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Posts Tagged ‘sinus pause’

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

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Sick sinus syndrome  or sinus node dysfunction (SSS, SND ) is one of the common cause of  symptomatic bradycardia .The other cause for  pathological bradycardia is complete heart block.Together , these two entities share 99% of indications for permanentpacemaker implantation.

The sinus node can get affected in various diseases . The commonest cause for SND is age related.This is manifested  as inappropriate bradycardia .The  other common presentation of  SND is exaggerated bradycardia to betablockers and calcium blockers.In fact , some consider drug  induced bradycardia  is  nothing but  , unmasking of underlying SND.Pathological states that result in SND include  hypothyrodism , infiltrative   and inflammatory diseases . (Surprisingly ,  ischemic  SND  is a lesser  clinical problem when considering  the  rampant CAD in our population )

What is  is a fundamental difference between SND and complete  heart block* ?

Sinus node is the proximal most pacemaker of the heart. When it fails the chances of  a  subsidiary pacemaker coming to the rescue is far greater than  a complete AV block. Further the quality and stability of the escape pacemaker is better in SND. In fact , in pure SND  ( With out AV nodal disease)  a sinus arrest is rarely fatal as escape rhythm  occur without fail.

* It should be emphasised  ,  there can be associated AV nodal disease in  significant (10%)  number of patients with SND .This may be present either at the  time of diagnosis or it can develop later in the course .This has important implication in the selection of   pacemaker .The discussion here is confined to isolated SND .

How common is ventricular escape rhythm in SND ?

It is very rare. the ventricle never gets a chance to come to the rescue as invariably junctional pacemaker takes over at times of extreme sinus pause/arrest.For the same reason , pause dependent VT (Brady dependent ) is also less common in SND .

What is  stokes Adam’s attack ? How  common it is  seen in SND  ?

It is the cardiogenic  syncope due  to extreme bradycardia. This classically occurs in complete heart block , when

the the escape rhythm becomes either very slow or temporarily goes for sleep .This results in a huge  pause (unlike sinus pause  of   , the pause  here is  ventricular pause  , this is  actually an  asystole  )  it  can  immediately trigger an VT or VF .

If  SND is not life threatening why pace maker is indicated in them ?

The pacemaker is primarily indicated for prevention of dizziness , near syncope or syncope.So primary impact is on improving quality of life  , not reduction in mortality. While in CHB  pacemakers improve  symptoms and survival.

Which form of SND can be dangerous ?

When SND is associated with rapid atrial fibrillation  some times it can trigger a VT/VT if ,  these patients also have

a fast accessory pathway with short refractory period. (<250msec)

Final message

If you have only one pacemaker at your disposal , but there are  two patients ,  one with SND and other with CHB please put the pacemaker to  the patient with CHB , even if the later has insurance coverage and the former is not .You are justified in  diverting  the pacemaker !

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