Accelerated Idioventricular Rhythm

Accelerated idioventricular rhythm (AIVR) is a regular, wide complex ventricular rhythm at 40 to 120/min (usually 60 to 100/min), faster than a ventricular escape rhythm and slower than ventricular tachycardia.

It comes from an automatic focus in the Purkinje network or ventricular muscle that takes over when the sinus rate falls to just under the focal rate. Sinus and ventricular rhythms then compete, with isorhythmic atrioventricular dissociation and fusion and capture beats.

Episodes last seconds to minutes, occasionally hours, and end when the sinus rate rises or the focus slows. It is a common finding in the hours after reperfusion for ST elevation myocardial infarction (reported rates vary widely, from about 10% to 50%), but it does not reliably confirm reperfusion.

Other settings are digoxin toxicity, cocaine use, myocarditis, cardiomyopathy, hypokalaemia, general anaesthesia, cardiac surgery, and healthy people including athletes, young adults and neonates.

Pathophysiology

Enhanced automaticity of a ventricular focus, and occasionally triggered activity, drives the ventricles slightly faster than the sinus node. Acceleration of the sinus rate (exercise, atropine) suppresses the focus by overdrive.

In reperfused myocardium, washout of metabolites, potassium shifts and heightened sympathetic tone promote the focus. The rhythm is usually haemodynamically benign and rarely degenerates into ventricular tachycardia or fibrillation, although a premature beat landing on the T wave can trigger it.

• Usually asymptomatic and found on a monitor or ECG.

• Palpitations or a slow, irregular pulse. Loss of atrial contribution to filling can cause lightheadedness, dyspnoea or hypotension in patients with poor ventricular function.

• Cannon a waves in the jugular venous pulse and a variable intensity of the first heart sound from atrioventricular dissociation.

• Features of the cause: ischaemic chest pain, digoxin toxicity (nausea, visual disturbance), stimulant exposure, or signs of myocarditis or cardiomyopathy.

• 12-lead ECG and rhythm strip. Regular wide QRS (usually 120 ms or more) at 40 to 120/min, with a ventricular rate close to the sinus rate (usually within 10 to 20/min). Onset and offset are gradual, with fusion beats at both ends and capture beats in between. Atrioventricular dissociation is typical.

• Telemetry for duration, rate, and transition to other rhythms.

• Laboratory. Potassium, magnesium, troponin, digoxin level, thyroid function and toxicology.

• Echocardiography for ventricular function, regional wall motion and myocarditis or cardiomyopathy.

• Exercise test or ambulatory ECG in athletes or young patients. Suppression at higher heart rates favours a benign focus.

• Cardiac MRI when structural disease is suspected, and coronary angiography when ischaemia is unresolved.

• Usual course: no treatment. Observe on telemetry for 24 to 48 hours after myocardial infarction. Do not suppress the rhythm with lidocaine or other antiarrhythmics, because they can abolish the escape focus and cause asystole when sinus rate is slow.
• Treat the cause: complete reperfusion, correct potassium to 4.0 to 5.0 mmol/L and magnesium to the normal range, stop stimulants and arrhythmogenic drugs, and treat anaemia, pain and hypoxia.
• Haemodynamic compromise from loss of atrioventricular synchrony:
  • Atropine 500 micrograms intravenously every 3 to 5 minutes, maximum 3 mg, to raise the sinus rate and suppress the focus. Doses under 500 micrograms can cause paradoxical bradycardia. Use with care in acute ischaemia, narrow angle glaucoma and urinary retention.
  • Atrial pacing through a temporary wire at a rate over the ventricular rate.
• Digoxin toxicity with life threatening arrhythmia: stop digoxin and give digoxin specific antibody fragments. Vials = serum digoxin (ng/mL) multiplied by weight (kg), divided by 100, where each 40 mg vial binds about 0.5 mg of digoxin. Empirical dosing is 10 vials for acute ingestion of unknown amount and 3 to 6 vials for chronic toxicity. Recheck potassium, which can fall sharply after treatment.
• Rate over 120/min, instability, or doubt over the diagnosis: give synchronised cardioversion at 120 to 150 J biphasic under brief sedation if the patient is awake, because the rhythm cannot be told reliably from ventricular tachycardia.
• Persistent AIVR with cardiomyopathy or reduced ejection fraction: investigate the substrate (cardiac MRI, ambulatory ECG, electrophysiology assessment) and treat the underlying disease.

Special groups.

• Athletes: asymptomatic AIVR that suppresses on exercise, with normal echocardiography and ECG and no family history, needs no restriction.
• Neonates and children: usually benign and transient, with no treatment.

Monitoring. Continuous ECG until the rhythm has resolved and the cause is treated. Repeat ECG and echocardiography at 3 months when structural heart disease was found. Ambulatory ECG yearly for patients with underlying cardiomyopathy.

Referral and escalation. Refer to cardiology when AIVR occurs outside reperfusion, with structural disease, symptoms, or recurrent episodes. Urgent for haemodynamic compromise, rate over 120/min, polymorphic ventricular tachycardia or digoxin toxicity.