Archive for February, 2012

Can you  safely rule out  heart disease before  non cardiac surgery without echocardiography  ?

Yes  ,  in most situations  .  Experience suggest  If the clinical examination is normal  ,  ECG and  X ray  do not show any abnormality  , significant heart disease is ruled out 95/ 100 times.

  Please note  : ECG and X-ray can not  R/O  Coronary  artery disease by  any  degree of   specificity  .Echo cardiogram  also  miserably fails to predict future CAD. But  EST / TMT does this very efficiently!

So where does the  echo comes in the   routine  protocol  in the screening of  heart disease*  ?

“No where” to be precise.  It is only a gimmick . But  many   physicians  and anesthetists are obsessed  with  echo estimated LV EF %  They     invariably   ask for pre  operative echo  for   cardiac risk  stratification.

* On the other hand EST has a strong case for inclusion as a routine screening test before surgery.

What about diastolic dysfunction  ?

ECG and X ray will not miss  a manifest myocardial disease  . However concealed diastolic  dysfunction can not be detected  without echo. It is very common to detect early forms of diastolic relaxation abnormalities in echo . Significance of this is not clear especially  if it is grade 1 . In this situation patient’s  functional capacity comes to our rescue.  In a non functional patient any degree of diastolic dysfunction may increase  the   pulmonary capillary  wedge pressure. These patients must be  monitored and fluid administration should be  be judiciously used.

Final  message

Echocardiography   rarely  comes*  in the  routine  scheme of things in the pre -operative   cardiac risk assessment.


First question to ask   before non cardiac surgery is  about the  symptoms and functional capacity . ( Do you climb 3 floors  ? Walk 6 km /hr . lift 20kg over a flight of stairs , objectively walk 9 mts on treadmill with std Bruce)  If  he is asymptomatic and his functional capacity is good , for all practical purposes he will be fit for  surgery in cardiac point of view .

Next  , we need to look  the ECG and X ray chest . If one of them shows  some evidence for chamber enlargement / q waves etc ,an echocardiography is ordered .

If  you  really suspect CAD  one should  go for EST or doubtamine stress ECHO.

* Cardiologist lack professional freedom in new age medicine  :

In this funny medical world , a cardiologist can not do what he wants to do . I have encountered surgeons and anesthetics refusing to take a patient for surgery without knowing the  ejection fraction ! Once when  I gave a  surgical fitness without taking an echo there was a furore  from the corporate  desk  of  a  big hospital . How can you  make decision without these modern gadgets they seemed  to  ask  !  Future looks lovely for cardiology !

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I stumbled upon this presentation which deals  how to approach to a problem of  congenital heart disease. In a newborn or an infant . It is clearly a master piece .  A life time experience  of a pediatrician  condensed in  130 slides . It is from Kerala .India.

Link to the  presentation

To  quote an  example  from this presentation.

When you want to rule out  urgently a congenial cyanotic heart disease in the bed side *  What will you do ?

What is  hyperoxia test  ?

Axminster 100 % O2 . Measure satutration.If the  PO2 crosses  200 ,  virtually any cyanotic heart disease is ruled out.

If it is less than 150 , it  is very much  likely the baby has  a CHD !

(* Echocardigram may not be available everywhere . Even if it is there it needs a certain expertise to do it  new-born  )

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The key word for  successful  primary PCI  is

  •  Suction &  Aspiration of thrombus  with   micro catheters like  export catheters
  • One can do away with a stent during primary PCI but can never do away aspiration
  • Distal protection as concept is rapidly dying out as we aim to remove all the thrombus .

Tips for effective thrombus aspiration

  • Apply continuous negative pressure once catheter reaches the thrombus do not release  it till you enter back into the guide.
  • Make sure  you are sucking only  blood  products  not the  endothelium
  • Watch out for  side branch spill over.
  • 7F sheath 7F catheter ideal for aspirating  with a  micro catheter
  • Please be informed some thrombus require more negative pressure especially  in the late  presenters of STEMI

* During dire emergency when you do not have a specialized suction catheter do not hesitate to push  even a diagnostic catheter into the coronary .We have  saved few lives !

Crazy   questions  in primary PCI  ( or Is  it futuristic )

Can we connect the suction apparatus into LAD micro catheter ?

Do we have camera guided suction catheter ?

Can you flush the thrombus if you are not succeeding in aspiration ?

Is ultrasonic desiccation  of thrombus possible ?


Some of the tips were  gathered from the recently concluded  India Live  2012  conference   in New Delhi .

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Blindness  brings  doom to most life situations , paradoxically it is supposed make us wiser in medical research .

We are made  to  believe , the shrewdness and the accuracy of  a study is directly related to the  degree of blindness .

Is blindness  such a great thing ?

The fact that medical research requires  tight  blindness  for  maintaining  truthfulness  ,    implies  there is a  huge   potential   for contamination  by vested  vision .

Our experience suggest  the purpose of blinding a study has entirely a different meaning in today’s world.

Telmisartan  is non inferior to  Ramipril  proved  by a double blinded RCT screams a headline in a popular journal !


Some of the definitions of blinding

Single blinded study

Patient does not know  . . . doctor knows

Double blinded  study

Both the  patient  the doctor  do not know what is the study the researchers knows it .

Triple blinded study

The  Researchers , the doctors and the patients   . . . no one knows what they are doing . Then who will know it ?

Please  be  reminded ,  few powerful men are always awake  to  manipulate the study.

Other forms of blindness (Cortical blindness !)

Who decides  which drug to be compared to which  drug   . . .  we are blinded

Who decides in which country the study  is to be  done  . . .   we are blinded

Who  appoints the principal investigator  . . . we are blinded

Who is steering the steering committee   . . . we are blinded

Who is going to  liaison with the journal editors for publishing the study   . . . .we are blinded

For the practicing doctors  the  blindness often  continues   even  after publishing the trial as vital information are with held.

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A young  man  fell  off the tread mill  soon  after complaining of chest pain in the immediate recovery  phase.

He had just completed 8 minutes of standard Bruce without any difficulty .

Even as the defibrillator was being  moved near him , he was  successfully   shocked with hands  of a hefty nurse !  ( 25 joules ? )   . He  got into this rhythm !

Note the ECG shows diffuse ST elevation .  The ECG soon settled and a diagnosis of  variant angina was  presumed.

He was shifted to CCU. There was no elevation of enzymes , though he showed a transient wall motion defect lasting up to 48 hours.

The subsequent elective  angiogram did not reveal any critical CAD favoring  Prinzmetal angina.

Provocative tests for vaso spasm is not practiced in our part of the world  (I wonder  whether it is still in vogue at all !)

* The classical  angina of prinzmetal is not related to exertion .  Can we call this as a variant of the variant angina ?

Final message

  • VTs are rare arrhythmias  during EST. However , there are important link between exertion ,  VPDs and VT .
  • Exercise induced RVOT  VTs are  supposed  to  more  common. However , ischemic VT during exercise has to be ruled out in every patient.
  • Non sustained VTs in patients who have baseline VPDs are usually benign .
  • Paradoxically VPDs disappear in many  during exertion indicating overdrive suppression by sinus rate .This again can be ignored.
  • Mono morphic VTs  would suggest structural defects.
  • Polymorphic VTs during exercise indicate either ischemia or electrolytic origin

Also read

Wrong concepts in coronary spasm


ECG Courtesy:  Dr G.Gnanvelu MD,DM  Professor of cardiology . Madras medical college

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Measuring TR peak velocity is the most popular  method to assess pulmonary arterial  pressure.It is  universally  believed  TR jet predicts the systolic PA pressure fairly accurately. By all means it is  a wrong perception.

At best ,  it has only 40% correlation with cath  derived PAP  . In other words cardiologist are fooled by TR jet more often than not ! Here is an  elegantly done study  from American  Journal of  Respiratoty and critical care medicine  in  patients  who had undergone lung transplantation . It compared  systolic PAP derived from  Doppler vs cardiac  cath.

Source : http://ajrccm.atsjournals.org/content/167/5/735.full.pdf+html

Important observations about TR jet derived PAP

  • Over estimation is the key error.
  • Error of  under -estimation  less common .
  • Over estimation often occur in normal persons
  • Under estimation more frequent in patients with PAH.

(The above study documents  over estimation of 10mmhg  in systolic PAP in 50 out of  100 patients )

Final message

Nothing is perfect in science ,  especially in medical science.  In spite of the limitations  of  TR  jet  , it   will remain the corner stone in the hemodynamic evaluation of right heart pressures . (Forget for the moment . . . the umpteen variables  in  the modified Bernolui equation  , flow acceleration , viscous friction etc )

It is prudent ,  cardiologists  are expected to be aware of this harsh  fact  and  should be meticulous in tracing TR jet and  reduce the error.

One controversial  but logical  suggestion  would be  to drop the ritual of adding  empirical  RA pressure   5- 10mmhg  over the TR  jet  while  calculating PAP , as there is   60 %  error  of  over-estimation  that naturally occur with TR jet. 




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Pulmonary  arterial hypertension (PAH ) is  an uncommon manifestation of dilated cardiomyopathy .While pulmonary venous hypertension of some degree is expected in most patients with DCM,  it is rare for these patients to go for severe arterial hypertension.

The reason for this may be the  natural history of DCM do not allow these patients to live that longer to manifest severe PAH.  Still ,  we encounter this problem  atleast in tertiary hospitals. Presence of moderate to severe PAH (> 50mm peak PAP) is a sinister sign in  DCM. They not only do badly , they also make  the transplant outcome dismal .

What causes this severe   PAH in DCM ?  The following observations are made in our institute .

Now we know , isolated  systolic dysfunction is  rarely associated with PAH  .It is the presence of  LV diastolic dysfunction (Often restrictive )  that raises the pulmonary pressures.  PAH of DCM is rarely progressive.

One important suggestion is the DCMs  which are associated with  severe  PAH may indeed represent  late stages of RCM , when the LV begin to dilate.

Associated mitral regurgitation   contributes  to PAH

Atrial fibrillation has a significant impact on elevating  pulmonary  venous and arterial  pressures in DCM.

Hypoxic PAH can occur in any medical situation  in susceptible population . DCM is no exception

For some reason  idiopathic DCM is more often result in PAH than ischemic DCM . (Is that possibel , some form of  idiopathic   PAH and DCM are etiologically  related ?)

Further , the positive inotropic agents when liberally used will worsen the diastolic  properties of LV.

Finally involvement of  right ventricle  in the cardiomyopathy  process can have an ameliorating effect on PAH.  A good RV function is essential to lift the PA systolic pressure. If RV failure is causing a low PAP , do not be happy .It simply means RV is going to  say  good bye  . . .  for the final  time !

How to manage PAH in DCM ?

There is no specific management strategy .

We do not know yet  whether Sildenafil ,  Bosentan, and Epoprostenol  have any role in this  form of  PAH. These are all basically vasodilators. It’s use in DCM is vested with a risk of  catastrophic hypotension . Of course ,  we do have a role for balanced vasodilators in cardiac failure .(As most of these patients would be already on adequate ACEI )

Presence of PAH should be considered as an independent indication for anticoagulants as in situ  pulmonary thrombus is common.

The effect of  cardiac resynchronisation therapy in reducing the PAH of DCM is not convincing.

Final message

PAH  in DCM is an unwelcome development. It makes the situation  tough .  The mechanisms are diverse  .Understanding the mechanism would help us deal  this problem better .  Conventional anti failure treatment may help  ,but  it is wiser to try  reserve drugs.

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Clinical cardiac  problems can be very demanding at  times. Here  is a  situation even the toughest will struggle.

A 52 year old man comes with a wide qrs tachycardia  with a blood pressure of 90 /70 with class 4 dyspnea .He was restless , trying to sit up because of  orthopnea. The ECG showed  a definitive ventricular tachycardia  with LBBB morphology.The patient was   connected  the   oxygen line ,  cardiac monitor, oximetery, etc

The consultant  on call instructed   immediate DC shock   and  he  warned  about  impending ventricular fibrillation .He  casually told the fellow to  do a echocardiogram also and rule out any structural heart disease. Even as  the staff was  arranging the defibrillator , the fellow did   a  rapid bed side echocardiogram . He was  shocked to find a  large mobile LV clot   with a  dilated ,  severely dysfunctional left ventricle  having an  EF  of  25 % .

Now comes  the critical time . Should we shock this man with VT and LV clot?

What will be your option now ?

  1. I will not mind the LV clot  ,  will go ahead with DC  Shock . Let him dislodge his LV clot . If It is his fate  let it be !
  2. Defer the   DC shock . Fall back on medical cardioversion like  Bretyllium, Amiodarone or magnesium  . After all . . .  it is not a pulse less VT. He is not in cardiac arrest . He can afford to wait .We can’t risk a stroke .
  3. Give a low energy  shock  25 joules  with paddles  avoiding the LV apex.  .It may not dislodge the apical clot , still  VT may be terminated.
  4. Try overdrive  pacing instead of DC shock
  5. Refer the patient for emergency surgical removal of LV clot
  6.  Suck out the LV clot with a   LV suction catheter and plan elective DC version*
  7. Insert a temporary Aortic filter and shock the patient **

*  Such catheters are in preliminary stage of development . Is  that true ?  ( If  no I  should get the royalty for the idea  ! )

(Read the related article in my blog )

** A loud imagination . Such filters do not exist.( If  IVC  can be filtered   why not  Aorta ? )

What was finally done ?

After analysing each  of the above  , we decided   option one “Prey the  God  and shock the heart” ) After all if it is  a VF ,  this  issue becomes null and void !  . Luckily God was with us.  The  patient  was  reverted to sinus  rhythm with 50joules   and  had  no  untoward events . He was subsequently anti-coagulated .  He is being planned for CRT/ICD therapy

Final message

Critical care  medicine is all about risk taking .Many times , therapeutic maneuvers  confer a  significant   risk  to life  comparable  to the   index problem.  But that  should not be a deterrent .  A careful learned decision  is warranted.

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Localising  WPW syndrome is a favorite  time pass  for cardiologists in spite of  serious  limitations of surface ECG .Still , it is vital to generate a rough idea about the location of  these pathways ,  so that we can focus  our efforts  on  some sort of ablation procedure .

Arruda algorithm is probably a simple and fairly useful technique to remember. It asks us to climb 4 steps   and pause at each  step and look sideways   for the accessory  pathways !

Step 1 (Left free wall step )

Initially one need to look only two leads .

Look at lead 1  and  V1 for   delta wave and R/S ratio .After Identifying delta wave look for the polarity of delta wave (This can sometimes be really difficult ) .If there is iso-electric or negative delta it immediately  fixes the pathway  in left free wall . Similarly if V1 R >  S it also fixes in left free wall. To locate more precisely in left free wall  look  for  delta  wave polarity in  AVF  and proceed down*

If none of these finding are present then  Go to step 2 .

Step 2 (Coronary sinus step )

It is the most simple step . If negative delta  located in lead 2 (often mimic inferior MI)

Here the pathway is often located in coronary sinus /middle cardiac vein often as diverticulum.

After excluding left free wall and coronary sinus origin one has to look at possible septal  pathway  .

For this  go to step 3

Step 3  (Septal step ) And  again v1 lead  becomes important if v1 shows negative or iso-electric  go down  to septal  pathway decoding

After ruling out septal origin the scheme takes us to right free wall by default.

Step 4  (Right free wall step)  If the delta wave does not fit in  any   of the above three steps (Including  positive  delta in V 1 )  it  fixes  the right free wall  pathway

Arruda scheme summary

Arruda scheme  guides  us  to scan  systematically  for pathway from left free wall  to  septum and lastly  the right free  wall  (The key  to  locate  the APs is  to look at  delta waves in lead  1, 2  AVF and R/S ratio In V1 )

Here is a  simplified version for basic localization


  1. Arruda MS, McClelland JH and Wang X , et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. J Cardiovasc Electrophysiol 1998;9:2–12.

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Doctors would simply hate  this book   because  it tries to  expose them !

I would n’t agree with  the tone and conclusion of  this book . But one should soul search  , why such books are written  in the first place ?

The medical professionals  definitely  need to ponder over this  issue .

I stumbled upon this book  in Amazon book store



How  frequently doctors make blunders  ?   What  is your take ?

Would you like to vote in this poll  ?

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