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Where there is a will . . . there will be a way !

October 30, 2014 by dr s venkatesan

Caring shall be an inbuilt character in the  Noble profession ,need not be a value added service or a separate medical specialty !

image

Posted in Cardiology quotes, cardiology-ethics | Tagged , , | Leave a Comment »

Ignorance based cardiology : Electrical vs Mechanical Asystole

October 23, 2014 by dr s venkatesan

When  a life leaves the body  silently in CCU , an  undulating  flat line in the monitor has a hidden scientific tale  to tell !

 

A  56 year old obese women died a instant death immediately after engaging the Left main ostium  after first injection of 5cc dye. The monitor showed only  a short pause, few sinus beats , a long pause , asystole and death . In the last 2 minutes of survival she threw a random wave forms of suggesting EMD . At any point of time she never showed any evidence for ventricular fibrillation . 1o minutes of intense resuscitation failed that included temporary pacing , repeated shocks  and ventilation.(ECMO /LV assist excluded)

asystole_bad_day_in_the_cath_lab_tshirt-p235709389664476041uye8_400

What is the mechanism of death ?

  • Is it electrical or mechanical ?
  • Acute mechanical stunning / the stone heart ?
  • Is it a primary electrical asystole ? (Acute sinus arrest or AV block )

Post hoc analysis of CAG did not show any significant clues except a tight distal left main.Apparently the catheter has triggered the event .( Or is it the  dye ? as some body suggested it as anaphylaxis  ?)

Even though we conveyed the message to the relatives,  it’s was an unexpected massive heart attack , obviously we were not convinced with our  uttering  ! Mind you , she had  normal LV function but had recurrent angina prior.

asystole ecg 004

Image courtesy modified from http://www.ijaweb.org 2012 for representation purpose only.

We know if cardiac arrest is due to VF, it tends to give us  at-least some time and sense. Further,the VF protocols are more clear and success rate is more .

There is always an issue of  fine VF vs  asystole.If the flat line is indeed VF , there is more chance of revival as we try to pump adrenaline to make the fine VF  into coarse one  and shock again .The sequence can continue few times.

It is well known  asystole has a  dismal outcome .Even among the asystole there is some hope* if asystole is purely   electrical . (Like Stokes Adams in CHB or electrolytic asystole like hyperkalemia etc ) .But if asystole is due  mechanical cause , death ensues in spite of prompt temporary pacing .

* Important note : We have this  common  form of  treatable  mechanical asystole .It is called cardiac tamponade .It always present  with extreme bardycardia and asystole. It is extremely  rare to see a tamponade to present with VF. A prompt needle tap will do the job .It is vital  to recognise this in cath lab as our efforts are rewarding .

I would recommend a hand held echo machine , to hang like a catheter in every cath lab , ready to screen unexplained cardiac arrests with zero delay !

Why some hearts respond with VF  , while others go for asystole  with acute coronary insult ?

  • A million Rupee question ! We are yet to find a legible answer .What is probable is  the the heart doesn’t  even have energy to fibrillate !
  • The underlying disease need to be so intense .In this case it was left main stenosis supplying a truncated LAD and LCX. We could also see it supplying twigs to RCA  suggesting it to be a total occlusion .
  • So ,when a  “physiologically single” coronary artery that precariously  supply the entire heart is suddenly insulted the heart behaves violently with runs of VT/VF. Our ignorance is complete when we realise  the heart  can do the opposite as well .It does not react at all , goes for a deep slumber and result in electro-mechanical sudden death.
  • It is expected , in acute mechanical  deaths one may encounter flash pulmonary edema if the LV alone gets stunned. However , if both right and Left ventricle come to standstill in a synchronised sudden fashion , lungs will be as silent as deep sea . We believe this is what happened in our patient and it can be logically correlated  as  the critically narrowed left main was supporting the  RCA  as well.

Final message

Sudden cardiac deaths  9 out of 10 times is electrical . Majority  of them is  due to fibrillation. Next comes the electrical asystole ,Rarely (is that really rare ?) an ultra fast  sudden death due to mechanical asystole (Non -Tamponade ) is  possible , as experienced in our patient .

These mechanical asystole  are yet to be decoded.Whether it is a form  of Acute stunning , electro -mechanical uncoupling or mechano electrical standstill is not clear.

 

 

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ICD secrets : Appropriate shocks are not benign after all !

October 5, 2014 by dr s venkatesan

Inserting an ICD  for  DCM  may a be great therapeutic success  for the physician  as well as the patient . But there is one big truth hidden behind the statistical screen.

Following  study  provides dramatic data from Maanhiem in Germany in about 561 patients who had ICD .The long term patient outcome after appropriate shocks were much worse  than those without    shocks .This was more pronounced in Ischemic DCM .

appropriate and inappropriate shocks ICD

Source : Streitner et al ,University Medical Centre Mannheim, Mannheim, Germany PLoS One. 2013 May 10;8(5):e6391

The fact that these patients continue to throw VT , some thing is wrong in the cellular  milieu or a fresh scar / fibrosis / ischemia is progressing .Further , the VTs and the  subsequent  shocks  set in temporary  hemodynamic instability .We have evidence , EF can be depressed for days  worsening the long-term out come.

While it is easy  to blame it on natural course of DCM , there are  solid reasons to believe  , shock induced myocardial damage is definitely contributing to this  excess mortality.

One important  clinical tip is to screen  all  these so called Idiopathic DCM  patients  who  had appropriate shocks.  They should be monitored for fresh signs of any systemic illness  , like a  connective tissue disorder , chronic granulomatous lesions  like sarcoid etc .To our surprise  some specific  myocardial disease may unmask themselves in the natural history. Identifying them may offer a dramatic cure .

Final message

Some where along our EP mind-set  we are conditioned to think  , as along as there is an ICD in situ and it appropriately  shocks, every thing is bliss ! Blame it  on semantics . The  word “appropriate”  inappropriately  soothes  our nerves.

The fact of the mater is , every appropriate shock is a  grim reminder  that the heart  in question  is restless electrically and VT continue to emanate  from diseased  myocardium  . It could  mean either the LV   is destabilising  , or the original  disease  is   progressing  or a new disease  is evolving .

Mean while, paradoxically , inappropriate shocks give us a quixotic comfort , since the  heart is not really  throwing any dangerous arrhythmia, after all it is  the device related  false alarm   that  could be easily  reprogrammed!

Reference

ICD appropriate and inappropriate shocks

Posted in cardiac resynchronisation, Cardiology - Electrophysiology -Pacemaker, Cardiology -unresolved questions, Dilated cardiomyopathy, Electro physiology, ICD -Tips and Tricks, Infrequently asked questions in cardiology (iFAQs), Land mark articles in cardiology, Pace maker Tips and tricks, Permanent pacemaker | Tagged , , , , , , | Leave a Comment »

Learn the essence of Interventional coronary care in 180 seconds flat !

October 3, 2014 by dr s venkatesan

Your clock starts  now !

 

clock gif dr s venkatesan002

Chronic stable angina : Most can be effectively managed  by  optimal /intensive medicines and life style Interventions .About 10% will require PCI/CABG.

ACS – STEMI:  Primarily  managed  with  rapid and competent  pre-hospital care with prompt thrombolysis in or out of hospital .Patients  with  large STEMI who develop complications (Again about 10 %)   require PCI and few additional  lives can be saved.

ACS-NSTEMI : This is  the group that demand  an  important role for PCI . All true high risk UA/NSTEMI patients  should receive urgent coronary  angiogram and critical lesions  should either be stented or  sent for CABG  (If the lesions are multiple and complex ) The field of interventional  cardiology  is  expected  to play a major  role in  this category of  patients for the simple reason , we  not only give dramatic  relief from angina and also prevent a  potentially a huge MI that is waiting to happen !

* It is vital to emphasise  the “Aim and  objective” in  NSTEMI  management  is critically different from other two. We know ,  in CSA   the aim is to give relief  symptoms  and improve excercise capacity . Both PCI/CABG  are  unlikely  to prevent a future MI in CSA..In STEMI it has already occurred .The aim is to salvage myocardium  and prevent  future events. While PCI can do the former , it can’t do the later . In STEMI scenerio ,we have very good  alternate  modality called thrombolysis which can easily beat the  pPCI  in , cost , availability and time  (and  hence efficiency as well  in  most  countries !)

Counter thought

The above suggestion  is too simplified ,generalized , misleading , and  unscientific, should   strongly be disagreed. For those people who disagree , I provide an alternate scheme  .It is ultra short ,comes in  5 lines .Very practical  and  scientific too  !

In any  patient , who is  suspected to have either  acute or chronic  coronary syndromes ,take them to the cath lab in an  urgent or semi urgent fashion .Do an angiogram and stent all lesions  that you feel important . If  stenting is not possible  manage  with optimal medicines and /or send them to the surgeons.

Final message

The essence of catheter based coronary care is simple.We complicate it. To understand this concept  100’s of cardiology  journals  and as many conferences and infinite  number of books are churned out every year !

 

 

 

 

Posted in Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged , , , , , , | 1 Comment »

Why 40 days cool off period for ICD after STEMI ?

October 1, 2014 by dr s venkatesan

Current guidelines advice us to wait for 40 days following STEMI to implant ICD in most high risk patients.

Why this  cool off period.? *

  • Essentially  we are waiting for the Infarct healing process to be completed.
  • By this time electrical stability may be restored. The  risk of VT/VF  declines per naturalis.
  • LV function recovery  is possible. As stunned and hibernating myocardium resumes its mechanical function and patient might  jump out of the MADIT-2  cutoff point. (EF< 30%)
  • Introducing  ICD very early  after STEMI may be a myocardial irritant and that it self can generate  arrhythmias.
  • There is a possible interference by the leads in the physiological remodeling  process.

Final message

So the cool off period is  not only to reduce  the unnecessary  ICD implantation  but also to  avoid lead related issues .

*  This 40 day rule is based on one  large study from Germany. (DINAMIT, 2004  ) . However  few believe  the rule is not absolute. There can be individual   exceptions in high risk patients with critical LV dysfunction .

Other  wise   . . . How do you digest  a death occurring on  35th day  in a patient  who is waiting for an ICD scheduled one week later ?

Reference

DINAMIT trial ICD nejm

Link to  ACC/AHA  Guidelines for ICD Implantation 2013

New development

How to bridge the 40 day gap in really high risk post MI patient ?

We can’t keep him in CCU. Here comes the role of WCD (Wearable cardiovertor defibrillator.) Life vest is  from Zoll . WCD can act like a bridge till the 40 days when the patient becomes eligible for ICD.

http://lifevest.zoll.com/

 

Posted in Cardiology - Electrophysiology -Pacemaker, Cardiology -Pacemakers and ICD, Cardiology -Therapeutic dilemma, cardiology -Therapeutics, Cardiology -unresolved questions | Tagged | Leave a Comment »

World’s most glorious hospital : Sant Pau Hospital Barcelona !

September 30, 2014 by dr s venkatesan

One of oldest hospital  in the world , is now an  UNICEF heritage site. Santa Creu , Sant Pau original hospital built in 1400 AD rebuilt in 1900 by Catalonian modern architect Montaner.

sant pau hospital barcelona unicef

Architecture by Lluís Domènech i Montaner

sant pau hospital barcelona

inside-hospital-sant-pau-in-barcelona

sant pau hospital unicefReference

Hospital de Sant Pau

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What is time velocity Integral ? (VTI )

September 30, 2014 by dr s venkatesan

TVI  (or VTI)  is a hemo-dynamic  echo parameter measured from Doppler spectrum  across the valves ,usually in the outflow.This parameter is used to calculate cardiac output .VTI times the cross sectional area gives the stroke volume.

 

time velocity Integral TVI

A correction: TVI is multiplication of velocity into time not division as suggested in the cartoon   

Time velocity Integral

What is time velocity integral TVI echocardiography

Summary

*VTI is a Doppler parameter described in cm , it can be referred to as Stroke distance.This stroke distance when multiplied by  valve area gives the stroke volume from LV/RV  (or flow volume across AV valves or through any conduit)

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Creating new culprits during Primary PCI !

September 28, 2014 by dr s venkatesan

One of  the hottest debate in  the recent  world  cardiology forum in Barcelona WSC 2014 , was  about  how to tackle incidentally detected non IRA lesions  during primary PCI.

So far , the dictum is , one should not meddle  the non culprit lesions unless demanded by hemodynamic instabilty .The next option is to do a staged PCI for these  lesions. (Few days later). or just forget about these lesions unless they are critical.

Now new studies are appearing that suggest  doing all  “do-able” lesions must  be stented  in one go ! This is obviously inviting trouble .The worry is not  in the concept but with the  dubious  track record , fragile guidelines and potential  ethical debacle of the cardiology community !

Stent “As you want and as you please”  has  already  invaded our mindset in  the chronic coronary  scenario. Now in 2014 , we want more freedom  in acute coronary  syndrome as well ! We  can’t ask for a  referee less game of soccer !

We clearly know coronary  arteries  are to be respected and do not deserve indiscriminate stenting  especially  in ACS  where  the early hazard is  more.

A recent story  which I heard  was a  height of  futility . A semi experienced cardiologist in the suburbs of a big southern Indian city , opened  successfully a LAD  which was the IRA  and  subsequently caused  acute  LCX  STEMI , while trying  to tackle an insignificant  non culprit lesion due to procedural mishap ! (Some suggested migration of LAD thrombus !)

What a pity , when we are supposed to  arrest the culprit, in reality it is simply  chased  down to another territory !

 Here comes  unique  advantage of thrombolysis , you need not locate  the culprit  artery the drug chases it wherever it is , even if they are  multiple ! Read in this link :

 Final message

We call it as fate when  thrombus suddenly occlude  a coronary artery  and the IRA becomes  a  culprit . We  need not compete with fate and end up creating  potential new culprits.Let the  sixth sense prevail over the five .Use judicious discretion when trying to stent muti-vessel  CAD  during PCI. Please  realise ,the concept  of  multivessel stenting during pPCI is not wrong .  How we interpret is the issue !

There is no excuse  to indulge as you like  , simply because your intentions are good !

 

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Buddha’s Instant recipe for happiness !

September 25, 2014 by dr s venkatesan

One of my favorite quote  about Happiness from Buddha !

 

Happiness quote from Buddha

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How is chest pain of unstable angina different from Infarct pain ?

September 24, 2014 by dr s venkatesan

When a patient comes with angina at rest , it could mean two things .Either a  STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .

Can we differentiate these two by the  character of chest pain alone ?

Very  tough task isn’t  ? But there are some definite clues .

Infarct  pain

  • Is mostly sudden .
  • Likely to be crescendo , lasts more than 20-30 minutes .
  • Fails to get relived by rest or even  Nitrites.
  • Sweating due to sympathetic activation is more pronounced.

Unstable angina

  • Is rarely  sudden .Often has a pro-drome.
  • UA is  mostly precipitated by an increased demand situation or a stress.
  • It has  a typical waxing and waning  pattern . Rarely assume a true  crescendo character  as myocytes  does not necrose (Just threaten to die !)
  • The chest pain radiation   to  shoulder is less  conspicuous , instead it  tends to  reach  the  jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)

Mechanism of the difference : Epicardial vs Endocardial angina

The pain of UA is   due to subtotal occlusion and  endocardial ischemia , while STEMI is  sudden total occlusion  and the resultant  transmural  ischemia . In STEMI  epicardial  surface is always involved (Which lifts the ST segment in ECG .).We know epicardium  is same as  visceral layer of pericardium which is well innervated .Hence  pain  of STEMI   acquires  more of somatic character  than a  predominately visceral type pain  that occurs with  UA/NSTEMI where epicardial ischemia is absent.

Clinical importance

The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.

Post -amble

It is tricky issue  to differentiate the  chest pain of  STEMI and NSTEMI  .A significant overlap can occur  in  real coronary care scenario . We know   chest pain  that occurs in both   pre and post infarct  phase  is considered  as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating  them may even be termed as futile.

Still,clinical cardiology  can be  made  fascinating by indulging in such exercise !

 

Posted in Cardiology - Clinical, Cardiology -Clinical signs, Cardiology -Mechnisms of disease, cardiology- coronary care, Clinical cardiology | Tagged , , , , , | Leave a Comment »

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