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Tachyarrhythmias

Tachyarrhythmias: Where are they coming from?
Kursten Pierce, DVM

Arrhythmias, especially ventricular arrhythmias, can be life-threatening if not treated in a timely manner and with the right antiarrhythmic medication. Choosing an appropriate antiarrhythmic therapy depends on the type of arrhythmia, including origin (supraventricular vs. ventricular), arrhythmogenic mechanism, metabolic status of patient (evaluate for electrolyte imbalances), presence of underlying structural heart disease and/or congestive heart failure, and the patient’s co-morbidities.

Normal cardiac conduction starts with an impulse from the sinoatrial (SA) node, the primary pacemaker of the heart, and travels through the internodal pathways across the atria to the atrioventricular (AV) node, which is the gatekeeper of electrical activity to the ventricles. Next, the impulse travels from the AV node to the Bundle of His, bundle branches, and Purkinje fibers. The various components of the normal cardiac conduction can be evaluated with a surface electrocardiogram (ECG), either lead II rhythm strip or 6-lead ECG if available.

Arrhythmogenic mechanisms include altered automaticity (enhanced normal, abnormal), re-entry mechanism, or triggered activity (early or delayed afterdepolarization). Enhanced normal automaticity occurs when there is an inappropriate discharge from the normal pacemaker and is typically caused by adrenergic stimulation. An example would be inappropriate sinus tachycardia at rest. Abnormal automaticity occurs when there is an ectopic pacemaker, which occurs when a non-pacemaker cell such as an atrial or ventricular myocyte spontaneously depolarizes at a rate faster than the SA node. Ischemia and hypoxia of the myocardium can create a focus for ectopic beats. A re-entry arrhythmia can occur when there is repetitive propagation of an impulse around an area of non-conducting tissue (anatomic or functional obstacle). Examples of a re-entry arrhythmia include atrial fibrillation, atrial flutter, or an accessory pathway. Arrhythmia can also be triggered by a preceding beat and spontaneously depolarize the ventricular myocytes leading to ventricular tachycardia or Torsades de Pointes.

Depending on the degree of tachycardia, it may be difficult to sort out the origin of the arrhythmia. Clues for distinguishing between supraventricular (SVT) and ventricular tachycardia (VT) can include evaluation of the QRS duration, morphology and cycle length regularity (AV conduction). SVT is a rapid rhythm (heart rate (HR) >180-200 bpm) originating from above the ventricles and typically has a narrow complex (QRS < 70 ms dogs, < 40ms cats). VT is a wide complex tachycardia (HR > 160 -180 bpm) originating from an ectopic ventricular focus. Other important clues to help better classify the arrhythmia include whether there is a constant QRS morphology (monomorphic) or a beat-to-beat variation in appearance (polymorphic) and whether the cycle length is normal (constant R-R interval) or irregular (variable R-R intervals).

It is important to rule out sinus tachycardia, which may be characterized by a regular rhythm with heart rate > 160 bpm with visible P waves on ECG and a constant PR interval. There may be a ramp up and slow down of the arrhythmia, which may respond to a vagal maneuver (ocular pressure, carotid sinus massage) and result in gradual slowing on the HR. Patients who are in pain, shock, hypovolemic, anemic, excited or CHF may exhibit sinus tachycardia; the underlying cause should be treated with no specific anti-arrhythmic treatment.

If a narrow complex tachycardia is identified and sinus tachycardia has been ruled out, there may be evidence of atrial activation (P’, flutter, or fibrillation waves) that can provide evidence for determining the type of SVT. Keep in mind that atrial waves may be hidden in the previous ST segment or T wave, especially at faster heart rates. There may be an abrupt onset and termination of the arrhythmia, usually with a single beat. Treatment of SVT is mostly aimed at slowing AV nodal conduction. Common types of SVT include atrial fibrillation (irregularly irregular R-R intervals, absence of P waves, +/- fibrillation waves) and atrial flutter (typically regular R-R intervals, saw-toothed oscillations). Other types of SVT include focal atrial tachycardia (FAT) or an accessory pathway (OAVRT), where an early P wave (P’ wave) or delta wave (wave seen on the upstroke of the QRS indicating ventricular pre-excitation) with short PQ interval may be visualized, respectively. If SVT is causing hemodynamic compromise such as poor perfusion (weak femoral pulses, pale mucus membranes) or collapse, emergency medications include IV diltiazem, esmolol or procainamide. In general, SVT is rarely life-threatening and is managed with oral medications such as diltiazem (first choice), digoxin, sotalol or amiodarone. Typical doses for treating atrial fibrillation and atrial flutter are diltiazem (Dilacor®) ER 1-3 mg/kg PO BID and digoxin 0.003 -0.005 mg/kg PO BID (do not exceed 0.25 mg PO BID).

If a wide complex tachycardia is present, when in doubt treat for ventricular tachycardia as this is life-threatening arrhythmia that can lead to ventricular fibrillation and death. The exception for a wide complex tachycardia not being ventricular in origin would be atrial fibrillation in conjunction with a bundle branch block. In this scenario, treating for VT with lidocaine (2 mg/kg IV bolus) will not cause harm to the patient. A common approach to treating VT includes administering lidocaine IV boluses (2mg/kg) to convert to sinus rhythm and if successful start on a lidocaine CRI at 50 mcg/kg/min. Generally, three doses are administered before determining that the lidocaine was unsuccessful. If this occurs, procainamide IV boluses (2 mg/kg IV repeated up to 4-6 times) can be administered and followed by a CRI. Procainamide is effective for conversion for VT as well as SVT. If the VT is refractory to lidocaine and procainamide administration and the dog is able to receive oral medications, sotalol 1-3 mg/kg can be administered; however, if that patient is hemodynamically compromised then amiodarone should be administered IV (1-2 mg/kg IV boluses (up to 3-5 mg/kg) followed by a CRI. Oral antiarrhythmic drugs used to maintain sinus rhythm and control ventricular arrhythmias include sotalol, mexiletine, beta-blockers such as atenolol in combination with mexiletine, or amiodarone. Sotalol and amiodarone are class III antiarrhythmics and work well for patients with a combination of supraventricular and ventricular arrhythmias.

Antiarrhythmics that are negative inotropes (diltiazem, sotalol, beta-blockers) should be used with caution in patients with poor contractile function or in active congestive heart failure. Amiodarone should be avoided or used with caution in patients with thyroid disease and liver disease as side effects include thyroid dysfunction and hepatopathy (both of which are reversible with discontinuation of the drug).

When choosing appropriate antiarrhythmic therapy, one should take into account the type and origin of the arrhythmia (+/- mechanism of the arrhythmia), patient’s metabolic status, underlying structural heart disease and other co-morbidities.

If you have a patient with an arrhythmia and have any concerns regarding treatment or would like to send your patient for referral, please do not hesitate to call Dr. Pierce at 781.684.8387.