Posts Tagged ‘reperfusion arrhythmias’

Reperfusion arrhythmia was described originally  in the thrombolytic era .

It can be any of the the following .

  • AIVR(Accelerated Idio Ventricular rhythm)
  • Sinus bradycardia (In Infero posterior MI )
  •  VF can occur as  Re-perfusion  arrhythmia.

Does these arrhythmia occur following primary PCI ?

It should  isn’t ? 

In fact it  must be  more pronounced  as we  believe PCI is far superior modality for reperfusion !

Busy Interventional  cardiologists  of the current era  either do not  look for it or fail to document it . These arrhythmias occurs only  with early Primary PCI (Say less than 2-3 hours) .If re-perfusion arrhythmias are  really less common with primary PCI , are we missing some thing ?



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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.


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


(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.

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Conduction disturbance is a fairly common occurrence following  MI. Inferior STEMI is especially prone for AV blocks. This is because  the  blood supply to AV nodal  tissues and the inferoposterior surface of the heart  share the same arterial territory . AV node gets it supply  90% of time by right coronary artery(RCA )  and 10% by  LCX. Very rarely from both .

The common bradyarrhytmias that we encounter in inferior MI are

Sinus bradycardia

Sinus pauses ,SA blocks

AV blocks






ECG types

1  degree AV block

2 degree  AV block – Type 1 Wenke bach

Complete heart blcok


The inferior aspect of the heart has rich innervation of vagal nerve terminals (While the  sympathetic adrenergic system is concentrated in the anterior surface) . The moment infero posterior MI occur it stimualtes the vagus and a prompt bradycardic response occur .Many times the classical hypotension /bradycardia reaction is simply a reflection of heightened vagal tone.

Consequence of vagal tone on SA nodal and AV nodal conduction

As expected, vagal stimulation can result in a spectrum of arrhythmias from the  simple bradycardia to complete SA block  to  AV block. Extreme bradycardia , may release the junctional pace maker and result in junctional rhythm with a rate of around 40-50. There can be a functional AV dissociation between SA node and AV node. Careful ECG analysis is required here ,  as it can mimic organic AV block.The simple way to differentiate between organic AV block from simple AV dissociation is to look at the p waves.In AV dissociation both atrial rate and ventricular rate are nearly equal or VR  is slightly more than AR .In CHB atrial rate  exceeds ventricular  rate.

SA and AV block occur due to various mechanisms in inferior  MI

  • High vagal tone
  • Ischemia of SA/AV node
  • Necrosis of AV node
  • Drug effects -Like morphine
  • Reperfusion bradycardia*

Ischemic AV nodal arrhythmias are  some times very difficult to differentiate from vagotonia especially if occur within 24h.

Irreversible AV nodal block due to necrosis is rare.But if occur , usually  associated with extensive inferior mI/RVMI/ .AV block  that  persist beyond 48-72hours should raise the suspicion of damage to AV node.( As vagal tone is very unlikely;y to last beyond 48h)

* Some time a an episode of sudden severe  bradycardia  can be manifestation of RCA reperfusion.Flushing of SA nodal or AV nodal branch of RCA might trigger this. This has a potential  to  bring the heart to asystole.The resultant extreme bradycardia often triggers VT/VF .The reported high incidence of primary VF in infero posterior MI is attributed to this sudden RCA perfusion.

Medical management for CHB

Brady arrhythmia’s due to high vagal tone are generally benign .No specific intervention is required.Atropine will be suffice in most situations.Some times isoprenaline may be required. Aminophyline , now Ivabradine may have a role. Atropine not only corrects the HR it raises the BP also as  it counters  both cardioinhibitory and  vasodepressive  limbs of vagal stimulus mediated by  acetyl choline .

Pacing for Bradycardias in inferior MI.

  • Generally not necessary for sinus bradycardia.
  • Few with CHB require it
  • Persistent hypotension and RVMI  needs it often.(Dual chamber temporary pacing preferred as AV synchrony is vital here.)

Weaning of temporary pacing in inferior MI.

This could be a tricky issue. It can be weaned off in less than a week.A practical way is to use temporary pacing  only in back up mode at a heart rate of few beats less than the patients rhythm.Pacing for long hours  at high rates may delay the resumption of patients own rhythm and may result in false diagnosis of irreversible CHB and a subsequent PPM

How many will require permanent pacing following infero posterior MI ?

Only a fraction of patients with CHB require long term pacing . There are some centres tend to overuse PPM in this situation. Wait and watch policy may be the best.A unnecessary lead  within a  infarcted ventricle  has a potential to create problems .There have been  occasions a stable RV MI has been destabilised due to RV pacing lead triggered recurrent VF.

Tachycardias in inferior MI

It is relatively uncommon.Atrial involvement is more common with infero posterior MI and hence a greater incidence of atrial fibrillation .

RV MI can induce ventricular tachycardia arising  from the RV myocardium

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