Identifying the Rhythm: The Normal Activation Sequence

The physiologic electrical impulse normally originates in the sinus node, and propagates through the atria, entering the ventricles through the atrioventricular (AV) node, the His bundle, and Purkinje fibers. Normal ventricular tissue does not discharge spontaneously unless no other impulse arrives in a suitable period of time. This happens because the sinus node discharges in a higher frequency, followed by the auxiliary pacemakers in the AV junction, and ventricular conduction system. This is the so called "overdrive suppression", i.e., while the ventricular myocytes respond to a higher command, their automaticity is suppressed (the most rapid rhythm dominates). When a higher pacemaker does not discharge, then the conduction system cells can discharge spontaneously and "rescue" the rhythm. This happens, for example, when sinus node does not discharge, as in a sinus arrest or when there is an atrioventricular block, and we observe a ventricular escape complex. The ventricular escape complex happens after a pause, and occurs as an idioventricular rhythm, which discharges at 20-40 times/minute in a dog. This is not a ventricular arrhythmia, and must not be treated as so.

When the impulse arises prematurely from the ventricle, it is called ventricular premature complex (VPC). VPCs may be isolated, may appear in pairs, triplets, runs (more than 3 VPCs), or as paroxysmal or sustained (>15-30sec) ventricular tachycardia. Rapid, repetitive ventricular premature complexes can lead to a low cardiac output, reduced arterial blood pressure, reduced organ perfusion and signs of hypotension. Besides that, ventricular arrhythmias may become electrically unstable and degenerate to fatal ventricular fibrillation.

Isolated VPCs pose little risk for mortality and have minor effects on blood pressure. However, VPCs may be a risk marker for fatal arrhythmias in some breeds (Dobermann and Boxer).

Possible Causes

Ventricular arrhythmias may be associated with various cardiac and systemic (non-cardiac) problems, as ventricular hypertrophy (concentric or eccentric), hypoxemia, hypovolemia, hypotension, acid-base imbalances, electrolyte disturbances, trauma, cytokines (systemic inflammatory diseases, as pancreatitis, sepsis), drugs (digitalis, barbiturates, antiarrhythmics), myocardial hypoxia, pain, coagulopathies, gastric dilation-volvulus, shock. Therefore, it is necessary to determine the primary cause of the arrhythmia to have a better chance of successful treatment.

A complete history and physical examination, as well as ECG, echocardiogram, thoracic radiograph, arterial blood pressure, complete blood cell count, biochemical profile, and even cTnI levels should be performed to determine cardiac involvement. For a correct diagnosis of the arrhythmia, an ECG must be recorded.

Treat Or Not To Treat?--That's the Question!

We must remember that not all ventricular arrhythmias require treatment. As the treatment does not always have beneficial effects, and may cause adverse effects, we must be careful in what we choose to treat.

We assume that treating a dog with ventricular arrhythmias, it will reduce the risk of death. This is difficult to evaluate--and there is no evidence that the treatment will increase survival or avoid sudden death. It is very difficult to predict which animals are truly at risk for sudden death. We also hope that there will be a decreased frequency of dangerous arrhythmias, and that the treatment will abolish or improve related clinical signs.

The first rule is to correctly identify the arrhythmia. The second and third rule: every antiarrhythmic is potentially arrhythmogenic!

What Arrhythmias Need Emergency Treatment?

 Extremely urgent: Ventricular fibrillation (VF). There is no heart beat when ventricles are fibrillating--no pumping of blood.

 Relative urgency: Ventricular tachycardia.

When Therapy Should be Indicated? Current Criteria to Grade the Arrhythmia Severity

 Hemodynamic alteration: When the patient is symptomatic secondary to the arrhythmia (syncope, weakness, collapse, hypotension, exercise intolerance, respiratory effort, restlessness, worsening of heart failure).

 Presence of cardiac enlargement.

 Pairs, triplets of VPCs.

 When there is danger of rhythm progressing to ventricular fibrillation, i.e., multiform/polymorphic ventricular complexes; sustained /fast ventricular tachycardia (>180-200bpm); R-on-T phenomenon (R wave falling very close to the T wave of the preceding QRS complex).

Current considerations

 Arrhythmia malignancy--dependence on baseline heart rate: VPCs in the presence of elevated heart rate appears to have increased possibility to progress to fatal arrhythmia (VF).

 OBS: It is not known if VPCs in a normal/ low heart rate indicates less possibility of VF occurrence.

 Class I antiarrhythmics are considered more proarrhythmic (humans with asymptomatic VPCs treated with class I antiarrhythmics were more prone to sudden death than the patients who received placebo).

 Class III antiarrhythmics (Sotalol, Amiodarone, Bretylium) are considered safer, but still with no concrete evidences.

 In humans, some β-blockers increase survival.

Goals of Treatment

 Provide hemodynamic stability

 Decrease ventricular rate

 Decrease number of ventricular ectopic complexes

 Arrhythmia conversion to sinus rhythm

 Prevent arrhythmia recurrence

General Measures

 Confirm arrhythmia diagnosis with an ECG

 Treat primary cause

 Correct electrolyte (K+, Mg++) and acid-base disturbances, anemia, hypovolemia, hypoxia, azotemia

For immediate treatment of ventricular tachycardia in dogs, lidocaine is the drug of choice. For sustained VT, use lidocaine (2-4mg/kg bolus--over a minute) and repeat up to 8mg/kg (total dose over 10 minutes). If successful, perform constant rate infusion (CRI) of lidocaine (40-80mcg/kg/min). If no response to lidocaine, try procainamide (3-6mg/kg IV, followed by 10-50mcg/kg/min IV CRI) or 6-15mg/kg/4-6h IM). Magnesium may be tried. Next possibility would be a β-blocker [esmolol (50-100 mcg/kg boluses/5min up to 500 mcg/kg max; then 10-100 mcg/kg/min IV CRI), propranolol (0.02mg/kg IV bolus, max 0.2mg/kg). Selective β-blockers (atenolol, metoprolol) are better tolerated than propranolol. Avoid β-blockers in decompensated heart failure.

For maintenance (chronic management), mexiletine, β-blocker, sotalol, or amiodarone are the options. It is important to know the side effects of all the antiarrhythmics before prescribing. Association of mexiletine + β-blocker (atenolol) may be considered. For boxer arrhythmogenic cardiomyopathy, sotalol, mexiletine + atenolol, and even mexiletine + sotalol may be tried. Unfortunately, in Brazil, mexiletine has not been available in the last 2-3 years. Omega-3 fatty acids have been shown to reduce arrhythmia in animal models and humans, and reduced ventricular arrhythmia in a clinical study with Boxer right ventricular arrhythmogenic cardiomyopathy. Further studies are needed to determine the ideal dose regimen.

Important: Since the chronic therapy is still not based on clinical evidence, Holter monitoring is essential to choose the best antiarrhythmic regimen for individual dogs before initiating treatment, and for response follow-up. The therapeutic endpoint is not necessarily the termination of the arrhythmia.

References

1.  Billman GE, Kang JX, Leaf A. Prevention of ischemia-induced cardiac sudden death by n-3 polyunsaturated fatty acids in dogs. Lipids. 1997; 32 (11):1161-1168.

2.  Meurs KM, Spier AW, Wright NA, Atkins CE, DeFrancesco TC, Gordon SG, Hamlin RL, Keene BW, Miller MW, Moise NS. Comparison of the effects of four antiarrhythmic treatments for familial ventricular arrhythmias in Boxers. J Am Vet Med Assoc 2002; 221:522-527.

3.  Moïse NS. Diagnosis and management of canine arrhythmias: In: Canine and Feline Cardiology. 2nd edition. Fox, P. R., Sisson, D. D., Moïse, N. S., editors. Philadelphia, W. B. Saunders Company 1999, p. 331-385.

4.  Moïse NS. Chronic management of tachyarrhythmias in the dog. Waltham-OSU Symposium, 2002.

5.  Plumb DC. Veterinary Drug Handbook, 4ed., Iowa State University Press, Ames 1999.

6.  Smith CE, Freeman, LM, Rush JE, Cunningham SM, Biourge V. Omega-3 fatty acids in boxer dogs with arrhythmogenic right ventricular cardiomyopathy. J Vet Intern Med 2007; 21 (2):265-273.

7.  Smith Jr FWK. Ventricular tachycardia. In: The 5-minute Veterinary Consult. Tilley LP, Smith Jr FWK. Lippincott Williams & Wilkins. 2000, 390-391.

8.  Tilley LP. Essentials of Canine and Feline Electrocardiography. 3rd ed. Philadelphia. Lea&Febiger, 1992.