A 7-year-old 523-kg (1,151-lb) Morgan gelding was referred for evaluation of signs of depression, fever (40.9°C [105.6°F]), tachypnea, and tachycardia. Flunixin meglumine (1.1 mg/kg [0.5 mg/lb], IV, once) was administered prior to admission. On examination, the horse was lethargic and profusely sweating. Mucous membranes were pale and dry with a capillary refill time of 2.5 seconds. Heart rate was 84 beats/min, respiratory rate was 50 breaths/min, and rectal temperature was 36.7°C (98.1°F). The horse was assessed to be 7% dehydrated. No arrhythmias or murmurs were noted, and peripheral pulses were normal and synchronous. Respiratory effort and results of pulmonary auscultation were considered normal.
Transcutaneous ultrasonographic examination of the thorax revealed no pulmonary abnormalities or pleural effusion. Ultrasonographic examination of the abdomen revealed that the right ventral colon wall was markedly thickened and heavily folded. Abdominocentesis yielded yellow, cloudy fluid with a total protein concentration of 5.5 g/dL (reference interval, < 2.5 g/dL), lactate concentration of 10.5 mmol/L (reference range, < 2 mmol/L), and nucleated cell count of 7,500 cells/μL (reference interval, < 5,000 cells/μL). A CBC revealed a leukocyte count of 2,980 WBCs/μL (reference interval, 6,000 to 12,000 WBCs/μL); neutrophil count was 1,400 cells/μL (reference interval, 3,000 to 6,000 cells/μL), and band neutrophil count was 179 cells/μL (reference interval, < 100 cells/μL). A serum biochemical profile revealed an albumin concentration of 2.3 g/dL (reference interval, 2.7 to 4.1 g/dL), globulin concentration of 2.7 g/dL (reference interval, 2.8 to 4.4 g/dL), and iron concentration of 41 μg/dL (reference interval, 129 to 173 μg/dL). Results of a serum electrolyte profile indicated that potassium concentration was 2.3 mmol/L (reference interval, 3.5 to 4.5 mmol/L), chloride concentration was 89 mmol/L (reference interval, 91 to 111 mmol/L), magnesium concentration was 1.0 mg/dL (reference interval, 1.7 to 2.1 mg/dL), and total calcium concentration was 9.3 mg/dL (reference interval, 10.5 to 12.9 mg/dL). All other biochemical variables were within reference intervals.
A presumptive diagnosis of acute colitis of unknown cause was made for the horse on the basis of a history of fever, leukopenia characterized by neutropenia, dehydration, electrolyte derangements, and the ultrasonographically detected thickened right ventral colon wall. Intravenous fluid therapy with balanced polyionic crystalloid fluids (Hartmann solution) at a rate of 60 mL/kg/d (27.3 mL/lb/d) was initiated. Flunixin meglumine (1.1 mg/kg, IV, q 12 h) and lidocaine hydrochloride (initial bolus of 1.3 mg/kg [0.59 mg/lb], IV, administered over a period of 15 minutes, followed by continuous rate infusion of 0.05 mg/kg/min [0.02 mg/lb/min], IV) were provided. Given the horse's marked leukopenia, prophylactic antimicrobial treatment was instituted with penicillin G potassium (22,000 U/kg [10,000 U/lb], IV, q 6 h) and gentamicin (6.6 mg/kg [3 mg/lb], IV, q 24 h). Distal limb cryotherapy was used for laminitis prophylaxis. Food and water were withheld from the horse.
Eight hours after starting the initial supportive treatments, the horse remained mildly dehydrated; its heart rate was decreased (48 to 52 beats/min) and clinical demeanor was improved. Diarrhea was noted. A repeated serum electrolyte profile revealed a potassium concentration of 2.2 mmol/L, magnesium concentration of 1.0 mg/dL, and total calcium concentration of 9.1 mg/dL. The horse received IV supplements of potassium chloride at a rate of 25 mEq/h, calcium gluconate at a rate of 2.3 g/h (10.7 mEq of ionized calcium/h), and magnesium sulfate at a rate of 1.5 g/h (12 mEq of ionized magnesium/h). Cardiac arrhythmia was auscultated 2 hours after electrolyte supplementation began, with intermittent periods of tachycardia (88 to 92 beats/min), which prompted echocardiographic and ECG evaluations.
ECG Interpretation
Base-apex ECG (Figure 1) revealed sinus tachycardia at a rate of 60 beats/min. An abrupt transition occurred, and a ventricular rhythm began with an idioventricular beat followed by ventricular complexes at 100 beats/min. At this time, the horse's plasma potassium concentration was 2.2 mmol/L, and its magnesium concentration was 1.0 mmol/L. All ventricular beats were morphologically uniform. Transient atrial standstill was excluded by the presence of p waves during the arrhythmia. Short periods of rapid ventricular beats at a rate of 80 to 100 beats/min were evident, each of which was followed by a transition into ventricular beats at a rate of 40 to 45 beats/min (Figure 2). Normal sinus rhythm was maintained between each period of paroxysmal ventricular rhythm, although the rate was mildly elevated (48 to 60 beats/min). Single, isolated, premature ventricular contractions were not observed outside of these intermittent runs of ventricular ectopic beats.
Base-apex ECG tracings obtained at the initial evaluation of a 7-year-old Morgan gelding that was evaluated because of signs of depression, fever, tachypnea, and tachycardia. The ECG examination was performed after auscultation of intermittent arrhythmia. A—Notice the sinus tachycardia at a rate of 60 beats/min. B—At this time, there is a transition from normal sinus rhythm to accelerated idioventricular rhythm (AIVR), initiated by a ventricular premature complex (arrow) and characterized by uniform ectopic ventricular rhythm of 100 beats/min. Atrial standstill was excluded by the presence of p waves (asterisks). The horse was known to have markedly low serum potassium and magnesium concentrations. C—In this tracing, notice the paroxysmal AIVR with multiple blocked p waves (asterisks). Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 254, 5; 10.2460/javma.254.5.591
Continuous base-apex ECG tracings obtained from the horse in Figure 1 during ongoing IV administration of electrolyte supplements and when intermittent AIVR was still present but at a slower rate than initially identified. Subsequently, the arrhythmia spontaneously resolved. A and B—Notice the intermittent AIVR with ventricular ectopy (arrowheads) at a rate of 40 to 45 beats/min. Intermittent sinus rhythm and blocked p waves (asterisks) are associated with a sinus rate of 48 to 60 beats/min. C—At 16 hours after the initial ECG examination, there is normal sinus rhythm at a rate of 46 beats/min. At this time, the horse's serum potassium concentration was 3.2 mmol/L. Paper speed = 25 mm/s; 1 cm = 1 mV.
Citation: Journal of the American Veterinary Medical Association 254, 5; 10.2460/javma.254.5.591
Echocardiography was performed to assess structure and function of the horse's heart. All echocardiographic variables were within reference limits, including cardiac chamber dimensions, systolic function, valve morphology, myocardial echogenicity, and transvalvular velocities. On the basis of clinical examination and diagnostic test results, a diagnosis of accelerated idioventricular rhythm (AIVR), most likely attributable to electrolyte imbalance and gastrointestinal tract disease, was made.
The horse was closely monitored for arrhythmia and clinical signs of cardiac compromise while receiving IV electrolyte supplements. The horse remained quiet and comfortable, and cardiac auscultation was repeated every 2 hours. Repeated ECG 16 hours (Figure 2) after previous cardiac diagnostic tests revealed a normal sinus rhythm and heart rate of 46 beats/min in the absence of administration of an antiarrhythmic dosage of lidocaine. At that time, the horse's serum potassium concentration was 3.2 mmol/L. There was no further evidence of AIVR detected during the ECG examination, and the heart rate normalized (40 to 44 beats/min). A constant rate infusion of lidocaine (0.05 mg/kg/min, IV) was continued for systemic anti-inflammatory purposes, and IV fluid therapy and electrolyte supplements were provided for 2 additional days until resolution of diarrhea. The horse maintained its serum potassium concentration within the reference interval and remained in normal sinus rhythm after discontinuation of IV electrolyte supplementation and lidocaine treatment. The horse's leukogram normalized within 4 days, and administration of antimicrobials was discontinued. No cause of the colitis was identified, and the horse recovered and was discharged from the hospital.
Discussion
For the horse of the present report, the 2 primary differential diagnoses for the ventricular rhythm were ventricular tachycardia (VT) and AIVR. A ventricular premature contraction (VPC) results from ectopic excitation within the ventricular myocardium; action potential conduction occurs through the myocardium instead of through conventional conduction channels, resulting in a wide, bizarre QRS complex followed by a compensatory pause.1 A single ectopic focus generates VPCs of uniform morphology. Those VPCs originating from multiple ectopic foci are characterized by variable morphology (multiform VPC), suggesting a more marked pathological change and greater potential for instability and progression to severe arrhythmias.1
Ventricular tachycardia refers to runs of > 3 consecutive VPCs, which develops when the myocardial ectopic focus takes on automaticity and results in a ventricular rate that is considerably greater than the sinus rhythm (typically > 100 beats/min in horses).1 This results in pulse deficits and decreased cardiac output because ventricular contraction occurs too rapidly for appropriate filling of the ventricles. Given the potential of VT to progress to ventricular fibrillation, it necessitates treatment typically with IV administration of lidocaine and magnesium sulfate (as first line treatment) as well as sotalol.2 For horses with VT, lidocaine is usually administered as IV boluses of 0.5 mg/kg (0.23 mg/lb) every 5 minutes up to a total dose of 1.3 to 1.5 mg/kg (0.59 to 0.68 mg/lb), followed by a constant rate infusion of 0.05 mg/kg/min.2,3 Without primary antiarrhythmia treatment, VT does not resolve spontaneously.
In human and veterinary medicine, case definitions of AIVR vary, but there are several diagnostic criteria such as the presence of 3 or more consecutive ventricular beats at a rate greater than sinus rhythm but slower than 100 beats/min, competition between the AIVR rhythm and sinus rhythm for control of heart rate (often with gradual onset or termination), fusion beats that occur when the 2 pacemakers are competing at similar rates and p waves are superimposed on AIVR beats, spontaneous resolution of AIVR and restoration of normal sinus rhythm when the systemic disorder causing AIVR is corrected, and presence of ventricular escape beats at a rate of 40 to 100 beats/min.4 The definition of an escape beat is an ectopic rhythm originating outside the sinoatrial node. Idioventricular rhythm refers to an ectopic ventricular escape rhythm with a rate of 20 to 40 beats/min. When the rate is accelerated and between 40 and 100 beats/min, it is called AIVR.2,4 There is no discrete cutoff for heart rate that can be used to differentiate AIVR from VT; however, a heart rate cutoff of 80 to 100 beats/min has been suggested for horses.2 In the horse of the present report, echocardiographic findings excluded structural and functional abnormalities of the heart, and AIVR was therefore likely attributable to an extracardiac cause. Although cardiac biomarkers of myocardial cell death were not evaluated, toxin exposure was not considered a likely cause of the ventricular arrhythmia. Therefore, a diagnosis of AIVR was made for the horse on the basis of the ECG criteria as well as the resolution of the arrhythmia with correction of the electrolyte imbalance and without administration of an antiarrhythmic agent at a recommended therapeutic dosage.
Heart rate is driven by whichever pacemaker tissue has the fastest rate of spontaneous depolarization (normally the sinoatrial node). Enhanced automaticity of the subordinate pacemaker tissues (the His-Purkinje system or closely associated ventricular myocardial tissue) results in AIVR.4 During AIVR, the passive inward flux of potassium and calcium that drives gradual diastolic depolarization (phase 4) of cardiac myocytes is accelerated by increased sympathetic tone, effects of certain drugs, and electrolyte (especially potassium, calcium, and magnesium) imbalance.1,5 Depolarization at the level of subordinate pacemaker tissues occurs at a faster rate than the intrinsic rate of the sinoatrial node, resulting in dominance by the ectopic rhythm (ie, AIVR).6 Compared with VT, AIVR has a slower rate, which allows for greater ventricular filling and does not generally result in hemodynamic compromise. However, if a horse with AIVR has clinical signs of poor perfusion or hypotension, antiarrhythmic treatment is warranted.5
Typically, AIVR develops from extracardiac causes, including systemic illness (ie, systemic inflammatory response syndrome, imbalanced sympathetic or parasympathetic tone, acid-base disturbances, or electrolyte imbalance), and can be induced by drugs that decrease the sinus discharge rate while increasing sensitivity to catecholamines (ie, α2-adrenoceptor agonists and halothane).2 In particular, hypokalemia is highly arrhythmogenic through several mechanisms; one that is most important in AIVR is acceleration of the rate of phase 4 diastolic depolarization, which increases dispersion of refractoriness and actively triggers automaticity within Purkinje fibers.7,8 Hypomagnesemia also plays an important role in arrhythmogenesis because it is an essential coenzyme for the Na+, K+-ATPase pump that drives cell membrane potential. Low circulating magnesium concentrations are linked with lower cell membrane potentials, increased spontaneous depolarization, and increased excitability in cardiac myocytes and Purkinje fibers.9,10 The combination of hypokalemia and hypomagnesemia has been linked with cardiac arrhythmias in humans and horses, and the horse of the present report had hypokalemia and hypomagnesemia at the time of AIVR development.5,9 Provision of appropriate supplements and resultant normalization of these electrolyte imbalances led to spontaneous resolution of AIVR in the face of ongoing gastrointestinal inflammation associated with colitis, making electrolyte imbalance the most likely cause of arrhythmia in this horse.
In the veterinary medical literature, AIVR has been described secondary to several different triggers. In a report11 of a warmblood gelding under anesthesia, AIVR was induced by multiple known triggers, namely administration of an α2-adrenoceptor agonist (ie, detomidine) and a catecholamine (ie, dobutamine) and the presence of hypomagnesemia. Accelerated idioventricular rhythm in dogs with severe systemic inflammation that resolved within 48 hours after treatment of the primary condition has also been reported.12,13 There is also a report14 of AIVR in 2 apparently normal horses before and after racing. Potential causes in those cases included increased ectopic automaticity owing to high sympathetic stimulation as well as the effects of prerace administration of furosemide, which can cause subclinical or clinical hypokalemia.
The horse of the present report had no evidence of heart disease and developed AIVR in the face of marked electrolyte imbalances and systemic inflammation. The AIVR spontaneously resolved after supplemental electrolytes were administered and serum electrolyte concentrations were subsequently normalized. The horse had no further development of cardiac arrhythmias.
References
1. Cardiovascular system. In: Muir WW III, Hubbell JA, eds. Equine anesthesia: monitoring and emergency therapy. 3rd ed. St Louis: Elsevier Health Sciences, 2008;40–48.
2. Cardiovascular diseases. In: Reed MS, Bayly WM, Sellon DC, eds. Equine internal medicine. 3rd ed. St Louis: Saunders Elsevier, 2010;423–424.
3. Sleeper MM. Equine cardiovascular therapeutics. Vet Clin North Am Equine Pract 2017;33:163–179.
4. Accelerated idioventricular rhythm. In: Lang F, ed. Encyclopedia of molecular mechanisms of disease. New York: Springer Science & Business Media, 2009;3–4.
5. Grimm W. Accelerated idioventricular rhythm. Card Electrophysiol Rev 2001;5:328–331.
6. Riera ARP, Barros RB, de Sousa FD, et al. Accelerated idioventricular rhythm: history and chronology of the main discoveries. Indian Pacing Electrophysiol J 2010;10:40–48.
7. Spiegler PA, Vassalle M. Role of voltage oscillations in the automaticity of sheep cardiac Purkinje fibers. Can J Physiol Pharmacol 1995;73:1165–1180.
8. Osadchii OE. Mechanisms of hypokalemia induced ventricular arrhythmogenicity. Fundam Clin Pharmacol 2010;24:547–559.
9. Stewart AJ. Magnesium disorders in horses. Vet Clin North Am Equine Pract 2011;27:149–163.
10. Tobey RC, Birnbaum GA, Allegra JR, et al. Successful resuscitation and neurologic recovery from refractory ventricular fibrillation after magnesium sulfate administration. Ann Emerg Med 1992;21:92–96.
11. Karrasch NM, Scansen BA, Aarnes TK, et al. ECG of the month. Accelerated idioventricular rhythm during anesthesia. J Am Vet Med Assoc 2013;243:1260–1262.
12. Guglielmini C, Diana A, Civitella C, et al. Accelerated idioventricular rhythm in 9 dogs. Vet Res Commun 2006;30:305–307.
13. Diana A, Fracassi F. ECG of the month. Accelerated idioventricular rhythm. J Am Vet Med Assoc 2005;226:1488–1490.
14. Slack J, Boston R, Soma L, et al. Occurrence of cardiac arrhythmias in Standardbred racehorses. Equine Vet J 2015;47:398–404.
