ecgsweep

Idioventricular Rhythm

caution
Lead II
25 mm/s10 mm/mV
HR72bpm
RR833ms
QT358ms
Type

A wide-complex ventricular rhythm at 50–110 bpm, most commonly the reperfusion arrhythmia after STEMI treatment; usually benign and needing no treatment of its own.

Updated

On the trace

Read the strip in the order it happens.

Try each step, then check it.
  1. Start in sinus rhythm.
    Show Narrow complexes with P waves, at a rate that drifts.
  2. Watch the sinus rate fall below the focus.
    Show A ventricular focus firing steadily at 80 bpm starts to arrive first. At the handover, sinus and ventricular impulses meet and draw fusion beats (the arrows): part narrow, part wide.
  3. Read the AIVR.
    Show Wide, regular complexes at 80 bpm with no P wave of their own. The sinus P waves are still there, marching through the wide complexes at their own rate, sometimes just in front of a QRS but too late to conduct: AV dissociation.
  4. Spot the captures.
    Show Now and then a P arrives early enough to conduct, and a single narrow beat interrupts the run.
  5. See it hand back.
    Show When the sinus rate climbs above 80 again, sinus rhythm takes over, gradually, with fusion beats again.

How to recognise it

FeatureValueNotes
Rate50–110 bpmFaster than an idioventricular escape; around 100 and above, manage as VT.
RhythmRegularSlight irregularity at the handovers as sinus and focus compete.
QRS width> 120 msThe same wide complex as a PVC from that focus.
P wavesDissociatedMarching through the QRS at the sinus rate.
Fusion beatsCommonAt the start and end of each run.
OnsetGradualThe focus takes over when the sinus slows, and gives way when it speeds up. A sudden start without fusion suggests VT.
ContextReperfusion, athletes, toxinsThe setting often gives the diagnosis.

The strip

Thirty seconds of lead II in which sinus rhythm gives way to accelerated idioventricular rhythm, drawn by the simulator. Work through the steps above on it, in the order it happens.

Mechanism

A focus in the His-Purkinje system or ventricular muscle fires faster than the ventricle's usual 20–40 bpm, through enhanced automaticity, but not fast enough to be VT. Whenever it is faster than the sinus node it takes over; whenever the sinus is faster, the sinus wins. That competition is what gives AIVR its gradual start, its fusion beats and its captures.

After reperfusion of an infarct, the recovering ischaemic zone briefly fires this way before the myocardium settles, which is why AIVR is a marker of restored flow and why it resolves on its own.

Go deeper

One focus, three rates

  • Idioventricular rhythm, 20–40 bpm: the escape when everything above has failed. Needs pacing.
  • AIVR, 50–110 bpm: an accelerated focus competing with the sinus. Usually benign.
  • Ventricular tachycardia, over 100 bpm: a different risk and different management.

A wide rhythm at 85 bpm after PCI is almost certainly AIVR. At 115 bpm, treat it as VT.

Other causes

  • Athletes and high vagal tone: the sinus slows below the focus. Benign.
  • Digoxin toxicity: through triggered activity rather than automaticity. Cocaine and some anaesthetics have also been reported.
  • Electrolytes: hyperkalaemia and low magnesium.
  • After resuscitation: often among the first organised rhythms after ROSC.
  • Cardiomyopathies: hypertrophic, arrhythmogenic right ventricular and ischaemic.

Clinical impact

A ventricular focus at 50–110 bpm takes over whenever the sinus is slower
AV dissociation removes the atrial contribution to filling, lowering output modestly
Palpitations or mild light-headedness at mostUsually Well Tolerated
Instability suggests severe LV dysfunction or dependence on the atrial kickRarely Unstable

The main risk is treating it: recognise it, and it usually resolves on its own as the cause settles or the sinus rate recovers.

Management

1

Observe

If the patient is stable, watch. AIVR stops when the sinus rate rises above the focus or the cause resolves.

2

Treat the cause, not the rhythm

After thrombolysis or PCI it signals reperfusion: leave it. For drug toxicity, remove the drug; for digoxin toxicity, give digoxin-specific antibody fragments.

3

If it causes compromise: speed up the sinus

Atropine (500 micrograms IV) or temporary pacing faster than the focus lets the sinus take the ventricles back. Cardioversion is not indicated.

4

Never suppress it with antiarrhythmics

Lidocaine, amiodarone and other Class I or III drugs suppress ventricular automaticity; if the focus is the dominant pacemaker, the result can be asystole.

Differential

Monomorphic Ventricular Tachycardia

Also wide with AV dissociation, but over 100 bpm with an abrupt start. In the 100–110 bpm overlap, context decides; when in doubt above 100, manage as VT.

Idioventricular Rhythm

The same wide complex below 50 bpm, when the higher pacemakers have failed. It needs pacing; AIVR does not.

Atrioventricular Nodal Re-entrant Tachycardia (AVNRT)

SVT with aberrancy is usually over 140 bpm and starts suddenly, with any visible P waves in a fixed relationship to the QRS and no fusion beats.

References

  1. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death — European Heart Journal, 2022
  2. 2023 ESC Guidelines for the management of acute coronary syndromes — European Heart Journal, 2023