Ventricular Tachycardia

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Tyson, a 6-year-old neutered boxer dog, was presented for evaluation of 3 exercise-induced collapsing episodes over 2 hours. During each episode, Tyson appeared to briefly lose consciousness and then abruptly “woke up.”

Case Summary

Figure 1. A 3-lead ECG (paper speed, 25 mm/sec; sensitivity, 10 mm/mV) demonstrating a single VPC (arrow) followed by 2 sinus complexes, then an abrupt onset of rapid monomorphic ventricular tachycardia.

On presentation, Tyson appeared depressed, had pale mucous membranes and a prolonged capillary refill time (3 seconds), and was tachycardic (300 bpm), with frequent femoral pulse deficits. No murmurs or abnormal lung sounds were heard on auscultation. An ECG revealed frequent ventricular premature complexes (VPCs) and periods of sustained ventricular tachycardia (VT). (See Figure 1.) Differentials for ventricular arrhythmias include primary cardiac disorders (congenital or acquired valvular heart disease, cardiomyopathies, myocarditis, infiltrative neoplasia), systemic disorders (electrolyte derangements, acid-base imbalances), and intra-abdominal disorders (hepatic/splenic disease, pheochromocytoma). Based on the signalment and morphology of the VPCs, Tyson was presumptively diagnosed with arrhythmogenic right ventricular cardiomyopathy (ARVC).

Related Aricle: Obtaining a Diagnostic Electrocradiogram

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Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC)

  • ARVC is a familial myocardial disease primarily of boxer dogs characterized by fatty or fibrofatty infiltration of the myocardium resulting in primarily ventricular arrhythmias.9
  • Ventricular premature complexes typically have an upright QRS morphology in leads II, III, and aVF, indicative of an origination of ectopy from the right ventricular myocardium.10
  • The prognosis is typically good, though sudden death is always possible even with therapy. Development of myocardial dysfunction and CHF warrants a guarded prognosis.11 
  • The true prevalence of ARVC in boxer dogs is unknown, though 1 study found increased ventricular ectopy in 25% of clinically normal adult boxers.12

Treatment Plan

The primary differentials for acute collapse include syncope and seizures. A detailed history and thorough physical examination are imperative. Even with ancillary diagnostic testing, a definitive diagnosis is not always identified.1,2 Syncope, a transient loss of consciousness and postural tone caused by decreased cerebral perfusion, is characterized by rapid onset, brief duration, and spontaneous recovery. Causes include both cardiac and noncardiac disorders. (See Table 1.) 

Related Article: Client Emergencies: Not Just About the Pet

Table1
Pathophysiologic Mechanisms for Syncope
CardiovascularMetabolicReflexive

Arrhythmias

  • Bradyarrhythmias
  • Tachyarrhythmias
Anemia

Situational syncope

  • Cough, micturition, defecation

Reduced myocardial contractility

  • Dilated cardiomyopathy
HypoglycemiaVasovagal syncope

Reduced cardiac filling

  • Pericardial effusion/tamponade
  • Hypertrophic cardiomyopathy
Hypoxia 

Obstruction to outflow

  • Valvular stenosis
  • Heart base and intracardiac tumors
  • Pulmonary hypertension
Electrolyte derangements 
Right-to-left cardiac shunts  
CardiovascularMetabolicReflexive

Arrhythmias

  • Bradyarrhythmias
  • Tachyarrhythmias

Reduced myocardial contractility

  • Dilated cardiomyopathy

Reduced cardiac filling

  • Pericardial effusion/ tamponade
  • Hypertrophic cardiomyopathy

Obstruction to outflow

  • Valvular stenosis
  • Heart base and intracardiac tumors
  • Pulmonary hypertension

Right-to-left cardiac shunts

Anemia

Hypoglycemia

Hypoxia

Electrolyte derangements

Situational syncope

  • Cough, micturition, defecation

Vasovagal syncope

 

Auscultatory findings of murmurs, gallops, muffled heart sounds, and arrhythmias can suggest underlying cardiac disease. If no obvious cause is apparent on physical examination, additional diagnostics (eg, CBC, chemistry panel, blood pressure, ECG, thoracic radiographs, echocardiogram) are warranted.

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No studies have evaluated the effect of antiarrhythmics on long-term survival or risk reduction for sudden death. The decision to treat ventricular arrhythmias is often dependent on the presence of clinical signs and hemodynamic compromise, as well as the frequency of VPCs and the complexity of the arrhythmia. (See Table 2.) IV lidocaine is the preferred treatment for acute management of VT in hemodynamically unstable patients. 

Table2
Indications for Treatment of Ventricular Arrhythmias
Clinical SignsNo Clinical Signs (but ECG evidence of either):
Exercise intolerance, fatigue, syncope

Increased frequency

  • >1000 VPCs/24h
 

Increased complexity

  • Multiform VPCs
  • Couplets, triplets
  • Ventricular tachycardia
  • R-on-T phenomenon
Clinical SignsNo Clinical Signs (but ECG evidence of either)
Exercise intolerance, fatigue, syncope

Increased frequency

  • >1000 VPCs/24h

Increased complexity

  • Multiform VPCs
  • Couplets, triplets
  • Ventricular tachycardia
  • R-on-T phenomenon

 

ECG telemetry is essential for monitoring therapy response. Once VT has resolved, a constant rate infusion (CRI) of lidocaine is necessary because of its short half-life. 

For chronic antiarrhythmic management, oral therapy with a β-adrenergic blocker, potassium channel blocker, and/or a sodium channel blocker can be considered. If systolic function is normal, the author prefers single agent therapy with sotalol, a potassium channel blocker with additive β-adrenergic blocking properties. If systolic dysfunction is present, then single agent therapy with a sodium channel blocker such as mexilitine or procainamide is often chosen, as the negative inotropic effects of β-blockers can exacerbate myocardial failure. 

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When possible, pre-treatment Holter monitoring (ie, 24 hour ambulatory ECG) should be performed to further characterize the arrhythmias and guide therapy, with repeat Holter monitoring 2 to 4 weeks after initiating therapy. Given the high degree of day-to-day variation in the frequency of arrhythmias in boxers with ARVC, greater than 85% reduction in the frequency of ventricular ectopy is required to document efficacy of therapy. If single agent therapy is ineffective at reducing the complexity of arrhythmias or the frequency of VPCs by more than 85%, then additional antiarrhythmic therapy is warranted. Sotalol monotherapy and therapy with a combination of mexilitine with either sotalol or atenolol have all been shown to reduce the frequency of arrhythmias.3,4 Supplementation with fish oils may also reduce the frequency of arrhythmias.5 No studies have evaluated the effects of antiarrhythmics on long-term survival or risk reduction for sudden death; however, a recent retrospective study found no difference in survival when using either sotalol, mexilitine and atenolol, or procainamide therapy.6 Periodic echocardiographic evaluation is also recommended for detection of myocardial dysfunction. 

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Outcome

Figure 2. A lead II ECG (paper speed, 25 mm/sec; sensitivity, 10 mm/mV) demonstrating conversion of ventricular tachycardia to a sinus rhythm after 2 mg/kg of lidocaine was administered IV.

Tyson’s VT resolved after he received a lidocaine bolus (2 mg/kg IV over 30 seconds). (See Figure 2.) A constant rate infusion (CRI) was subsequently initiated at 40 mcg/kg/min. A proportion of boxers may present with or eventually develop myocardial dysfunction, which may resemble dilated cardiomyopathy and can result in CHF and shorter survival times.7,8,11 Tyson’s echocardiogram revealed no structural abnormalities and his systolic function was normal. Therapy with sotalol at 2 mg/kg PO twice a day was initiated. After 24 hours, the lidocaine CRI was discontinued with no recurrence of ventricular ectopy and Tyson was discharged. 

Holter monitoring 3 weeks later revealed only infrequent VPCs. Tyson’s arrhythmias appeared adequately controlled and he remains free of clinical signs 3 years post-diagnosis. 

Team Roles

The Role of Veterinary Nurses in Case Management of Cardiac Arrhythmia

In small animal practice, the veterinary nurse plays an important role in the case management of a cardiac arrhythmia patient and should be involved in several key steps during the diagnostic and treatment processes.  

Step 1

The veterinary nurse should make initial contact with the patient while triaging and obtaining temperature, pulse, and respiration (TPR) and collecting patient history. The client may indicate that the patient is fainting or collapsing, or has had a seizure. Distinguishing between seizure and syncope can be challenging. Important historical information can be obtained by asking questions like these: 

  •  How often do the events occur and how long do they last? 
  •  Are they associated with exercise or activity (eg, excitement when the client arrives home)? 
  •  Does the pet take any medication? 
  •  Was there any possible exposure to toxins? 
  •  Were the muscles rigid or relaxed during the event? 
  •  Did the patient seem confused before or after the event? 

A video of the event made by the client is helpful for the veterinarian to make the diagnosis. A seizure diagnosis is generally made after ruling out syncope.

Related Article: Skills for Veterinary Technicians: IV Catheter Placement

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Step 2

Once a diagnosis of VT is suspected, the veterinary nurse may assist with diagnostics, including:

  • Recording a diagnostic quality 6-lead ECG with the patient in right lateral recumbency. It should include a short strip of leads I, II, III, aVL, aVR, aVF; a strip of lead II recorded at a paper speed of 50 mm/sec; and a long strip of lead II recorded at 25 or 50 mm/sec. The patient’s heart rate dictates the appropriate paper speed to easily characterize the ECG complexes.
  • Restraining the patient during an echocardiogram.
  • Measuring non-invasive blood pressure (BP) that will be used to determine the hemodynamic significance of any arrhythmia. 
  • A veterinary nurse skilled in either Doppler or oscillometric BP measurement is needed. An appropriate BP cuff will be ≈40% as wide as the circumference of the limb to which it is attached.13 
  • Placing an intravenous (IV) catheter. The importance of good vascular access cannot be over-emphasized. The IV catheter will be used to deliver intravenous therapy for the arrhythmia and is often placed at the initial suspicion of VT. “The biggest catheter you can get in” rule does not necessarily apply. It is unlikely the patient will need large boluses of fluids quickly. It is more important to have a well-placed, secure catheter that will remain patent for 2 to 3 days. 

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Step 3

Continuous ECG monitoring is required for these patients. Any ECG system can be employed, but an ambulatory telemetry system is ideal. Electrodes can be placed on the trunk to allow for normal postural movements. The veterinary nurse can place the white (RA) electrode on the patient’s right thorax cranial to the heart in the axilla or the thoracic inlet, and the black (LA) and red (LL) electrodes on the patient’s left thorax caudal to the heart. Both electrodes can be placed in close proximity, provided both are caudal to the apical impulse, similarly to the base-apex lead used in large animals. With the ECG monitor set to display lead I or lead II, this will provide essentially a lead II ECG appropriate for identification of arrhythmia. A light bandage can be placed over the thorax to prevent electrodes and wires entangling. 

Client Communication

Clients may call the practice to ask the veterinary nurses questions about their dog’s prescribed oral medications. Below are key points about the most common antiarrhythmic drugs (ie, sotalol, mexilitine, atenolol):

  • Sotalol and atenolol are β-adrenergic receptor blockers (β-blockers); sotalol also can delay myocardial repolarization. These drugs may cause the dog to be less active and experience hypotension. To limit adverse effects, the dosage of these drugs can be gradually increased over several weeks.
  • Mexilitine is similar to lidocaine but is active in an oral form and may cause nausea or vomiting. This drug should be given with a meal, and is typically administered 3 times a day.

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Clients should contact a veterinarian if patients experience any adverse effects. 

Clients may also call to ask what constitutes an emergency in their pet. An emergency visit is always warranted if syncopal events increase in frequency or duration, or new signs develop relating to underlying structural heart disease (ie, cough, increased respiratory rate, loss of appetite, exercise intolerance, distended abdomen).

Related Article: The Art of Triage

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Grief Support

Despite therapy, patients with arrhythmia may be at increased risk for sudden death or, if structural heart disease is also present, developing chronic heart failure (CHF). The practice team, including veterinary nurses, should be familiar with grief counseling options and able to share resources with owners who have lost or are facing the loss of their pet. The Association for Pet Loss and Bereavement website is a valuable resource. 

Team
Takeaways

Veterinarians:

Prompt assessment and aggressive treatment for hemodynamically unstable dogs with ventricular tachycardia is necessary, yet most patients will respond favorably to antiarrhythmic therapy. 

Nursing Team:

Veterinary nurses should be skilled at several key steps in the diagnostic and treatment process of a cardiac arrhythmia patient to allow the veterinarian to talk with the client while ECG, BP, and IV catheter procedures are in progress.

Client Care Team:

Grief counseling or triage may be necessary in the event of a patient emergency situation or sudden death, and the team should have resources available to help the client. 

References and author information Show
References
  1. MacKie BA, Stepien RL, Kellihan HB. Retrospective analysis of an implantable loop recorder for evaluation of syncope, collapse, or intermittent weakness in 23 dogs (2004-2008). J Vet Cardiol. 2010;12(1):25-33.

  2. Barnett L, Martin MW, Todd J, et al. A retrospective study of 153 cases of undiagnosed collapse, syncope or exercise intolerance: the outcomes. J Small Anim Pract. 2011;52(1):26-31.

  3. Meurs KM, Spier AW, Wright NA, et al. Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. JAVMA. 2002;221(4):522-527.

  4. Prosek R, Estrada A, Adin D. A comparison of sotalol and mexilitine versus stand-alone sotalol in treatment of boxer dogs with ventricular arrhythmias [abstract 135]. In: Proceedings of the American College of Veterinary Internal Medicine Forum. 2006; Louisville, KY; 777.

  5. Smith CE, Freeman LM, Rush JE, et al. Omega-3 fatty acids in boxer dogs with arrhythmogenic right ventricular cardiomyopathy. JVIM. 2007; 21(2):265-273.

  6. Caro-Vadillo A, Garcia-Guasch L, Carretón E, et al. Arrhythmogenic right ventricular cardiomyopathy in boxer dogs: a retrospective study of survival. Vet Rec. 2013;172(10):268.

  7. Meurs KM, Stern JA, Reina-Doreste Y, et al. Natural history of arrhythmogenic right ventricular cardiomyopathy in boxer dogs: a prospective study. JVIM. 2014;28(4):1214-1220.

  8. Baumwart RD, Meurs KM, Atkins CE, et al. Clinical, echocardiographic, and electro-cardiographic abnormalities in boxers with cardiomyopathy and left ventricular systolic dysfunction: 48 cases (1985-2003). JAVMA. 2005;226(7):1102-1104.

  9. Basso C, Fox PR, Meurs KM, et al. Arrhythmogenic right ventricular cardiomyopathy causing sudden cardiac death in boxer dogs: a new animal model of human disease. Circulation. 2004;109(9):1180-1185.

  10. Kraus MS, Moïse NS, Rishniw M, et al. Morphology of ventricular arrhythmias in the boxer as measured by 12-lead electrocardiography with pace-mapping comparison. JVIM. 2002;16(2):153-158.

  11. Palermo V, Stafford Johnson MJ, Sala E, et al. Cardiomyopathy in boxer dogs: a retrospective study of the clinical presentation, diagnostic findings and survival. J Vet Cardiol. 2011;13(1): 45-55.

  12. Stern JA, Meurs KM, Spier AW, et al. Ambulatory electrocardiographic evaluation of clinically normal adult boxers. JAVMA. 2010; 236(4):430-433.

  13. Binns S, Sisson DD, Buoscio DA, et al. Doppler ultrasonographic, oscillometric sphygmomanometric, and photoplethysographic techniques for noninvasive blood pressure measurement in anesthetized cats. JVIM. 1995;9(6):405-414.

Authors

Stacey Leach

DVM, DACVIM (Cardiology) University of Missouri

Stacey Leach, DVM, DACVIM (Cardiology), is assistant teaching professor of veterinary cardiology and serves as director of the small animal rotating internship program at University of Missouri. Stacey earned his DVM from Texas A&M University and completed a 1-year rotating internship in both small animal medicine and surgery and a 3-year residency in cardiology at University of Missouri. He has authored numerous publications, lectured at both regional and national levels, and serves as a reviewer for several veterinary journals.   

FUN FACT: In his free time, Stacey can be found in the gym or enjoying the outdoors with his 2 4-legged kids—Tyson, a Labrador retriever, and Layla, a standard schnauzer.

H. Edward Durham Jr

CVT, LATG, VTS (Cardiology) Ross University School of Veterinary Medicine

H. Edward Durham Jr, CVT, LATG, VTS (Cardiology), is a senior veterinary technician in the anesthesia service at Ross University School of Veterinary Medicine. Ed is a charter member of the Academy of Internal Medicine for Veterinary Technicians and serves as the director at large (cardiology). He began his work in veterinary medicine in 1976 and is also a national and international speaker in veterinary cardiology.

FUN FACT: Ed is a dedicated martial artist, trained in Japanese and Filipino styles of self-defense. He lives in the Caribbean, on Saint Kitts and Nevis, and practices on the beach.

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