Archive for December, 2011

A middle-aged obese man was referred  to me  for  an emergency  echocardiography

The patient was unable to lie  either supine or left lateral  . He could lie down only  right lateral posture  that too for a minute .An ultra fast echo gram was completed . It  was  entirely  normal . His ECG was also normal.

When I  asked for x ray there was a surprise

Note the shrunken thoracic space  on both sides .The  fundus of stomach is  almost fighting for place with left ventricle in the thoracic cavity .

No wonder he is severely orthopnic  (But fairly comfortable on erect posture )

He has a distended abdomen .He is  now waiting for a GE consult. His other complaint is belching   . Is that some form of gastric obstruction ?

I’m posting this image to re-emphasise the  classical  teachings in medicine .

Human body is  a highly integrated  biological  system .We in the name of modern science  has  disintegrated in to  multi organ entity.

This patient was labeled as acute pulmonary edema and the treatment was about to be started.

Here is a patient  with dyspnea and orthopnea  entirely  due to a non-pulmonary and non- cardiac cause !

                                                        All youngsters  . . .  always be alert  . Clinical medicine  is  notorious  for  throwing   surprises , especially when you least expect it !

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There were times medical  profession’s  only purpose was to take care of the sick . Modern  principle of living  has contaminated  every walk of life .Medical profession  leads  by example in this race .

How can one justify celebrating a disease in a grand manner in public domain  in the name of increased awareness  ?

I am shocked to find an ad in a recent  The  Hindu Ad  (25-11-2011)

Some of the words  used are terrible and highly objectionable . It amounts to an  insult to all diabetic patients.

  • Diabetes award !
  • Diabetic  Carnival !
  • Join us in the fun of diabetes !
  • Glitz and glamor of diabetes!
  • Festival of diabetes !

How can a patient celebrate his illness ?

I think  the news paper  which  publish such ads  should also show some sensitivity .

I agree there are lakhs of diabetic patients who do require  intensive treatment  but the fair held in the air conditioned corridors of  a trade center is  never  going to address  this issue.

( Can I ask these organizers to  help and  serve the real diabetic burden in ill equipped public hospitals  across  our state ? )

It  is simply a commercial extravaganza   creating a fear complex among the healthy , rich men and women and make a living

out of   human anxiety . 

Who sponsors these medical  award nights ?

For those who are unaware  of the games doctors and pharma companies play,  here is a shocker – large amounts  of money is pumped into  such public events.

This is part of  a  larger board  room  strategies ( Can it be a conspiracy  !) to increase the per capital consumption of drugs of our population . And no doubt   doctors are integral part of this scheme with or without intention .

While MCI can penalize  a individual doctor  even for accepting a pen as gift from pharma company ,

they can do nothing but simply watch  as millions are  exchanged  in the name research , health education ,  and awareness .

The height  of  the  irony is  , these events are sponsored by WHO and the world  forums as well  !

Ironically   the  doctrine of  modern medicine  seems to suggest   . . .“Ethics is   primarily for individual physicians and do not  apply   for institution ”  This is the single   most dangerous  concept that is  playing havoc with human health”

It closely mimics the principle  of   war justice  . An  individual shooting another individual  is a definite  crime ,  while  multiple  individuals  killing  multiple   individuals   is not a crime , it is a war !


The author has no  personal grudge  against any hospital or organization instigation. It ‘s   an expression  against so many commercial activities that occur  in the medical filed on day-to-day basis !

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WPW syndrome is the prototype of cardiac pre- excitation . The accessory  AV pathway short circuits the ventricle .Since  there are two options  available   for the  incoming  atrial  impulse  to reach ventricle ,  often  times  the qrs is contributed by both .Hence a  fusion  occurs  within qrs complex and stretches it wide   ,  it also  generates a delta wave and short PR interval .

The complexities of  conduction   properties and refractionaries of AV node and  accessory  pathways determine the degree of pre- excitation. When an optimally timed  APD  gate crashes  into the  accessary pathway it gets blocked ,  only to recover little late ,  unfortunately  invites AV nodal impulse  from below  . This facilitates a  re- entry circuit from ventricle to atria and result in classical AV reciprocating tachycardia .

Antegrade conduction through AV node is  physiological and  benign as it inherently checks the heart  rate . Antegrade conduction  occurring through the  accessory pathway  (which  constitutes the pathological  component  ), is   potentially  dangerous  as it lacks the  electrical breaks (Technically called decremental conduction )

What  is the  specific  ECG evidence for  antegrade conduction thorough accessory pathway  in ECG ?

Delta  waves

So,  what does it mean if there is absent delta waves  in WPW syndrome ?

It can mean three things

  1. Concealed pathway
  2. Manifest pathway , but intermittently  blocked pathway.
  3. It is not WPW syndrome at all .

We know concealed  pathways are  safe* as it allows only retrograde conduction. ( Safe  regarding   risk  of  sudden cardiac death ,  still unsafe for AVRT !)

Intermittent WPW

Intermittent pathways are equally  safe  as intermittent absence of  pre-excitation   indicate  the  presence   of naturally occurring     breaking system within accessory pathway . Are these  accessory pathways blessed with some AV nodal cells ?  May be !  . Histological studies do suggest that .This explains   intermittent missing of delta waves  which is  electro-physiologically a good sign

(We also know   there are exclusive slowly conducting accessory pathways like  Mahim and variants  )

If  one is lucky to observe this phenomenon in ECG  it can be termed as  a poor man’s  EP study  . ( Which requires specialized methods to document the refractory period of accessory pathway  to be   < 250 msec)

Techniques to  screen for or / unmask this concept.

Whenever  we  diagnose  WPW one has to look   ,  whether the patient  harbors  this phenomenon .

  • Holter monitoring has a useful role in this regard .
  • If there is nocturnal   disappearance of pre- excitation it would  suggest a safe  accessory pathway.
  • Similarly , if pre- excitation disappear during exercise  stress  testing it  would indicate a  type of intermittent WPW syndrome.

Final message

An astute cardiologist shall  look for this intermittent nature of delta waves  and  help avoid a costly and  potentially harmful EP study !

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How early one can shift a patient for rescue PCI after failed thrombolysis ?

  1.  Wait for at-least 24  hours.
  2. A minimum  cool off period of 2 hours is required.
  3. It is never an issue . Rush the patient  immediately to cath lab
  4. The question does not arise  . Often times ,  rescue PCI is a dead concept  as  sufficient damage has happened !


The irony of  medical science  lies in our belief that every medical query  has a specific answer ! In reality it is rarely true.   In this instance , any of  the above can be a correct response.

A patient with  failed thrombolysis can belong to any of the  64 possible combinations*  based on  time of  thrombolysis , extent of  MI,  associated complications, co- morbid conditions , presence of symptoms . (For example there is  a sub groups of patient with  failed thrombolysis still  asymptomatic  and comfortable )

The issues for rescue PCI  do not  arise  in a   sinking STEMI (Cardiogenic shock ) , or  STEMI with persistent angina. There  is  no  management issues in  these patients  .They need to be rushed to cath lab. Unfortunately  in  impending  LVF or manifest LVF (But not in shock )  decision making is tough , as doing a PCI in patients  with basal crackles  and hypoxia is a real challenge .These are the patients who are likely  to hit hard  from the hazards of the procedure .Extreme caution is required.

I have seen  significant cohort  of  asymptomatic hypotensive patients getting converted into   drug resistant, IABP dependent refractory shock after PCI  ,  making every one look  pathetic  !  The  only solace for the interventionist  is  the gratification  of  stenting the  IRA !

This  happens  , in spite  of having  multi national trained  in house critical care anesthetics and  dual core processing IABP  . Realise  what we need is delicate decision making ,  So use extreme diligence in selecting patients with impeding shock .

Your medical management can  provide  more teeth to stabilise your patient than a PCI .If you are doubt discuss with your learned colleagues .  ( If you  do not  ask for evidence for  this statement , probably  it would confirm  you  as  an  experienced   cardiologist  !)

Real issues pushed to the sidelines ?

While the real issue  in the timing of rescue PCI  may be  different , the discussion traditionally  revolves around   hemo-rheological aspects . We know  the lytics and PCI do not combine well for two reasons.

  • Pro-coagulant nature of lytic state .
  • Excess bleeding risk at puncture site.

Now ,  we have evidence to say fibrin specific lytics  TPA, TNKTPA has less of this issue . ( NORDISTEMI)

Patients who receive  fibrin specific lytics  can  safely  be  taken for rescue PCI  in case it is needed without any increased risk .

Bleeding complication  has dramatically reduced as radial procedures are done often even in emergency setting.

Vascular occlusive devices  have added to our comfort.

* The definition of failed  thrombolysis by  itself is not standardized . Is it symptom guided ?  or ECG / enzyme / echo guided  ? A patient with  infarct  related chest pain (dull aching )  after thromolysis can be labeled as post infarct refractory angina and rushed for emergency angiogram .(This is due to our ignorance  about  the  residual pain signals  through  type c pain fibres  for up to 24 hours )

Final message

The indication and  timing of rescue PCI is  primarily  related   to the  overall   patient profile  rather than the bleeding or pro-coagulant issues .

Although   pro-coagulant  lytic state is based on weak scientific  foundation , it  is a blessing in disguise  as it  can  act  as a deterrent  in restricting  inappropriate rescue PCI !

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 Delta waves  are initial 20 ms  (or is it up to 40ms ?)  segment of  qrs complex that is  inscribed due to pre-excited depolarisation of the ventricle due to an accessory pathway .

It is more of a  fusion complex with  native normal qrs complex. The leads in which appear , the polarity and magnitude of these delta waves are determined by

  • Site of APs
  • Rapidity of  conduction through this AP
  • The quantum of native AV conduction
  • Influence of Autonomic tone  and the  refractory period of these accessory pathways .
  • Heart rate , distal conduction velocity , also can influence .

Can delta occur without AP ?
Like any other variation  isolated delta waves are reported in routine ECG finding.   It can be  be present in 0.15% to 0.25% of the general population. A higher  prevalence of 0.55% has been reported in first-degree relatives of   patients with accessory pathways.

How do you account for delta in general population ? We know concealed pathways can not record delta  . . . then it is possible some from of accelerated AV conduction  with twin pathway should be quiet common . ( It is very much possible  dual AV nodal pathway with grossly different conduction properties and distal insertion sites  inscribe a delta wave .)

  The crux of the discussion  of WPW syndrome revolves around  identifying delta wave and its direction .  If  the delta wave is well inscribed this job is easy  but at times  it  can be really difficult .

Many moods of delta wave

  • Positive delta  wave inscribes  above baseline. (See the above ECG  showing different delta in same patient )
  • Negative below baseline  and  iso-lectric on the baseline .
  • Please note , delta wave polarity and QRS polarity need not be in the same direction . If  they are in  the opposite  direction many time it appears as  small a pathological “q”  or pathological  “r”
  • It is likely  a delta wave can also drag  and  change the direction of qrs depolarisation  if  the  quantum pre-excitation  is large and with a fast conduction property.
  • It is also possible  the combined contribution of  negative delta with negative qrs together make a  deep  q waves . (Typical example is the LBBB type ECG in type B WPW in Ebstein anomaly )
  • Rarely the entire QRS can be  due to pre-excited  tract and native AV conduction contribute less.(This exactly happen in anti-dromic tachycardia ) but  this phenomenon is extremely rare to occur without tachycardia.

Final message

WPW  syndrome is such a dynamic  entity ,  one can realize how futile it will be to formulate fixed rules for ECG localization based on this wave .In fact,  we suffer from a  fundamental  electrical ignorance .How often delta wave polarity is discordant with qrs polarity and what is the  mechanism ? Standard text books do not discuss this issue . Many of the EPs skirt this question ! For this , we need  to critically decode the mechanisms of delta wave generation . Hope our youngsters take up the job !

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