Cardiac arrhythmias by nature connote a serious implication ,especially so with ventricular ones. Here is an arrhythmia which arise from the ventricle by excessive automaticity , fires independently , still very benign compared to others ventricular arrhythmias.
Why AIVR is a stable arrhytmia ?
Primarily due to its low rate.
Since it is a reperfusion arrhythmia the outcome is good.
Mechanism
It is not due to reentry , it is thought to be due to enhanced automaticity without pathological intra-myocytic calcium spikes (Like true VT )
Absence in surface ECG does not mean it is not existent. In-fact there is some evidence to call this arrhythmia as a form of ventricular parasystole.
Focus of arrhythmia
Since it is a reperfusion arrhythmia it has to arise somewhere from re-perfused myocardium.
The fact that it can occur in both RCA and LCA reperfusion indicate the focus can be in any of the ventricle .
Usually it follows the reciprocal rule of bundle branch block pattern (RBBB in LV focus LBBB in RV focus.)
Septal AIVR can have either RBBB or LBB morphology. Usually left axis is noted .
How to differentiate it from non sustained VT ?
- Ventricular rate in AIVR should be between 60 -110 .(Note -The inherent ventricular rate is 35/mt .There is three fold acceleration )
- Basic idoventricular rhythm is about 35. Three times accelerated
- Characteristically AIVR starts with an escape beat rather than an ectopic beat .
AIVR is common in RCA or LCA reperfusion ?
It is supposed to be more common in infero-posterior MI as sinus slowing is an important predisposing factor for releasing the idio ventricular rhythm.
AIVR after primary PCI
Is not reported much as current interventional cardiologists do not bother much to watch about this arrhytmias
Other causes for AIVR
- Myocarditis.
- Digoxin toxicity
Management
(The commonest issue with AIVR could be . . . Nurses /Fresh interns may mistake it as VT and pressing the false alarm ! )
- Rarely requires treatment .
- Atropine ,Isoprenaline to increase sinus rate.
Dr.S.Venkatesan MD 
Very interesting. I had a STEMI patient back a few months ago that was back & forth between IVR (38-ish) & AIVR (63-ish). It looked nothing like this, rather extremely wide QRS, no P’s, & massive ST-elevation in II, III, avF; ST-Depression in I, avL; ST-E in V5 & V6, ST-D in V1 & V2. Patient woke his wife up with moaning & she assumed hypoglycemia like before, waited 2 hours to call 911 & when we got there, he was semi-conscious, non-verbal, moaning & writhing in pain; entire bed soaked in diaphoresis, skin death cold, & he was pale from head to feet, mottled from neck to legs. BP for me was 70’s systolic, no radials or pedals w/ weak carotid – no time for a right-side 12-Lead. ER physician cancelled my alert & cath team & said it was a AAA (ultrasound said three times it wasn’t) & she still didn’t believe it; CAT scan also said no & she ordered an MRI (he was sedated & intubated by now) with a BP of 50/22 after 6 full liters of saline & cont’d IVR. He coded before the MRI took place & his troponin came back at 29.0 µg/L. Sadly he did not survive & it has been a call that still angers & saddens me.