Feeds:
Posts
Comments

Posts Tagged ‘inferior wall mi’

Can you diagnose inferior MI with poor R waves ?

No , you need  a “Q ” that’s  for sure !   Do not diagnose inferior MI without a  q wave  . ( The luxury of diagnosing MI without q waves  is available  only for LAD region )

Any axis deviation ( even 30 degrees) from  base line  can alter the inferior lead qrs morphology to a great extent. R wave amplitude is  primarily determined by the  initial septal depolarisation .  So if the  inferior septum is intact  it will never allow to inscribe a q wave  . Further ,  limb leads are bi polar leads and they are   sum-mated  potential  reflected along the entire  bottom half of the  torso . Hence it is not  reliable to attribute  significance  to presence or absence of  r wave (Unlike  chest leads).

The lung and diaphragm  exert  not only electrical insulation but   also mechanical  alteration of septal profile with phases  of respiration.

Counter point

Not really  . . .  you do not need a  Q   waves  to diagnose inferior MI  ,  electrically  diminutive R  is same as  “Q”

There is  an alternate way of  reasoning  too  . R wave is muscle , We diagnose LVH with tall  R waves so muscle loss should be equivalent to R wave loss .We have innumerable examples where  low voltage R waves are  recorded in inferior leads after a well documented inferior MI.

How do you diagnose old inferior MI by ECG ?

  1. Near normal ECG with degeneration of q waves and regeneration* of  R waves
  2. Residual T wave inversion
  3. Simple low voltage inferior leads
  4. Slurred or notched qrs  complex in 2 3 AVF
  5. Rarely with atrial abnormalities and AV nodal prolongations

The concept of regenerated R is well established . And it brings to the age-old debate of R with live muscle Q is dead muscle

Regeneration is salvaged muscle (Natural salvage , awakening from hibernation etc)

How good is Echocardiogram in diagnosing old Inferior MIs ?

Surprisingly , echocardiography do not help much either .Technically inferior transmural MI  is expected to  leave  a residual wall motion defect.  But many times it do not. Many non q inferior MI (Is there such an entity ?)  do look perfectly normal by echo .

The primary reason  for this is ,  infero-posterior surface is anatomically remote and it makes  wall motion analysis difficult .Newer tissue motion analysis (Velocity vector imaging)  could aid us better.

Some times a trivial or mild  mitral regurgitation is the only sign of   old inferior MI  as  the pap  muscle  lags behind in it’s  functional recovery  while  free posterior wall is  fully salvaged and contracting well .

Final message

It needs  that extra bit of   of  knowledge to  expose  our ignorance.

Even in this  maddening   scientific  era  we have valid  reasons to  go back to fundamentals  of  R wave and Q  wave genesis in MI ,  where clarity  is lacking .

Read Full Post »

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

Read Full Post »