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Archive for June, 2012

While their cardiology colleagues are extravagantly indulging in coronary arteries   ,It is heartening to note the pediatricians our country has  silently come out with the first India specific  criteria for Acute Rheumatic fever diagnosis and management.

It was long over due . . . three cheers to them !

* It is ironical  these guidelines came in 2008,many of us are aware about the  existence  such guidelines , still  every one is after PTMC  for a full blown mitral stenosis !

http://www.indianpediatrics.net/pdf/acute_rheumatic_fever.pdf

Highlights and Summary

  • WHO criteria  of 2001 is adopted
  • ASO titre positivity alone has less value  in the diagnosis .Hence the importance of which is down graded
  • Steroids  are mandatory in all grades of carditis for 12 weeks
  • Benzathine  penicillin  should be administered weight  based and to be given  every 15 days in children less than 27 kg.

More high lights will be posted.

Secondary prophylaxis of  for Rheumatic fever

Note the Important advice regarding weight based penicillin prophylaxis.

 

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What are  the blind spots of aorta in Tans thoracic  Echo ?

What are pseudo  dissection flops in aortic arch ?

How to differentiate true from false lumen ?

Can  TEE  also  miss any  segments  of  Aorta ?

How is  Aortic Intra mural hematoma differentiated form true dissection?

Spend a minimum of 30 minutes in this 14 page  article.  You will  be able to answer all these and much more The knowledge gained ,   would easily beat  a  day  long   crash course on   Echocardiogram   !

Please thank  the European society of cardiology for providing this article free of cost !

Reference

http://ehjcimaging.oxfordjournals.org/content/11/8/645.full.pdf+html

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Tachycardia – Bradycardia syndrome is the hall mark of sinus node dysfunction.

  • The commonest tachycardia in sinus node dysfunction is Atrial fibrillation . Followed very closely by sinus tachycardia . In fact alteration between sinus tachycardia and sinus bradycardia without other pathological arrhythmia is rare . (Of course , we have a name for such an entity as inappropriate sinus tachycardia / bradycardia )
  • Atrial tachycardia occurs a distant 3rd
  • Ventricular tachycardia may be an exception (Please note , extreme bradycardias which lead to pause dependent VT is not directly related to sinus node disease )

The commonest bradycardia in SND is

  • Sinus bradycardia (This fact is undisputed unlike the tachycardia component of SND !)
  • Followed be sinus pause , SA blocks and sinus arrest .
  • AF with slow ventricular response ( Bradycardic AF) We are not sure about the rhythm here (Is it truly junctional /or conducted atrial ? )
  • Associated AV block can occur up to 20 % of patients .If AV block is present the true nature of SA node disease is masked and it’s function becomes almost irrelevant .

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Stress related wall motion defect  is a well-known entity . It is referred to as Takotsubo cardiomyopathy .

These stress are often

  • Emotional
  • Neurological
  • General systemic stress

The culprit seems to be pooling of adrenaline and nor adrenaline in myocardium .These remote  neurogenic stress can cause significant wall motion defect due to adrenergic  downpour

The image depicts the wide variation in the density of beta receptors in heart.The stress of MI can result in varying degrees of wall motion defect .It is important to realise the wall motion defect in STEMI has two components .One is related to ischemia and other is due to excess catecholamines. This explains many of the unexplained remote wall motion defects during STEMI .This  may be referred to as Intrinsic Takosubo effect !

Then   . . . the following    questions arise

When systemic stress can have a profound  effect on myocardium , what   about local stress ?

Acute STEMI  is  a huge stress for the heart   . . .   isn’t  . If  so , can it   alter  the wall motion defect in adjacent  or remote myocardial segments  independent of ischemia ?

With the distribution  of adrenergic receptors  showing  huge variation ,  we do not know how an acutely ischemic heart  spills the adrenaline all over .  Is there a pattern to it  ?  or it happens at random ?  Further , the  response to  accumulated  catecholamines  is  not  going to be  uniform. This will explain why certain patients  go into ischemic  LVF  , very early in the course of STEMI  even before the myocardium is necrosed. It will  also explain  the  benefits that accrue in selected patients  who receive early IV beta  blockade  ( Which is  of course currently not popular after COMET study ! )

Final message

We  have seen at least  two patients  with severe  transient ballooning  wall  motion defect in LAD region  (LV apex)  with isolated RCA lesion and inferior Infarct .

The question raised is this 

Can  the  stress of  Inferior  STEMI   . . . result in  apical Takatsubo  like  effect ?

Reference

http://www.medscape.org/viewarticle/567069_4

http://www.takotsubo.com/

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IRA localization for both LAD and RCA , LCX  is a fascinating  exercise for cardiologists.I suspect  our understanding  about this crucial issue is  far from complete .While  localizing  level of lesion within LCA  or RCA requires more precise data and erring is acceptable  , it is not uncommon to  call  even the  IRA wrong  especially in multi -vessel disease.

Why current   criteria of IRA localisation goes awry many times  ?

The  factors  that operate are not few   . . .  it  runs into a dozen  at least  !

  1. Dominance  is never considered during IRA localization  (A right dominate system can vastly influence the LAD localization  algorithm PLV branches  can protect LV postero- lateral segments in spite of proximal LAD lesions )
  2. The length of  mid LAD   IS  controversial entity ( Traditionally  it refers  to  the  segment  between first major diagonal to second  major diagonal or septal  leads to faulty   coronary mensuration .It is not uncommon to have a  mid LAD measuring few  mm  when  full the full  length of  LAD  is about 15-19cm
  3. Diagonal vs OM  trade off occurs  in every alternate patient which is ignored  !
  4. Ramus  is never considered worthy enough  to be included in the IRA  localization scheme (In spite its presence  in 20 % )
  5. Type of LAD is not given allowance.
  6. Finally &  most importantly these rules of IRA localization will not apply in  the setting of  multivessel  CAD
  7. In the presence of Pre existing CTO
  8. STEMI following chronic stable angina
  9. Extensive collaterals
  10. Re Infarctions
  11. Post CABG etc

Final message

Decide for yourself  . . .  how good is the value of IRA localization  after  considering all the above variable. . It is not a great thing to predict  correctly RCA from LCX in an  inferoposterior MI  with a  70 % accuracy  . (It actually means  20 % accuracy  )    statistically when there are only two options  . . .  we are blindly  right 50% of times   !

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There was a big debate in one of my classes with cardiology fellows  regarding the shunt quantification  of ASD . We were talking about the significance of ASD shunting . We suddenly realised  2:1 left to right shunt is not a  simple equation  to comprehend . I was  thinking 2:1 shunt would mean pulmonary flow would be twice the systemic flow . It  was not to be !

Is the ratio of shunting and  Qp/Qs convey the same thing ?

No . Qp /Qs is the ratio of pulmonary to systemic blood flow  flow . When we want to quantify shunt we  express it in two different ways .

1. The amount of blood shunted form left side to right side of the heart .

2. The amount of pulmonary blood flow  to systemic blood flow in absolute terms .

Though both are closely linked entities  they do not denote the same meaning . When we say 2: 1 shunt  we refer  to the  shunted blood across the  defect but when we  calculate pulmonary blood flow  we take into account venous blood  which does not take part in the shunting .

The confusion arises because we use both terms interchangeably.The following illustration will try to  prove  A  2: 1 shunt would actually correspond  to  a qp/qs of  three  (Pulmonary flow is 3 times  the systemic flow !)

Let us begin with a hypothetical  ASD patient who  has  systemic  cardiac output of 4 liters.

He shunts 2  :  1   from left to right  . ie he shunts 2 /3  of three parts  into RA (66%  ) .

A patient who delivers 4 liters from LA in the presence of  2;1  ASD shunt  would mean he would  receive 12 liters from the lung  as pulmonary blood flow.

Final message

I am still not fully convinced about the above reasoning . I guess  it is correct.  I argue  the fellows  to give further insight into this equation. The complexities in bi- directional shunt and effective pulmonary blood flow in Eisenmenger syndrome is going beyond my heads !

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                                           Essential qualification for becoming a great medical  researcher  is  the    “Fine art of  mis-interpretating  data “                                                     Venkatesan sangareddi MD .Chennai .India

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