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Determinants of “P” wave location in narrow qrs tachycardia ?

July 6, 2012 by dr s venkatesan

Identifying the P wave is the key to decode  any  narrow QRS  tachycardia . Though the  the relationship to  p and  qrs is vita ,  many times it is  not  easy to  relate them.More easily one  may  get  a  clue to the mechanism by analysing   P wave timing .This is the basis of calling narrow qrs tachycardia as short RP and long RP.

Wonder   . . .  why  the  relation “P to R” became  “R to P” here !

Since  in the   common narrow qrs tachycardias  AVNRT/AVRT  ,  atria  activates  the atria  in a  retrograde manner , we look  for the relationship of qrs complex on subsequent P wave . Hence the interval between R to P become the focus.

In other words RP interval indicates retrograde  conduction property of AV tissue .

If it is slow the P wave will be well separated from QRS .

If it is fast it will be close to QRS complex .

If it is ultra fast as in some AVNRT ,it can fall within the qrs complex and completely invisible .

(The so called  r’ prime in classical AVNRT is nothing but a distorted p wave on the terminal qrs complex.)

Based on  RP interval  the following classification is used (List is incomplete)

Short RP Tachycardia

  • AVNRT (Slow-Fast )
  • AVRT

Long  RP tachycardia

  • Atypical AVNRT(Fast -slow)
  • Atrial tachycardia*
  • Sinus tachycardia*
  • SA nodal re-entry*
  • Some forms of AVRT

* Please note ,  here the P wave is not determined by the preceding qrs unlike other tachycardia in the list.

What is the  cut off point to call it is Short RP /Long RP ?

It is arbitrary . Following may help

If RP interval > PR interval it is long RP.

If the absolute RP interval is >  100  ms  with the heart rate of > 160 it would  generally  Indicate a long RP tachycardia .

The timing  of  retrograde P can be very complex than we believe  as the following factors heavily influence it.

  • The autonomic tone
  • Site of retrograde atrial  breakthrough point .
  • Atrial size ,
  • Atrial  refractionaries
  • Effect of drugs
  • Intact-ness of inter atrial conduction
  • Chances of the retrograde atrial activation capturing Internodal pathway

Final message

The P wave location in narrow qrs tachycardia is primarily determined by the retrograde VA  conduction and less  on the antegrade AV conduction  . Looking at the interval between R and P is a  quick way of getting the VA conduction in the bed side.

Once we get an  idea how the VA  circuit  conducts , we can narrow down the possibilities  in  Narrow qrs tachycardias !

Comming  soon

What determines the morphology of retrograde P waves in AVNRT/AVRT ?

Posted in cardaic physiology, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG | Tagged , , , , , , , , , , , , , | 1 Comment »

What are the mechansims of mitral regurgitation in Acute Rheumatic Fever ?

July 5, 2012 by dr s venkatesan

Rheumatic valvulits , Valvular inflammation and edema  is the traditional answer .A detailed Echocardiographic study from All India Institute of medical sciences New Delhi  ,India  which was published in circulation 1996 answers this question most authentically .

From a meticulous  Echocardiographic  study of about 70 patients  (with both first and recurrent episodes of carditis ) the following findings were observed.

After reading this article one should be able to answer variety of  questions in RHD  such as

  • How common is MVPS in RHD ?
  • How often MR dissapear with Aspirin etc ?
  • Echocardiographic correlates  for care -coombs murmur ?

Reference

http://circ.ahajournals.org/content/94/1/73/T5.expansion.html

Posted in acute rheumatic fever, Cardiology - Clinical, Cardiology -unresolved questions, echocardiography, Infrequently asked questions in cardiology (iFAQs), rheumatic heart disease, valvular heart disease | Tagged , , , , , , , , | Leave a Comment »

How to identify culprit artery in unstable angina ?

July 3, 2012 by dr s venkatesan

It is estimated multi-vessel CAD occur in about  70 % of NSTEMI/UA.In high risk NSTEMI early invasive strategy is popular (Though it is not yet  an undisputed choice !) .Tackling the culprit artery and restoring the blood flow ,   providing immediate  relief from angina is the primary aim  . Myocardial salvage is a lesser aim !

The lesion that is immediately  responsible for  angina is referred to as culprit  lesion and artery .(Ideally may  be called as Angina related artery ARA .)

If we have  multiple culprit like  lesions  it is difficult to identify the target lesion. Inexperienced cardiologists  may not consider  this as an    issue !

The following features  may be helpful

  1. The tighter the stenosis , it is  more likely to be a culprit . (Of course , blind  belief on this rule  can result in huge errors ! )
  2. Eccentric lesions
  3. Thrombotic lesions
  4. Grafts /Post PCI lesions if present carry high chances of becoming culprits.
  5. ECG characteristics may  be use full (Global ST depression can not occur with isolated  RCA/LCX NSTEMI   .It  generally indicate LAD  lesion to be  the  culprit.
  6. Deep ST depression in V1 to V3 would indicate LCX a definite culprit .(It could even be a STEMI equivalent )
  7. Echo – Angio correlation can provide a useful clue in identifying the culprit. (Example : In a patient with Multi vessel CAD  , if there is severe resting wall motion defect in Infero -Lateral segments with relative sparing of septum   LCX lesion should be the culprit .)

Exceptions

  • It is not always easy to identify the culprit artery .There can be multiple active  plaques .
  • Diffuse inflammatory vessel are reported in few with NSTEMI
  • Occasionally there can be no  culprit lesion at all (No active plaques ) ,  as the rest angina may be related to excess demand like fever or anemia with  a stable non critical plaque.

Final message

The  delicate   exercise of identifying the angina related  artery is  important  for two reasons.

  1. We can not afford to   prolong the PCI procedure in the setting of ACS  as increased procedure time is clearly related to peri- procedural events.
  2. Secondly , stenting a wrong lesion   and persistence of angina after a  PCI  will take  away  the  hard earned credentials  of  cardiologists  instantaneously !

Reference

Read a related presentation

Posted in Cardiology -Interventional -PCI, Cardiology -unresolved questions | Tagged , , , , , , , | Leave a Comment »

The first Indian guidelines for Acute rheumatic fever diagnosis and management .

June 30, 2012 by dr s venkatesan

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.

 

//

Posted in acute rheumatic fever, rheumatic heart disease, valvular heart disease | Tagged , , , , , | Leave a Comment »

A comphrehensive review and guidelines for Echocardiogram in Aortic diseases

June 29, 2012 by dr s venkatesan

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

Posted in Aortic diseases, cardiology -Therapeutics, general medicine | Tagged , , , , , | Leave a Comment »

Which is the commonest tachycardia observed in Tachy-Brady syndrome ? (Sinus node dysfunction)

June 26, 2012 by dr s venkatesan

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 .

Posted in cardiology -ECG, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias | Tagged , , , , | Leave a Comment »

Crazy concepts in STEMI : Intrinsic Takotsubo effect !

June 24, 2012 by dr s venkatesan

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/

Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology- coronary care, Cardiology-Coronary artery disese, Clinical cardiology | Tagged , , , , , , , , | 3 Comments »

Why Localising IRA with ECG is essentially a guess work ?

June 24, 2012 by dr s venkatesan

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   !

Posted in Cardiology - Clinical, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Cardiology-Arrhythmias | Tagged , , , , , , , , , | Leave a Comment »

2 : 1 shunt in Atrial septal defect means what ? Is it same as qp/qs ?

June 20, 2012 by dr s venkatesan

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 !

Answer found after a decade

All the above cartoons are wrong

The word shunt itself has been mis interpreted by us . Shunt at the level of ASD is different from Qp/ Qs ie excess flow to pulmonary circuit.

Correct explnnation for a 2:1 Shunt:

  • Right Atrium (RA): Receives 1 unit (venous return) + 1 unit (shunt) = 2 units total, which goes to the right ventricle and lungs (Qp = 2).
  • Left Atrium (LA): Receives 2 units from the pulmonary veins, of which:
    • 1 unit (~50%) crosses the ASD to the RA.
    • 1 unit (~50%) passes through the mitral valve to the LV (Qs = 1).
  • Pulmonary-to-Systemic Flow Ratio: Qp/Qs = 2/1 = 2, confirming the shunt ratio.

Posted in cardaic physiology, Cardiology - Clinical, cardiology -congenital heart disease, Cardiology -Interventional -PCI, Cardiology -unresolved questions | Tagged , , , | 10 Comments »

Modern medical quotes : Medical research

June 18, 2012 by dr s venkatesan

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

Posted in Uncategorized | Tagged , , , , , | Leave a Comment »

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