 9, November 1, 2013

a rhythm that predominately develops in relation to high parasympathetic influence and relates to regulation of arterial blood pressure.5 After recovery from anesthesia, during which sympathetic tone is likely to predominate, the PR interval for the horse described in this report normalized at 360 milliseconds in association with a regular sinus rhythm. First- and second-degree AV block are considered common arrhythmias in horses5 and were observed both at rest and during anesthesia in the horse of this report. Second-degree AV block can be categorized as Mobitz type I (Wenckebach) or Mobitz type II. Mobitz type I second-degree AV block is characterized by a progressive elongation of the PR interval, eventually resulting in a P wave that is not followed by a QRS comFigure 1—Base-apex lead ECG tracings obtained from an 11-year-old horse during an initial evaluation, during a pe- plex. Conversely, Mobitz riod of light exercise, and during anesthesia. A—Base-apex ECG tracing recorded when the horse was at rest dur- type II second-degree AV ing the initial evaluation. An underlying sinus rhythm (heart rate, 40 beats/min) with Mobitz type I second-degree atrioventricular (AV) block is evident. This is characterized by an incrementally increasing PR interval and blocked block is defined by a fixed P waves. The PR intervals of the conducted QRS complexes range from 480 to 560 milliseconds. In addition, PR interval with intermitabnormal QRS complexes (asterisks) are apparent. This ectopic rhythm (rate, 29 beats/min) was initiated during tently blocked P waves and pauses caused by intermittent AV block; AV dissociation is apparent. Paper speed = 25 mm/s; 1 cm = 1 mV. B—A Lewis (ladder) diagram of the rhythm in panel A. The upper zone represents atrial activation (A), the middle zone is thought to more likely represents AV conduction (AV), and the lower zone ventricular activation (V). It is evident from this analysis that represent intrinsic or struconly the second and third P waves are conducted to the ventricle and all others are blocked in the AV conduction tural disease of the conducsystem. The first, fourth, fifth, and sixth QRS complexes originate in the ventricle and represent escape activity. tion system. However, these C—Base-apex ECG tracing recorded immediately after the horse underwent light exercise. Normal sinus rhythm is present (heart rate, 45 beats/min). The PR interval is slightly prolonged at 520 milliseconds (reference range, relationships are complicat< 500 milliseconds), which is consistent with first-degree AV block and 1:1 AV conduction. Paper speed = 25 ed, and in humans, the PR mm/s; 1 cm = 1 mV. D—Base-apex ECG tracing recorded after premedication of the horse with acepromazine interval may be unchanged and detomidine. An underlying sinus arrhythmia (atrial rate, approx 35 beats/min) is evident with Mobitz type I second-degree AV block. Paper speed = 25 mm/s; 0.5 cm = 1 mV. E—Base-apex ECG tracing recorded during or even shorten in the abanesthesia and administration of a dobutamine infusion. The rhythm is initially a sinus rhythm but after the third sence of any structural conQRS complex, a premature ventricular complex initiates a relatively slow ventricular rhythm (arrowheads) with duction disease.6 evidence of AV dissociation. Paper speed = 25 mm/s; 0.5 cm = 1 mV. F—Base-apex ECG tracing recorded when Mobitz type I secondthe horse was standing during recovery from anesthesia. A sinus rhythm is present and the heart rate ranges degree AV block is characterfrom 40 to 45 beats/min with a PR interval of 360 milliseconds. Paper speed = 25 mm/s; 1 cm = 1 mV. istic of high vagal tone and can typically be abolished by the administration of parasympatholytic drugs or by an inDiscussion crease in sympathetic tone; however, increasing blood pressure in the setting of an inappropriate sinus tachycardia can The PR interval is the time required for current to reach lead to a resumption of AV block because baroreceptors are the ventricular myocardium after the impulse has exited the activated.7 Treatment with parasympatholytic drugs can result sinoatrial (SA) node. This interval involves the atrial myocarin gastrointestinal tract discomfort in horses.8 Therefore, we dium and specialized internodal pathways, the AV node, and elected to exercise the horse of the present report to investithe His-Purkinje system. The PR interval can be influenced by gate the underlying cause of the AV block. The second-degree respiration, arterial blood pressure, body temperature, heart AV block largely resolved following light exercise, suggesting rate, and autonomic tone.2 Because of the high influence of that vagal tone either was the direct cause or an important vagal tone in horses, the PR interval is known to be variable; influence. The finding of persistent first-degree AV block durvalues in healthy large-breed horses have been reported to ing exercise in the horse was interesting and unexpected. It is range from 200 to 500 milliseconds.3–5 The PR interval of the possible that the sympathetic stimulation of only light exerhorse of the present report was variable, initially ranging from cise was adequate to abolish second-degree AV block, but was 480 to 560 milliseconds at rest and remaining equivocally not sufficiently high to completely normalize AV conduction; prolonged at 520 milliseconds after light exercise. Elevated alternatively, it is possible that increases in arterial blood presvagal tone is the most likely explanation for the prolonged PR sure activated vagal efferents preferentially to the AV node9 or interval given the presence of Mobitz type I AV block at rest, JAVMA, Vol 243, No. 9, November 1, 2013

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that the horse did in fact have concurrent conduction disease. The last option was considered unlikely in light of the ECG tracing obtained from the horse when it regained a standing position following recovery from anesthesia. The use of detomidine as a premedicant in this horse may be considered contradictory given the potential of α2-adrenoceptor agonists to increase vagal tone and exacerbate underlying conduction disease. However, the abolition of second-degree AV block with exercise, coupled with the need for profound sedation prior to induction of anesthesia, justified the use of detomidine in this case. In addition, administration of acepromazine prior to detomidine and guaifenesin administration immediately prior to ketamine administration allowed a reduced dose of detomidine to be used, thereby limiting the likelihood that hemodynamically important increases in vagal tone would develop. In mammals, subsidiary pacemakers are present within the specialized conduction system of the AV node and ventricular Purkinje fibers. These pacemakers may be apparent on surface ECG tracings during slowing of the sinus rate or during periods of SA arrest or AV block. Escape (idioventricular) rhythms, by definition, are initiated after a pause in ventricular activation because these foci are not considered protected from overdrive suppression.10 The horse of the present report had a fairly rapid ventricular escape focus, which was evident repeatedly at rest following slowing of the sinus rate as well as after periods of AV block. When the escape focus discharged at a rate comparable to the underlying sinus rate, the atrial and ventricular rhythms became dissociated, as seen in the initial ECG tracing. The similar rate of discharge for both atria and ventricles resulted in the P waves marching through and on the ventricular complexes, a phenomenon termed isorhythmic AV dissociation.11 Interestingly, the horse also had isorhythmic dissociation during dobutamine administration under anesthesia. However, the ventricular rhythm during anesthesia was initiated by a premature complex with a shorter coupling interval than the idioventricular rhythm that was present at rest (Figure 1). It is likely that this ventricular rhythm developed as a result of increased automaticity of a ventricular focus induced by the administration of anesthetic agents (including ketamine) and the catecholamine infusion.12 It is possible that the same ventricular focus was operative both at the initial evaluation and during the dobutamine infusion, but this is speculative. Under certain conditions in mammals (eg, endotoxemia, autonomic imbalance, acid-base disturbances, and electrolyte abnormalities), a subsidiary pacemaker may discharge at a rate that is equivalent or more rapid than the sinus rate.10,13 Such rhythms have been termed an accelerated idioventricular rhythm (AIVR) and are defined by ventricular depolarizations that occur faster than expected for a subsidiary pacemaker; fusion beats also commonly occur as the idioventricular rhythm and sinus rate compete for control of the ventricular rhythm.14 There are no defined ranges for AIVR in horses, but some authors propose a range of 60 to 80 beats/min.5 It is also possible that the rhythm detected at the initial evaluation of the horse of the present report was an AIVR originating from an abnormal subsidiary pacemaker. However, a ventricular escape rhythm was considered more likely because no fusion complexes were documented and the rate of discharge at 29 beats/min was considered appropriate for a subsidiary escape pacemaker. The rhythm recorded during the dobutamine infusion, however, was characterized as an AIVR because it was initiated with a premature complex. α2-Adrenoceptor agonists 1262

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have been reported to slow SA discharge rate while increasing the subsidiary pacemaker sensitivity to catecholamines.15 The presence of premature ventricular complexes and an AIVR during anesthesia was likely a result of the concurrent administration of detomidine and dobutamine, perhaps potentiated by mild hypomagnesemia,16 which is potentially proarrhythmic. No structural heart disease was identified in the horse of this report by auscultation or echocardiography, and the serum cardiac troponin concentration was within reference range, which suggested no ongoing intrinsic myocardial damage.17 An alternative explanation for the rhythm recorded during the dobutamine infusion is that a singular premature ventricular complex was initiated by the drug followed by a compensatory pause, which allowed the perpetuation of a ventricular escape rhythm to occur under the increased vagal influences of anesthesia. However, given the comparable morphology of the ventricular rhythm to the premature complex, it is the authors’ opinion that this dysrhythmia more likely represented an AIVR. References 1.

2. 3.

4. 5. 6. 7. 8. 9. 10. 11.

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13. 14. 15. 16. 17.

American Society of Anesthesiologists. ASA physical status classification system. Available at: www.asahq.org/For-Members/ Clinical-Information/ASA-Physical-Status-Classification-System.aspx. Accessed Aug 10, 2013. Hall JE. Rhythmic excitation of the heart. In: Guyton A, ed. Textbook of medical physiology. 8th ed. Philadelphia: WB Saunders Co, 1991;111–117. Schwarzwald CC, Bonagura JD, Muir WW. The cardiovascular system. In: Muir WW, Hubbell JAE, eds. Equine anesthesia: monitoring and emergency therapy. 2nd ed. St Louis: Saunders Elsevier, 2009;37–100. Fregin G. The equine electrocardiogram with standardized body and limb positions. Cornell Vet 1982;72:304–320. Bonagura JD, Reef VB. Disorders of the cardiovascular system. In: Reed SM, Bayly WM, Sellon DC, eds. Equine internal medicine. 2nd ed. St Louis: Saunders, 2004;372–487. Holm H, Gudbjartsson DF, Arnar DO, et al. Several common variants modulate heart rate, PR interval and QRS duration. Nat Genet 2010;42:117–122. Smetzer DL, Senta T, Hensel JD. Cardiovascular effects of amphetamine in the horse. Can J Comp Med 1972;36:185–194. Ducharme NG, Fubini SL. Gastrointestinal complications associated with the use of atropine in horses. J Am Vet Med Assoc 1983;182:229–231. Raymundo H, Scher AM, O’Leary DS, et al. Cardiovascular control by arterial and cardiopulmonary baroreceptors in awake dogs with atrioventricular block. Am J Physiol 1989;257:H2048–H2058. Vassalle M. The relationship among cardiac pacemakers. Overdrive suppression. Circ Res 1977;41:269–277. Waldo AL, Vitikainen KJ, Harris PD, et al. The mechanism of synchronization in isorhythmic A-V dissociation. Some observations on the morphology and polarity of the P wave during retrograde capture of the atria. Circulation 1968;38:880–898. Woehlck HJ, Vicenzi MN, Bosnjak ZJ. Anesthetics and automaticity of dominant and latent pacemakers in chronically instrumented dogs. I. Methodology, conscious state, and halothane anesthesia: comparison with and without muscarinic blockade during exposure to epinephrine. Anesthesiology 1993;79:1304–1315. Cornick JL, Seahorn TL. Cardiac arrhythmias identified in horses with duodenitis/proximal jejunitis: six cases (1985–1988). J Am Vet Med Assoc 1990;197:1054–1059. Campbell WB. EKG of the month: accelerated idioventricular rhythm with a “fusion” beat and premature ventricular contraction. J Tenn Med Assoc 1979;72:214–215. Taylor PM, Browning AP, Harris CP. Detomidine-butorphanol sedation in equine clinical practice. Vet Rec 1988;123:388–390. Pignide L, Hersch R. Efficacy and limits of magnesium therapy in extrasystole [in French]. Magnesium 1985;4:272–279. Nath L, Anderson G, Hinchcliff K, et al. Serum cardiac troponin I concentrations in horses with cardiac disease. Aust Vet J 2012;90:351–357. JAVMA, Vol 243, No. 9, November 1, 2013

ECG of the month. Accelerated idioventricular rhythm during anesthesia.

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