In the emergency setting, we are commonly confronted with cardiac arrhythmias either as a consequence of an underlying disease or as a primary cause of potentially life-threatening clinical signs. This refresher lecture aims to provide a practical summary of common tachy- and brady-arrhythmias in the emergency setting, their ECG diagnosis and initial treatment.

When confronted with an irregular heart rhythm, bradycardia (<60–70 bpm in dogs, <140 bpm in cats) or tachycardia (>160 bpm in dogs, >220 bpm in cats) in the emergency room, the basic questions to answer are:

1.  Is the arrhythmia hemodynamically significant?

2.  What is the rhythm diagnosis?

3.  What is the underlying cause (non-cardiac or cardiac)?

To answer these questions, the first steps to undertake are to monitor the ECG and to non-invasively measure blood pressure. Arrhythmias that cause a decrease in blood pressure require emergency management, most commonly these are severe tachycardias, very slow bradycardias, or tachycardias/normal heart rate followed by long pauses. These are often life-threatening and commonly have a primary cardiac cause.

Luckily, primary cardiac arrhythmias occur less frequently than arrhythmias due to underlying systemic disease. They are less likely to be acutely life-threatening, but nevertheless may have hemodynamic consequences, requiring adequate diagnosis and potential treatment.

Possible systemic causes for arrhythmias include (non-exhaustive list):

• Electrolyte abnormalities
• Hypoxia
• Abdominal disease: gastric-dilation volvulus, pancreatitis, splenic disease
• Intracranial disease
• Myocardial trauma/blunt chest trauma
• Heat stroke
• Hypothermia
• Intoxication/drug-related
• Infectious diseases
• Endocrine disease
• Vagotonia/dysautonomia
• Autoimmune disease
• Electrocution

Arrhythmias can be classified according to their rate into tachyarrhythmias or bradyarrhythmias, and according to their anatomical site of origin into ventricular arrhythmias and supraventricular arrhythmias. Tachycardias are often described as narrow complex tachycardias (QRS-duration <70 ms in dogs and <40 ms in cats) or wide complex tachycardias (QRS-duration >70 ms in dogs and >40 ms in cats). Usually narrow-complex tachycardias are supraventricular and wide complex tachycardias are ventricular in origin. However, conduction delays cause widened QRS-complexes and one needs to be aware that this can make a supraventricular tachycardia appear like a wide complex tachycardia.

Ventricular Arrhythmias

ECG Diagnosis

The hallmark of ventricular complexes is that they are too wide (>70 ms in dogs, >40 ms in cats), not associated with a P-wave and their T-wave direction is opposite to the main deflection of the QRS-complex. Ventricular premature complexes can occur as single premature beats, as couplets, triplets or as runs (≥4 complexes), that can be sustained (lasting more than 30 seconds) or non-sustained (less than 30 seconds). Importantly, when a ventricular complex occurs after a pause, it is an escape beat, functioning as a rescue mechanism and treatment is of course contra-indicated.

Assessment

To determine the danger of ventricular arrhythmias the first thing to assess is the rate and duration of the ventricular tachycardia. If the rate is in the normal range (within 10% of variation of the underlying sinus rhythm or in the dog arbitrarily ≤160 bpm) ventricular runs are usually called an ‘accelerated idioventricular rhythm.’ The ventricular rhythm is competing with the sinus rhythm often causing ‘fusion beats.’ It is usually monomorphic (1 QRS-morphology), non-sustained and repetitive with periods of sinus rhythm. Usually, this rhythm has limited hemodynamic significance and does not require treatment, unless cardiac structure or function is compromised. For example, a Great Dane with gastric dilatation volvulus and underlying dilated cardiomyopathy may need medical intervention for an accelerated idioventricular rhythm during postoperative care, whereas a dog with normal cardiac function may not. If ventricular runs are present at a rate higher than 160 bpm, they are often referred to as ‘ventricular tachycardia.’ Ventricular tachycardia (VT) can be caused by underlying systemic disease or can have a primary cardiac cause. They are described as monomorphic when there is a single QRS-complex morphology or pleomorphic when there are 2 or more different QRS-complex morphologies. Criteria to determine the immediate danger are again the rate, duration, and cardiac function.

Ventricular arrhythmias may also manifest as single premature ventricular beats, couplet, triplets, or in patterns such bigeminy and trigeminy. When these ectopic beats have a short coupling interval, e.g., the R-wave occurs close to the peak of the previous T-wave (R-on-T phenomenon) this may initiate ventricular fibrillation as a potentially fatal rhythm. In Dobermann Pinschers it has been documented that a fastest coupling interval of ≥260 bpm of ventricular ectopic beats is associated with a higher risk of sudden cardiac death.

Treatment

First line treatment for ventricular arrhythmias is IV lidocaine, in a bolus of 2–4 mg/kg IV in dogs (to be repeated up to a cumulative dose of 8 mg/kg) followed by a CRI of 25–80 µg/kg/minute. The dose in cats is lower, with 0.25–0.5 mg/kg boluses (up to a cumulative dose of 2 mg/kg) and CRI of 0.01–0.04 mg/kg/minutes. Amiodarone is another option, but water soluble amiodarone may not be readily available. If lipid soluble amiodarone is administered, this must be done very slowly (at least over 10 minutes) to reduce the risk of hypotension.

For ventricular fibrillation the treatment consists of electrical defibrillation (2–5 J/kg) potentially in combination with magnesium sulfate IV (20 mg/kg) in refractory cases as demonstrated in a recent case report. Alternatively, a precordial thump can be attempted or IV lidocaine or amiodarone.

Supraventricular Arrhythmias

ECG Diagnosis

The main ECG criterion of supraventricular complexes is that they are narrow (<70 ms in dogs, <40 ms in cats), except when there is an intraventricular conduction delay. Supraventricular tachycardias have a rate >180 bpm in dogs and >220 bpm in puppies and cats.

Sinus tachycardia must be differentiated from other supraventricular tachycardias (SVTs). In sinus tachycardia QRS-complexes are narrow, and p-waves have normal morphology with a physiologic PQ-interval, but sometimes are superimposed on the previous T-wave. The maximal sinus rate is poorly defined but probably lies around 250 bpm in dogs. Differentiation between sinus tachycardia and other SVTs can be made by treating the underlying cause of the sinus tachycardia, vagal manoeuvre, or sedation of a nervous animal.

Atrial fibrillation (Afib) is the most common supraventricular tachycardia. The ECG characteristics are an irregular, narrow complex tachycardia without visible p-waves. Instead, fibrillation waves are seen at a rate of 400–600 bpm. Luckily the AV node slows the ventricular response to an average rate of 130–260 bpm in dogs and 200–280 bpm in cats. When there is aberrant conduction, QRS complexes can be wide and in that case Afib mimics VT. The key criterion to differentiate Afib with aberrant conduction from VT is the presence of irregular R-R intervals in Afib.

Other SVTs include atrioventricular tachycardias mediated by accessory pathways, junctional tachycardias, focal atrial tachycardia, and atrial flutter. Usually, these tachycardias have non-sinus p’-waves (or in the case of atrial flutter, F-waves), which distinguishes them from Afib, where p-waves are absent. It is outside the scope of this lecture to discuss the ECG diagnosis of all these tachycardias.

Assessment

Clinically, SVTs are better tolerated than VTs and also less likely to degenerate into ventricular fibrillation and death in the emergency room. However, when incessant they cause tachycardia-induced cardiomyopathy, a myocardial dysfunction mimicking dilated cardiomyopathy. When confronted with a narrow complex tachycardia, first steps are to define the ventricular rate and analyse the regularity of the R-R intervals, this will help to decide if it is Afib or a different SVT. Distinction between Afib and other SVTs is crucial because it influences treatment choice. Atrial fibrillation mainly occurs in 3 clinical scenarios: vagally mediated, associated with structural heart disease and ‘lone’ Afib in large breed dogs without structural heart disease. Differentiating these scenarios is important because they require a different therapeutic approach.

Treatment

Most commonly Afib is associated with underlying structural cardiac disease and the patient presents in congestive heart failure (CHF). With appropriate management of the CHF, the Afib rate will decrease and there usually is no need for emergency treatment with IV drugs. Vagally-mediated Afib is likely to occur in large breed dogs (as atrial mass is important in Afib) in situations with sudden alterations of vagal tone, for example anaesthesia/analgesia with opioid drugs, gastrointestinal surgery or pericardiocentesis. In this case IV lidocaine is the drug of choice, especially when administered <1 hour after onset of Afib. Large breed dogs with lone Afib usually have slow ventricular rates without hemodynamic compromise and do not require emergency treatment. In these dogs the arrhythmia usually is an incidental finding. Care must be taken with the administration of lidocaine in SVTs other than vagally-mediated Afib. Although it can be effective, a recent case-series described potential adverse effects, including ventricular fibrillation and cardiac arrest.

For other types of hemodynamically important SVTs (usually very high rates e.g., around 300 bpm), IV drugs that may be used in initial management are diltiazem, verapamil, or esmolol, usually a bolus followed by a CRI.

Bradycardias

Most bradycardias in the emergency setting are secondary to systemic disease such as sinoventricular rhythm due to hyperkalemia or sinus bradycardia associated with increased vagotonia, increased intracranial pressure, or hypothermia. Some patients present with clinical signs due to severe bradycardia caused by high grade second degree or third degree AV block, which usually has a primary cardiac cause.

ECG Diagnosis

High grade degree AV block is characterised by blocking of 2 or more consecutive p-waves, with normal QRS-complexes following the conducted p-waves and a normal or prolonged PQ-interval. In third degree AV block, p-waves are not conducted to the ventricles at all. The ECG shows p-waves that are completely unrelated to a ventricular (wide QRS) or junctional (narrow QRS) escape rhythm at a rate <40–60 bpm in dogs and between 80–140 bpm in cats.

Assessment

Severity is assessed by the heart rate, systemic blood pressure and clinical signs. Very slow (<30 minutes), irregular or variable escape rhythms may be at higher risk to stop abruptly than faster, regular, and uniform escape rhythms.

Treatment

High-grade second degree may be responsive to atropine, but third degree AV block generally is not. In clinically unstable dogs with very slow heart rates and hypotension, often the only effective emergency treatment is temporary pacing. This can be achieved with a temporary pacing lead inserted into the right heart via the jugular or saphenous vein, or via external placement of defibrillation patches on the chest wall and use of the pacing function of a defibrillator.

References

1.  Santilli R, Moïse NS, Pariaut R, Perego M. Electrocardiography of the Dog and Cat. Diagnosis of Arrhythmias, 2nd ed. Milano, Centro Leoni: Edra S.p.A.; 2018.

2.  Willis R, Oliveira P, Mavropoulou A. Guide to Canine and Feline Electrocardiography. New York, NY: John Wiley & Sons Ltd; 2018.

3.  Klüser L, Holler PJ, Simak J, et al. Predictors of sudden cardiac death in Doberman pinschers with dilated cardiomyopathy. J Vet Intern Med. 2016;30(3):722–732.

4.  Somberg JC, Cvetanovic I, Ranade V, Molnar J. Comparative effects of rapid bolus administration of aqueous amiodarone versus 10-minute cordarone IV infusion on mean arterial blood pressure in conscious dogs. J Invest Med. 2005;53(2):S359–S359.

5.  Gatson BJ, Swift S, Paranjape V. Successful treatment of prolonged refractory ventricular fibrillation in an anesthetized dog. J Vet Emerg Crit Care. 2022;32(1):129–134.

6.  Pariaut R, Moise NS, Koetje BD, et al. Lidocaine converts acute vagally associated atrial fibrillation to sinus rhythm in German shepherd dogs with inherited arrhythmias. J Vet Intern Med. 2008;22(6):1274–1282.

7.  Johnson MS, Martin M, Smith P. Cardioversion of supraventricular tachycardia using lidocaine in five dogs. J Vet Intern Med. 2006;20(2):272–276.

8.  Seo J, Spalla I, Vazquez DMP, et al. Rhythm disturbances associated with lidocaine administration in four dogs with supraventricular tachyarrhythmias. J Vet Emerg Crit Care. 2022;32(1):106–112.

9.  DeFrancesco T, Hansen B, Atkins C, et al. Noninvasive transthoracic temporary cardiac pacing in dogs. J Vet Intern Med. 2003;17(5):663–667.

10.  Syring RS, Costello MF, Poppenga RH. Temporary transvenous cardiac pacing in a dog with diltiazem intoxication. J Vet Emerg Crit Care. 2008;18(1):75–80.