Download What is the mechanism of complete AV block in inferior MI

What is the mechanism of complete AV block in inferior MI ?
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
Functional
Vagotonic
Organic
Ischemic
Necrotic
ECG types
1 degree AV block
2 degree AV block – Type 1 Wenke bach
Complete heart blcok
Mechanisms
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