Accelerated Idioventricular Rhythm

Ventricular rhythms that are faster than ventricular escape, but slower than classical ventricular tachycardia are termed accelerated ventricular rhythms. Most ventricular escape rhythms have an inherent heart rate of 20-45 beats-per-minute (bpm) in the dog. Ventricular tachycardia is present if the rhythm is ventricular and the heart rate is arbitrarily over 180 bpm. Everything in between (heart rate 45-180 bpm) is considered to be accelerated, and usually the result of increased normal or abnormal automaticity occurring in the Purkinje fibers of origin. This may be the result of ischemia with subsequent reperfusion, hypoxia, electrolyte abnormalities as well as drugs (digitalis intoxication). The term accelerated idioventricular rhythm is used if atrioventricular dissociation is present. If ventriculoatrial association is present, then the term accelerated ventricular rhythm is used. This means the ventricular focus completely depolarizes the atrioventricular node retrogradely, capturing the atrial myocardium and sinus node from the bottom up. Most of the time, atrioventricular dissociation is present, and thus the prefix idio- is retained.

Atrioventricular dissociation is a condition that refers to the atria and the ventricles beating independently of one another. This is a broad category that involves multiple different electrocardiographic phenomena. This means that “atrioventricular dissociation” is not an electrocardiographic diagnosis, but rather a symptom of an underlying arrhythmic mechanism. Ventricular tachycardia, accelerated idioventricular rhythm, automatic junctional tachycardia and accelerated idiojunctional rhythm (both types of supraventricular tachycardia), block/acceleration dissociation and third degree atrioventricular block all may create atrioventricular dissociation.

Atrioventricular dissociation is termed "incomplete" (or “interference” atrioventricular dissociation) if fusion complexes or capture beats occur. A ventricular fusion complex is the result of an impulse originating at or above the atrioventricular node that merges with a depolarization initiated in the ventricle. The resultant QRS complex is intermediate in morphology between that of the supraventricular (usually sinus) focus and that of the ectopic focus in the ventricles and is preceded by a P wave, often with a short P-R interval. A capture beat is the first supraventricular beat (again, usually sinus) that occurs following a run of ectopic rhythm. If atrioventricular dissociation is incomplete, then the atrioventricular node is still capable of impulse transmission only if it is no longer refractory. Often the sinus rhythm is irregular (i.e. a sinus arrhythmia), and as it slows down a focus in the ventricles may take over until the sinus node outcompetes it again. Whichever focus is faster will dominate the rhythm. Atrioventricular dissociation is termed "complete" if no fusion complexes or capture beats occur, and the atrioventricular node is incapable of impulse transmission. This really only occurs in the setting of 3rd degree atrioventricular block, when the atrioventricular dissociation occurs by default.

Paper speed 50 mm/s, 1 cm/mV, lead II, canine with right atrial mass and pericardial effusion, sinus arrhythmia, incomplete atrioventricular dissociation secondary to usurpation by accelerated idioventricular rhythm. A right ventricular focus (producing a left bundle-branch block pattern) captures the rhythm before the second sinus beat is conducted, resulting in an accelerated idioventricular rhythm. The 5th complex is a sinus capture beat, accelerated idioventricular rhythm resumes after the 6th beat, and the 11th beat is another capture (the P wave is hiding in the T wave of the last ventricular complex). The sinus rate is approximately 111-150 bpm and the rate of the ventricular focus is similar at 130 bpm.

Paper speed 25 mm/s, 1 cm/mV, lead II, canine with immune-mediated hemolytic anemia. Sinus arrhythmia, incomplete atrioventricular dissociation secondary to usurpation by accelerated idioventricular rhythm. A left ventricular focus (producing a right bundle-branch block pattern) captures the ventricles with the 3rd complex (which is a fusion beat). The resulting accelerated idioventricular rhythm is hemodynamically well-tolerated by the dog since the sinus rate and the rate of the ventricular focus are both at around 125-150 bpm.

 

It is important to distinguish whether atrioventricular dissociation is occurring secondary to usurpation or by default. A rapid ventricular or junctional focus that outpaces the sinus node and takes control of the ventricles often results in atrioventricular dissociation. This is also termed atrioventricular dissociation due to usurpation, and the atrial (usually sinus) rate is normal or fast, but still less than that of the ventricles. Automatic junctional tachycardia, accelerated idiojunctional rhythm, ventricular tachycardia and accelerated idioventricular rhythm all may cause atrioventricular dissociation via usurpation. If atrioventricular dissociation is secondary to usurpation and the ventricular rate becomes unacceptably fast and hemodynamically compromising (i.e. during ventricular tachycardia with a HR of 250-300 bpm), then intervention is indicated. Slowing of the sinus rate, sinus arrest, atrial standstill and atrioventricular block may result in atrioventricular dissociation by default, in which case a junctional or ventricular escape rhythm may take over. When atrioventricular dissociation occurs by default, suppression of the rescuing focus may result in life-threatening bradycardia.

Otherwise known as “slow ventricular tachycardia,” accelerated idioventricular rhythm is usually monomorphic and only rarely polymorphic, irregular or associated with R on T phenomenon. If a premature beat depolarizes the ventricles again (producing an R wave) right when the ventricles are repolarizing from the previous beat (during the T wave), then ventricular fibrillation can result. This is termed “R on T,” and since it only happens when the heart rate is fast, it is uncommonly associated with accelerated idioventricular rhythm. The QRS complexes are typically prolonged at 0.06s or greater. The on and off-set of accelerated idioventricular rhythm is commonly associated with various degrees of ventricular fusion, occasionally confusing the examiner with multifocal ventricular arrhythmias. In the hospital setting, these arrhythmias are often described as “runs of ventricular premature complexes.” Arguably the most overtreated arrhythmia in veterinary medicine, accelerated idioventricular rhythm is quite common among our patients that have gastric-dilatation/volvulus, hemoabdomen from ruptured splenic or hepatic neoplasia (usually hemangiosarcoma), pericardial effusion (post-pericardiocentesis, usually secondary to ruptured right atrial mass from hemangiosarcoma), immune-mediated hemolytic anemia, or traumatic myocarditis (hit-by-car). Typically, NOT associated with excessively fast tachycardia or hemodynamic compromise, accelerated idioventricular rhythm responds poorly to typical antiarrhythmic therapy for ventricular tachycardia, is secondary to non-cardiac issues, and often will resolve on its own following correction of the underlying disorder.


 

Paper speed 25 mm/s, 1 cm/mV, lead II, canine. Sinus arrhythmia, incomplete atrioventricular dissociation secondary to usurpation by accelerated idioventricular rhythm. The idioventricular rhythm is interrupted by periods of sinus rhythm. Note that the ventricular focus takes over when the sinus rate slows. This patient had a splenic infarction following a gastric dilatation/volvulus and surgical gastropexy. Accelerated idioventricular rhythm is very common following this kind of surgery and is typically well-tolerated by the patient, poorly-responsive to antiarrhythmics, and self-limiting. Persistent arrhythmias and colic in this patient more than 72 hours post-operative indicated an unresolved problem. Timely splenectomy resulted in resolution of the arrhythmias.

While it is important to monitor patients with ventricular arrhythmias, especially while hospitalized, pharmacologic intervention in patients with accelerated idioventricular rhythm is almost never warranted. Generally if the heart rate is under 200 bpm and the patient’s blood pressure is within normal limits, then antiarrhythmic therapy is of no real value. The most commonly used intravenous medication for ventricular tachycardia is the sodium-channel blocker lidocaine, which is frequently administered to patients with accelerated idioventricular rhythm. Lidocaine actually works well for ventricular tachycardia when the arrhythmia is secondary to reentry in patients with structural heart disease (i.e. dilated cardiomyopathy in Boxers and Doberman Pinschers). This is because the drug preferentially acts on diseased myocardial cells. When patients have accelerated idioventricular rhythm, the cytokines circulating in the bloodstream that are the presumed root cause tend to persist until the underlying problem is resolved. An apparent therapeutic success is often attributed to lidocaine in such patients as the patients naturally go in and out of sinus rhythm as the sinus node competes for control of the heart with the focus producing the accelerated idioventricular rhythm. The best approach is to place these patients on telemetry, monitor the arrhythmias and continue to search for and treat the underlying problem until it resolves.


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