Archive for September, 2009

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Medical profession has  evolved over centuries with humble discoveries by genuine researchers in the past . As we  pursued  science vigorously  , we  looked  for innovations , when innovation  work ( or many times shown to work !) we jump to sky , even as  some of these  innovations fail and crash down  to earth , many times  we continue to be in the clouds . This is the fundamental problem of modern medical science . When  our expectations reached  unrealistic proportions ,   we tend to lose the common sense . Prolonging life and reducing human suffering may be the ultimate aim of the medical  profession , but  If we try to fight the death with science and money without application of mind , our current  life may become  miserable ! Thats what is happening for the majority of the population of this planet . After all ,  death is an essential and final  component of life !

Coming to the issue of CAD ,  in our country , a  rich gets a 4th generation drug eluting stent for a insignificant  asymptomatic PDA lesion , and poor fellow with left main dies without any intervention .This is  fairly acceptable   to this uneven world  , where a rich westerner  dies due to obesity related disease and a  poor African dies to malnutrition .

This article is in   response to  my  recent  experience  when  . . . I advised

Simple life style modification &   few drugs   for a patient with chronic multivessel   CAD  , I was  made to look   ordinary , inferior  and funny   by  many of the current generation cardiologists .

Further , the term optimal medical therapy(OMT)  for chronic stable angina has evoked laughter in one of the interventional cardiology  conferences  I  attended !

It is a sorry state of affairs  for the whole cardiology community , a  genuine scientific  fact , proven by  real life experience  as well,   is  being  ridiculed.

Richard  Conti tells in this excellent editorial in his journal   Clinical cardiology about the issue of medical management of CAD

“Respect in clinical trials”

Chronic stable angina pci vs cabg vs medical courage trial oat trial ethics in cardiology

Click here to reach the article  http://www3.interscience.wiley.com/cgi-bin/fulltext/122512853/PDFSTART

A similar study which  suggested  exercise  could be  better than PCI in the recent 2009 ESC is suffering the same fate !

What if regular exercise were as good as a stent for stable angina?


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Internet has revolutionised  in sharing our knowledge . But  , the  freedom it gives  has a trade off .Identifying   genuine  knowledge  in the  vast cyberspace is like searching for lost treasure in the ocean bed.

Have a look at this site which innovates medical teaching

great medical videos top cardiology web site drsvenkatesan

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Normal P waves

normal p wave ecg rae lae

What are the components of Pwave ?

RA component : The SA node depolarises the RA first  , so the initial part of  P wave represents  RA  current .After about 40msec  the wave front reaches LA and it begins it’s depolarisation .LA component :By the time LA is maximally depolarised the RA  already starts its repolarisation.So there is  overlap and also a short time lag between these two wave forms . This is very important to recognise as , even if the RA conduction is prolonged in pathology the RA component of P Wave still falls within the LA wave .Hence it is not shown in the ECG and P wave is not widened in RA enlargement. This is in contrast to LA enlargement , when the terminal half of P vector delayed it stretches the P wave wide beyond the normal 110ms .Hence LAE widens the Pwave.

Why P wave becomes taller in RA enlargement ?

In classical P pulmonale , the P wave is    tall >2.5mm. It is easy to explain why it not getting wide , than  why it is getting taller !

The atrial vector has two components .The initial RA vector , is directed  anteriorly .The main reason is due to the anatomical proximity  of RA to  the chest wall . Further the  atrial  electrical dp/dt is  fast  , so  the slope of  forward limb  is steep . Any RA voltage increase is  easily picked up by the chest leads.

rae right atrial enlargement ecg tall p p pulmonale p tricuspidaleright and left atrial enlargement how to differentiate lae rae

Why LAE can not produce tall P wave ?

The Left atrial vector which  follows RA vector  is mainly directed posteriorly and hence inscribe a  descending  limb of   P wave . This causes the P terminal force .  So  the direction of vector forces  and the anatomical locality  make a  tall & positive P  deflection highly improbable in   LAE .

*Of  course  when LAE is   huge , where a antero -supero vector from  roof of LA may inscribe a positive wave .

What happens in bi atrial enlargement ?

It can have features of both . Tall & wide P waves  .

Can RA generate a Q wave ?

Yes . When RA assumes a huge  size  , especially if the RV is also at high pressure as  in severe PHT or valvular PS   a  q wave is generated in the lead V1 .This q wave is nothing but the intra cavitary potential of the enlarged RA.

What is the difference between atrial enlargement, atrial dilatation, atrial hypertrophy, intra atrial block and inter atrial  block  ?

The p wave morphology has no  specificity to identify the various entities. In any pathology of atrium the first thing that happens is a conduction delay ! It is now realised the bulk of the changes we see in atrial enlargement especially in LAE is due to intra and inter atrial  blocks or more subtly conduction delay.

It is  obvious , a wide P wave can occur either  due to LAE or simple conduction delay .In elderly  hypertensive patients atrial fibrosis is more common , one can not confirm LAE  without echocardiogram .

A notched P wave  can be a very specific sign of   inter atrial block .Which is more common in severely diseased left atrium. A notch , slurred p wave is a good marker for impending AF or atrial flutter.


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Pharmacology is a major discipline in medicine where we learn how a drug acts in our body for various ailments . Now  in this era ,  doctors need not only how a drug acts but also how a drug company acts ! This has become vitally important   for the welfare of the mankind .

In this context one of the best books on medical pharmacology is from the

Famous Editor of New England  journal of medicine

A must read for all genuine medical professionals

ethics hippocrates ebm

Watch Marcia Angell  talk http://www.youtube.com/watch?v=ouF3ISihHLM

Full lecture of Mercia Angell  http://videos.med.wisc.edu/videoInfo.php?videoid=940

Click to buy/read the book  http://www.amazon.com/Truth-About-Drug-Companies-Deceive/dp/0375508465#reader

A Review  about the book  http://calitreview.com/176

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Wide qrs tachycardia has a unique place in clinical electrocardiography .It is  a much fancied and glamorous entity for the simple reason , it continues to be the  cardiologist ever solved puzzle .For over three decades of research, clinical debates , symposiums , seminars have effectively failed to take away the uncertainties in decoding the wide  QRS  tachycardia . (Specifically ,  VT vs SVT with aberrancy)

Some wondered , should we really waste our efforts in differentiating the two . In emergencies it never matters , in fact one need  not attempt to do this often futile exercise !

Few dedicated criterias like Brugada etc have helped us .

While the difficulties in differentiating between VT and SVT with aberrancy remain over the decades .A less reported  , but more common issue is  confronting  us .

It is  the big question of  differentiating a  wide  QRS tachycardia from a narrow QRS  tachycardia

wide qrs tachycardia vt svt aberrancy

This  occurs  more often than we realise  ,because we define wide  QRS  tachycardia in a vague manner

  • Normal qrs width between Up to 80 / up to 100 ms acceptable  ?*
  • Narrow qrs tachycardia 80 ms?
  • Wide qrs tachycardia i> 120ms  ?
  • Definitely wide qrs >140msec

* The confusion is mainly because 20ms difference between limb leads and chest leads .

In reality one may not be able to all  tachycardia into narrow or wide .

There is big  overlap zone that need to be labeled a intermediate qrs tachycardia

If we can  triage the tachycardias into three instead of two it may help us arrive  fast  ,  to the  correct diagnosis

Narrow QRS tachycardia ( qrs 80ms)

  • Sinus
  • All svtS (avnrt etc)

Intermediate QRS tachycardia 90-120

  • Most of the SVT with  aberrancy  ( Except antidromic SVTs which are really to wide !)
  • Septal VTs*
  • Fascicular VTs*
  • VT in PPM and ICD /CRT patients **

*  Any VT that arise near the major conducting system of ventricle conduct  fast and hence qrs are relatively narrow.

**These are rare entities where  base line wide QRS getting narrower with the onset of VT . (Ref : http://europace.oxfordjournals.org/cgi/content/full/eun254v1)

Wide qrs tachycardia >120ms

  • Most of the genuine VT (Ischemic , myocardial origin)
  • Post MI VTs
  • SVT aberrancy especially AVRT
  • Any SVT with preexisting BBB
  • Marked electrolytic disorders

Unresolved questions

  • Which lead we should look for measuring the width of qrs ?
  • Should we take the narrowest qrs or widest qrs or should we take the average ?
  • Should we calculate how much the tachycardia has widened the qrs from the baseline  width of a given patient ?  Is it not possible , what is wide for some may be normal for another !
  • If  there is no isoelectric line  and ST segment  blends with qrs complex  how to mark end of qrs ?
  • If  limb leads show a narrow qrs and chest leads shows  wide qrs what is the significance  ?
  • In precardial leads  if one lead alone shows a narrow qrs , what is the significance ?
  • Can a narrow qrs VT conduct  with aberrancy and making it  really  wide ?

Final message

When we are  able to solve   complex electrophysiological  problems  , we must also realise  even   simple  tasks can be demanding in medicne ! It is proposed to create a  new  group “Intermediate QRS tachycardia “that can help solve the issue where we have difficulty in labeling these  tachycardias which fall  in the  greyzone .We can try &  apply the modern EP based VT criterias  to this group and find out the hidden truths !

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The most popular criteria to differentiate VT from SVT aberrancy is  formulated by Brugada in 1991.

The greatness of  this  criteria is that  a single question asked  is able to confirm VT in vast majority of cases.

Is RS complex absent all  of the pericardial leads ? If  the answer is  yes  it is VT 100%

How is that,  we have been struggling for so long , a single question is able to solve the issue quite easily ?

wide qrs tachycardia vt svt aberrancy brugada

This is because , the term  “Absent RS complex ” actually means

Presence of  one of the  following three typical complexes Of VT.

  1. QS
  2. QR
  3. Monophasic R

Two of them  actually imply ,  q waves throughout   V 1-V6 .This  means a badly damaged ventricle and  with  little electrical activity coming towards the chest wall .This situation  almost always occur in VT.*

The third complex is Monophasic R .

A  monophasic , wide  QRS  complex  again indicate VT  as monophasic aberrancy is very rare as the supraventricular  impulse invariably conducts with  RSr’  (The right bundle  refractory period sees to that  at least a small r’ is inscribed however fast the SVT is !  )

So if there is no RS complex  it must be VT !

What  are the  difficulties  faced in applying this   first step of Brugada criteria ?

It is funny to note , in medicine criterias  often work perfectly in  text books only !

Is there a RS complex seems to be a very easy question ? There lies the catch !  .Even though this criteria may be 100% specific , differentiating RS from QS complex even by an experienced cardiologist may be difficult in a significant number of VT tracings.This  realistically ,  reduces    supposedly  100% specificity  of this criteria !

In fact we expect Brugada to develop an  another limb  to his now famous algorithm

Is there  absence  RS complex in precardial leads  ?  Yes / No / May be ,  not sure !

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