Posts Tagged ‘av block’

The bundle of his divides into two

  • Anterior fascicle
  • Posterior fascicle
  • Middle septal  fascicle*

Middle fascicle * Many  dispute  it’s presence .  One may wonder , how  can anatomy be  under  dispute  ? If you cut a heart you should be able to clear the dispute .  But medicine is not that simple . . . What you do not see may be more important than what we see.

The anterior  fascicular block (LAFB) is one of the common conduction disorder. It ‘s significance :  Can  be a  benign  or a  dangerous entity depending upon the clinical situation .The  problem with  LAFB  is , it is diagnosed primarily by the axis shift it inflicts on the QRS complex.

In a strict sense, it is not a ideal way .There is  a tendency to label all significant left axis (> -60*) deviations  as LAFB. This  practice has made diagnosing LAFB very common in elderly, hypertensives, etc. In these situations it may not mean anything ,  except to suggest a  delay in conduction in  left anterior  fascicle.

If we filter out all these  benign  axis shift  ECGs  , the true organic pathological LAFB  may  not be that common .

Organic , LAFB occurs in the following situations.

  • Degenerative  blocks (Part of Lev & Lenegre’s disease)
  • Aortic valve disease .
  • Hypertensive heart disease
  • Post MI (Either alone or part of bifascicular or trifascicular block )
  • In association with dilated cardiomyopathy

Even in degenerative  , ischemic conduction defects LAFB is far more common than LPFB why ?

The traditional explanations are

  1. Anterior fascicle is relatively sub epicardial in location
  2. It is a  long and thin  structure prone to damage easily
  3. Exposed to the mechanical   stress of   LVOT **
  4. Anterior fascicle has  only a single blood supply(LAD)

** Which experiences  the peak LV  pressure  at > 100mhg and a dp/dt  up to  2000mmhg  (While,  the posterior fasicle is located  away  in the inflow portion of LV  , which is exposed  to low pressure – at best 10mmhg filling pressure )

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It is the classical description of wenkebach AV block type 1 there is progressive prolongation of PR interval followed by a blocked p wave and hence a dropped qrs complex. The usual conduction ratio for wenkebach AV block is 3:2 or 4:3 .

It is well known wenkebach AV block is usually a benign form of AV conduction defect and it recovers spontaneously without any pacemaker support.The block is at the level of AV node and since the his purkinje conduction is intact and the prognosis is good. In type 2 AV block the disease is often(Not exclusively ) located in the infra hisian area .This makes this type of block very unstable and these patients have a high risk for going in for complete heart block and often require pacemaker implantation. The reason for the poor outcome in type 2 AV block is now more attributable to the more extensive myocardial damage these patients suffer than the location of the block itself .

So it is important for the physician to differentiate the two entities .

It is a simple task in most situations , but when the condition ratio is 2:1 one can imagine the difficulties as none of the classical criteria of wenkebach’s AV block are applicable .When alternate qrs complex is missing there is no question of progressive PR prolongation .

How common is 2:1 AV wenkebach ?

It is considered rare , but may not be recognised in surface ECG so real prevalence is under reported.

What are points to differentiate the two ?

  • The qrs width : A normal qrs width suggests wenkebach .A widened qrs indicate the block is infra hisian.
  • The conducted basic PR interval is usually normal in ttype 2 AV block. In wenkebach the PR interval is usually prolonged.(Not always though! )
  • Response to atropine *:Wenkebach tend to accelerate while type 2 AVblock tend to worsen.
  • Response to excercise :Wenkebach conduction ratio improves , type 2 does  not, some times worsens
  • Response to carotid massage: Wenkebach AV block worsens ,Non Wenkebach improves

*The principle behind the varying response is due to the fact that AV node is under the influence of vagal fibres than the his purkinje system.

**It should be noted the atropine effect on AV conduction  is a complex one .Atropine by it’s direct vagolytic action improves AV conduction , while it’s effect on sinus node accelerates the heart rate and make the AV node more prone for physiological AV delay (Decremental conduction: Increased refractionary period at fast hear rates) .This effect is in exact opposite of it,s direct action on AV node.So the net effect will be the balance between these two.Hence atropine effect on heart can be quite variable in both physiological pathological situations.

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atropine leafsAtropine ,  the extract from the  Belladona  plant  is an important cardiovascular  drug. It’s  presence is vital  in every crash carts .  This  unassuming molecule  probably has   saved more cardiac lifes than any other drug . It provides immediate  remedy for many of the bradycardias .It  works like a magic.  The physician buys  time with this molecule  and  proceed  on to resuscitate or  plan other interventional  procedures. It is most powerful antiarrhytmic agent known .It is an irony , many of  the standard cardiac texts do not even mention this while discussing anti arrhythmic agents .

In  this  era of  hyped  cardiac  care   , the  sartans ,  2b3a inhitors   , the fondaparinux’s  making merry !  we  have no spare time  to realise  ,   more  cardiac  deaths  have been prevented by atropine  than  all these   drugs    put together.  It is still working like a bull  across the coronary care units and cath lab world over. While  many mediocre  drugs  enjoy a  big  bash  time for  possibly  saving   few occasional  lives   , the atropine  like drugs never get the due recognition among cardiac literature for the simple reason ,  it being a  cheap  generic drug.This drug is available  for few  rupees , no marketing no advertisements, no celebrations.

Mechanism of action

The  biochemical  mediator :  Acetyl choline

Site of action :     It blocks the M2 (Muscaranic receptors) .

We will confine to the cardiovascular  actions.

  • SA nodal acceleration
  • AV nodal accelerated conduction

Effect on ECG

Sinus tachycardia

Short PR interval

Life saving situations in cath labs  in CCU.

Vagus  nerve richly innervate the heart and blood vessels . Acute coronary syndromes   especially involving the infero posterior territory  raises the vagal tone  , and can  in severe bradycardia and hypotension.  In cath labs , as we  manipulate  cardiac  structures with wires and  catheters  there is always  a potential to elicit the vascular reflex .It can occur  any where between the  access point , femoral or radial  artery to coronary arteries .

Further ,  whenever the  pain  intensity is more , the  central pain integrating  centre in  brain stem  and thalamus has a spill over effect into the vagal nucleus .

What happens if a vaso vagal reaction is left untreated ?

We have often  made  the term “vaso vagal  reaction” appear as an  innocuous  entity. The main reason for this perception is   due to the common occurrence of  “vaso vagal  syncopewhich  is largely a benign entity in the general population .This fact  has sensitised our brains . One should distinctly realise the vaso vagal syncope that occurs in  healthy people standing  in erect posture ,  from  vagal reactions that  occurs in  lying patient with a diseased heart  in a  cath  lab  or CCU.In the classical vaso vagal syncope , assuming the recumbent posture is the treatment and it  counters the hemodyanmic imbalance .No drug is required here. So the common vagal syncope can never be compared with potentially dangerous  vagal reflex that occur in CCUs and cath labs. If not recognised earlier and  immediately countered  it can lead on to asystole and death .Many of  the delayed deaths post PCI during sheath removal or an episode of vomiting are directly related to this.


Atropine is the Savior here . Can you imagine a  world without atropine .

The other reason we had always considered vaso vagal   reactions lightly is that the poor atropine is always available  in the side selfs and it acts   rapidly  and promptly with almost  100 % success  reversing the vagal action  in less than  60 seconds .

How often we here  this  “Oh it’s a brady . . . push  2cc atropine . . .  given sir, the rate has picked up . . .”

If only atropine has a failure rate of say  50%    we  would have  realised the full impact of   vaso vagal shocks (See … how we struggle with No reflow   with no effective drug available !)

Is there any other alternative  treatment  for vaso vagal shock other  than atropine ?

No.   (I guess so . . .Readers may correct me )

Other uses of atropine in cardiac practice

  • During stress testing along with dobutamine  to  increase the heart rate.
  • It can be used to differentiate AV blocks the two types of 2nd degree AV block. The mobitz type 2 worsens while type one accelerates.

Non cardiac uses.

Ophthalmology, pre anesthetic medication, bronchial asthma, various poisoning.

What is the future for this molecule ?

Remain bright .  But only very  few companies make this molecule.  It is a drug that can not  fill the cash boxes but  it is a drug to keep the human heart running at times of crises  . The only  threat to this drug  is  the  possibility of it being replaced with a  modified patented  version of this great  molecule  !

Final message

The evolution of medicine is based on strong foundations  put upon by clinical acumen   by great medical men of  past generation. Atropine was developed by such people   and it has withstood the test of time. This drug  probably  has saved ( and  continue to  save)  many  lives  than any  other drug  in cardiology . It should be recalled ,  another great cardiac drug   called digoxin  has almost succumbed to modern medical  forces  .Let us  keep developing   new molecules  ,  we shall also pay  tributes  to some of   the  unassuming drugs in cardiology .

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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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