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Home , Auscultation, Ventricular fibrillation, Ventricular tachycardia

—RESPIRATORY/CARDIOVASCULAR

How to Diagnose and Treat Ventricular

Amanda M. House, DVM, Diplomate ACVIM; and Steeve Gigue`re, DVM, PhD, Diplomate ACVIM

Authors’ address: Large Animal Clinical Sciences, College of Veterinary Medicine, University of Florida, PO Box 100136, Gainesville, Florida 32610; e-mail: [email protected]fl.edu. © 2009 AAEP.

1. Introduction booming sounds can occasionally be heard and Although ventricular are less common are associated with the simultaneous production of than atrial arrhythmias, they are more likely to be life two during periods of atrioventricular threatening and associated with underlying cardiac disassociation. can be uni- or a multisystemic disorder.1–3 Common eti- form (regular rhythm) or multiform (irregular ologies include electrolyte abnormalities (hypomag- rhythm). Multiform ventricular tachycardia is as- nesemia and ), drug administration, or sociated with more rapidly progressive signs of con- primary myocardial disease. Ventricular tachycar- gestive and increased electrical dia is characterized by a rapid cardiac rhythm that instability, which can result in ventricular fibrilla- originates in the below the bundle of His in tion. If the QRS complex occurs within the preced- the conduction system, in the surrounding ventricular ing , this is called the “R on T” phenomenon, myocardium, or both. It can be characterized by an and it is associated with an increased chance of irregular or a regular rhythm. Diagnosis of ventric- ventricular fibrillation. QRS complexes are wide ular tachycardia is straightforward with an electrocar- and bizarre and not associated with P waves (Figs. diogram, but identification of the etiology often 1–3). A series of four or more ventricular prema- remains a challenge for veterinary practitioners. ture depolarizations is diagnostic of ventricular Several treatment options exist, and a discussion of tachycardia.4 the anti-arrhythmic therapies is included below. A single lead (I) is sufficient to diagnose most A refractory case of ventricular tachycardia that was rhythm disturbances in the horse. ECG tracings in ultimately successfully treated with will ventricular tachycardia reveal abnormal QRS com- be presented to illustrate the diagnosis and principles plexes that are often wide and bizarre in appearance of therapy. and not associated with P waves. The T waves may be large and follow the QRS complex immediately. 2. Materials and Methods If a differentiation between ventricular and su- Diagnosis of ventricular tachycardia cannot typi- praventricular rhythms cannot be made, additional cally be made based on auscultation alone. Loud leads may be used. ECG evaluates the rhythm and

NOTES

308 2009 ր Vol. 55 ր AAEP PROCEEDINGS MEDICINE—RESPIRATORY/CARDIOVASCULAR

Fig. 1. Base apex ECG recorded in lead I. is detected (HR ϭ 60 bpm). The test is recorded at a paper speed of 50 mm/s and a sensitivity of 20 mm ϭ 1 mV.

Fig. 2. Base apex ECG recorded in lead I. The normal QRS complex (solid arrow) is followed by a run of ventricular tachycardia. The first abnormal complex is indicated (open arrow). The test is recorded at a paper speed of 50 mm/s and a sensitivity of 5 mm ϭ 1mV.

Fig. 3. Uniform ventricular tachycardia is detected. The R-R interval is regular. The P-P interval is regular, but the P waves (arrows) are often buried in QRS complexes or T waves. The test was recorded at a paper speed of 50 mm/s and a sensitivity of 5 mm ϭ 1 mV.

rate only. Because of the pathway of depolariza- myocardial injury, aortic root rupture, and auto- tion in the horse (the deeply penetrating Purkinje nomic nervous system imbalance have all been system and depolarization from ventricular endocar- associated with the development of ventricular dium to epidcardium occurring explosively and in tachycardia.4 Underlying gastrointestinal disor- many directions at one time), chamber sizes cannot ders or sources of sepsis should be ruled out. be determined. Usually a base-apex lead is used: A serum or plasma biochemical profile will deter- mine if electrolyte abnormalities are contributing LA (ϩ): Attach to behind left . to the conduction disturbance. Because ventric- RA (Ϫ): Attach dorsal to right scapular spine. ular tachycardia may be a consequence of myocar- RL (ground): Attach anywhere (usually right ditis, measurement of myocardial muscle enzymes side of the neck). such as creatinine kinase-MB (CK-MB), ␣-hy- droxybutyrate dehydrogenase (HBDH) lactate de- After the diagnosis of ventricular tachycardia hydrogenase (LDH 1 and 2), or preferably, cardiac has been established, additional diagnostic testing troponin I (Ͻ0.15 ng/ml) is recommended.5 However, for an underlying etiology should be considered. normal values do not rule out myocardial damage. , myocardial necrosis, fibrosis, neopla- Suspected viral etiologies of myocarditis in horses in- sia, bacterial , , , clude equine herpes virus and equine influenza. electrolyte or metabolic disturbances, , Testing should be considered in horses with a history drug administration, sepsis, endotoxemia, toxic of fever. Finally, an echocardiogram is necessary to

AAEP PROCEEDINGS ր Vol. 55 ր 2009 309 MEDICINE—RESPIRATORY/CARDIOVASCULAR determine if underlying cardiac disease such as valvu- hypomagnesemic horses, and it is particularly lar insufficiency or endocarditis is present. useful in quinidine-induced . Magnesium may cause hypotension 3. Treatment of Ventricular Tachycardia but has no other adverse cardiovascular ef- fects. In hypomagnesemic patients, magne- Treatment is indicated if there are signs of cardio- sium sulfate acts as a cofactor for the Na/K vascular collapse, the is excessively high ATPase pump. In horses with normal serum (Ͼ120 beats per min [bpm]), the complexes are mul- magnesium concentrations, a calcium chan- tiform, or there is detection of the “R on T” phenom- nel-blocking mechanism is believed to account enon. , if present, should be 7 treated with furosemide (1–3 mg/kg, IV or IM). for its action. The authors often use magne- Table 1 describes anti-arrhythmic therapies for the sium in combination with and other horse. The following list describes drugs that can therapies as a 25-g IV slow bolus twice daily be used in the treatment of ventricular tachycardia (in 1 l of isotonic fluids). in the order that they are usually attempted: Treatment with lidocaine and magnesium are con- sidered to be ideal therapeutic options in circum- 1. Lidocaine is often used as a first-choice ther- stances where continuous monitoring is not apy (0.5 mg/kg, IV bolus every 3–5 min for a available. The additional therapies listed below total of 1.5 mg/kg; therapy can then be contin- should be considered in hospitals where continuous ued as a constant rate infusion (CRI) at 0.05 monitoring and ECG are available. Referral of mg/kg/min). Lidocaine is a class IB drug, these cases for additional diagnostics and therapy which is a sodium-channel blocker and acts to should be offered if they are evaluated in the field. shorten the refractory period. The most com- Each of the following drugs has the potential to mon adverse effect is excitation. Neurologic cause life-threatening adverse effects and should be side effects can typically be controlled with administered under strict supervision. diazepam or a reduction in the rate of admin- 3. (2 mg/kg, IV bolus every 5–10 istration. Boluses and infusions are typically min up to a total of 20 mg/kg) is a class IA well tolerated and cause minimal hemody- anti-arrhythmic that also acts by sodium- namic or electrophysiologic changes at non- channel blockade. This drug has been re- toxic doses.6 ported to be the drug of choice for ventricular 2. Magnesium sulfate is the second choice for tachycardia in conscious horses.7 Unlike therapy (IV infusion of 1 g/min to a maximum quinidine, this drug does not interact with of 25 g). Magnesium sulfate can be effective . Although procainamide may have when added to fluids of normomagnesemic or similar side effects as quinidine, the authors

Table 1. Anti-Arrhythmic Therapy in Horses

Drug Indications Dose

Amiodarone AF, VT 5 mg/kg/h for 1 h followed by 0.83 mg/kg/h for up to 48 h Sinus , 0.005–0.01 mg/kg IV Vagally induced arrhythmias tosylate Life-threatening VT 3–5 mg/kg, IV (up to 10 mg/kg total dose) Ventricular fibrillation Digoxin SVT, AF (rate control) 0.0022 mg/kg, IV, q 12 h 0.011 mg/kg, PO, q 12 h Diltiazem SVT 0.125 mg/kg IV over 2 min (can repeat every 10 min up to a total dose of 1.125 mg/kg) Lidocaine VT 0.5 mg/kg, IV bolus every 3–5 min for a total of 1.5 mg/kg. Therapy can then be continued as a CRI at 0.05 mg/kg/min Magnesium sulfate VT 1 g/min, IV to a maximum of 25 g Procainamide VT, AF, atrial and ventricular 2 mg/kg, IV bolus every 5–10 min up to a total of 20 mg/kg; 25–35 mg/ arrhythmias kg,PO,q8h Propafenone* Refractory VT, AF, atrial 0.5–1 mg/kg in 5% dextrose slowly IV over 5–10 min; 2 mg/kg, PO,q8h arrhythmias Propanolol SVT 0.03–0.2 mg/kg, IV Unresponsive VT 0.38–0.78 mg/kg, PO,q8h

Quinidine gluconate VT, AF 1–2 mg/kg, IV bolus repeated every 10 min up to a total dose of 12 mg/kg Quinidine sulfate AF 22 mg/kg, NGT,q2hforfour doses followed by 22 mg/kg,q6h

*Intravenous formulation not available in the United States. VT ϭ ventricular tachycardia; SVT ϭ supraventricular tachycardia; AF ϭ atrial fibrillation.

310 2009 ր Vol. 55 ր AAEP PROCEEDINGS MEDICINE—RESPIRATORY/CARDIOVASCULAR have noted few toxic effects in conjunction reserved for life-threatening ventricular with its administration. tachycardia or ventricular fibrillation. Like 4. Quinidine gluconate (1–2 mg/kg, IV bolus amiodarone, it is a class III drug that length- repeated every 10 min up to a total dose of ens the refractory period through potassium- 12 mg/kg) is also a class IA drug, and it can channel blockade. The authors have not be used for multiple ventricular and supra- used this drug in clinical cases. ventricular arrhythmias. Quinidine gluconate is protein bound, and concurrent administration A period of rest (4–8 wk) is recommended after with digoxin can result in higher serum concen- successful treatment. Echographic and electro- trations of both agents from competitive bind- graphic evaluation is necessary before return to ath- ing. It is more cost effective than therapy with procainamide; however, it is contraindicated in letic activity. A 24-h ECG recording or exercising hypotensive patients, because it may cause ECG is more useful than just a brief resting ECG. peripheral vasodilation. Cardiovascular side Many horses can return to their prior level of per- effects of quinidine administration include hy- formance if there is no functional residual damage to potension, decreased cardiac contractility, the heart. prolongation of the QRS complex, rapid supraventricular tachycardia, ventricular 4. Results and Discussion arrhythmias, and sudden . Supraven- The case discussed is a yearling Quarter Horse tricular tachycardia is an idiosyncratic reac- colt who presented to the hospital with a history of tion rather than an indication of toxicity, and fever up to 105°F and tachycardia. The colt was it occurs because of a sudden release of vagal diagnosed with ventricular tachycardia and myo- tone at the atrioventricular (AV) node. Su- based on the results of ECG, echocardio- praventricular tachycardia (SVT) has tradition- gram, cardiac troponin I, routine laboratory ally been treated with digoxin (0.0022 mg/kg, evaluation, and additional diagnostics. Conversion IV, if heart rate [HR] is rapidly increasing and to was challenging and attempted not responsive to stimulation or 0.011 mg/kg, with lidocaine, magnesium sulfate, procainamide, PO, if HR is steady and returns to normal with and quinidine; ultimately, it was successful with stimulation). amiodarone. Additional supportive therapy in- 5. Amiodarone (5 mg/kg/h for 1 h followed by cluded furosemide, flunixin meglumine, dexametha- 0.83 mg/kg/h for up to 48 h) is a class III sone, broad-spectrum antibiotics, and judicious use of anti-arrhythmic agent. It has been used in IV fluids. humans to treat atrial fibrillation (AF), atrial Ventricular tachycardia is considered a life- flutter, and ventricular tachyarrhythmias. threatening condition in advanced cases. A step- In horses, amiodarone has been successfully wise approach to diagnosis and antidysrhythmic used to treat chronic atrial fibrillation and treatment will result in the best outcome. Thera- 8,9 refractoryventriculartachycardia. Amio- peutic monitoring during treatment must be done darone blocks sodium and calcium channels with periodic or continuous ECG readings; however, in addition to beta-adrenoreceptors. It also this limits feasibility of treatment to practitioners prolongs repolarizations and increases the with monitoring systems. Amiodarone should be 10 duration of the action potential. Oral bio- considered as a potential therapy in refractory availability of amiodarone in horses is low cases, and reports of its use in horses have increased 11 and variable ranging between 6% and 34%. in the past several years. 6. Esmolol is administered at 200 ␮g/kg over 1 min; if there is no response after 10 min, 500 ␮g/kg is administered over 1 min. If the References horse converts, CRI can be maintained at 25 1. Yamamoto K, Yasuda J, Too K. Arrhythmias in newborn ␮g/kg/min until switched to oral propano- Thoroughbred foals. Equine Vet J 1992;24:169–173. lol. Esmolol is a class II beta-adrenorecep- 2. Reimer JM, Reef VB, Sweeney RW. Ventricular arrhyth- mias in horses—21 cases (1984–1989). J Am Vet Med Assoc tor antagonist. Like propranolol, it works 1992;201:1237–1243. by slowing the cardiac rate. 3. Reef VB. Frequency of cardiac arrythmias and their signif- 7. Propafenone (0.5–1 mg/kg in 5% dextrose, IV, icance in normal horses, in Proceedings. 7th Annual Amer- slowly over 5–10 min) is a class IC drug that ican College of Veterinary Internal Medicine Meeting 1989; blocks sodium channels and is a beta-adreno- 506–508. 4. Reef VB, McGuirk SM. of the cardiovascular sys- receptor antagonist. IV propafenone has tem. In: Smith B, ed. Large animal internal medicine, 4th been used successfully in horses for refractory ed. St. Louis, MO: Mosby Elsevier, 2009;453–489. ventricular tachycardia.4 Unfortunately, the 5. Begg LM, Hoffmann KL, Begg AP. Serum and plasma car- IV formulation is currently not available in diac troponin I concentrations in clinically normal Thorough- the United States. breds in training in Australia. Aust Vet J 2006;84:336–337. 12 6. Meyer GA, Lin HC, Hanson RR, et al. Effects of intravenous 8. Bretylium tosylate (3–5 mg/kg, IV; it can be lidocaine overdose on cardiac electrical activity and blood repeated up to a total dose of 10 mg/kg) is pressure in the horse. Equine Vet J 2001;33:434–437.

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7. Bowen IM. Cardiac dysrhythmias. In: Robinson NE, ed. 10. Gill J, Heel RC, Fitton A. Amiodarone—an overview of its Current therapy in equine medicine, 5th ed. St. Louis, MO: pharmacological properties, and review of its therapeutic use Saunders, 2003;602–613. in cardiac arrhythmias. Drugs 1992;43:69–110. 8. De CD, Van LG, Baert K, et al. Intravenous amiodarone 11. De CD, Baert K, Croubels S, et al. Evaluation of the phar- treatment in horses with chronic atrial fibrillation. Vet J macokinetics and bioavailability of intravenously and orally 2006;172:129–134. administered amiodarone in horses. Am J Vet Res 2006;67: 9. De CD, Van LG, Baert K, et al. Treatment with amiodarone 448–454. of refractory ventricular tachycardia in a horse. J Vet Int 12. Reef VB. Arrhythmias. In: Marr CM, ed. of Med 2007;21:878–880. the horse. W.B. Saunders Elsevier, 1999;177–209.

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