Feeds:
Posts
Comments

Archive for the ‘Uncategorized’ Category

Great cardiology websites : This one is for cardiac radiology !

Posted in Uncategorized, tagged , on March 7, 2010| Leave a Comment »

Hunting for  treasures in medical jungle is no easy job

There are  thousands  of websites for learning  radiology  and then ,

This one  . . .

Hats  off  to   William Herring, MD,

http://www.learningradiology.com/toc/tocorgansystems/toccardiac.htm

Read Full Post »

How to identify pulmonary veins in transthoracic echocardiography ?

Posted in Cardiology - Clinical, cardiology -congenital heart disease, echocardiography, Uncategorized, tagged , , , , , , , , , on March 6, 2010| Leave a Comment »

Even though it is a great vein , often the imaging pulmonary veins by echocardiography is a not a pleasant excercise.

This is due to the following facts

  • The pulmonary veins are posterior structures
  • They occupy the far field of echocardiographic window
  • The pulmonary veins often enter obliquely into the LA
  • The course of PVs are highly variable ( Like RCA origin !) especially in ASDs ,where identifying PVs becomes all the more important

Hence no fixed imaging angle can be advised . But generally a pattern is observed.

  • Right pulmonary veins are best viewed in apical 4 chamber or 5 chamber or in between (Especially RUPV is  seen best in 4.5 chamber view !)
  • Left pulmonary vein , best visualised in  Para sternal  long and short axis view.

Other modalities for imaging pulmonary veins

TEE : Can be  very useful since it is brings the vein closer to the probe .But needs more expertice.

Contrast echo :Probably a simple and best modality often underutilised.

Very useful to clinch the diagnosis when PVs take abnormal course as in PAPVC .

MDCT , Spiral CT, MRI  are the new age modalities that can provide us  with dramatic  3d images of PVs.

The  echocardiogram will always prevail over these sophisticated gadgets for its simplicity and also it’s ability to give us the physiology of pulmonary venous flow which is vital in many diseases(Constriction, Diastolic function etc)

The following illustration is a gross attempt to simplify the imaging of PVs.Please note the rules may not be applicable in all.

Left upper and lower pulmonary veins in short axis view will be posted shortly .

Reference

The images are  based on  personal observations and  an  excellent insight  on the topic from  Department of Cardiovascular Medicine, Guangdong Provincial People’s Hospital, Guangzhou , China

http://ejechocard.oxfordjournals.org/content/9/5/655.full

Read Full Post »

A landmark study , but least popular among the interventional cardiologists !

Posted in Cardiology - Clinical, Uncategorized, tagged on March 3, 2010| Leave a Comment »

Are the drug eluting stents really better than bare metal stents ?
A million dolor question ? , No . . . a billion dolor question
A study which answered most convincingly with a huge data base  published in LANCET 2007.
  • 38 trials  , Metaanalysis
  • 18 023 patients with
  • 4 year follow-up of up to 4 years.
  • No mortality difference from bare metal stent vs DES
But unfortunately there is  no takers for this  study . The usage of DES continue to  surge ahead  .
The problem facing the medical science in the current era
It takes years  of research to get  into  the truth    and  still   longer time  for  us  to  accept it ! Ironically  falsehoods have immediate patronage and there is no incubation period !

Read Full Post »

Guideline violations in cardiology

Posted in Uncategorized, tagged on February 28, 2010| Leave a Comment »

Cardiology  is  among the top medical  specialty  in the current era. It deserves this  special status as it is probably  the  a specialty  which  is based on maximum  scientific evidence and  involves ,   the  most advanced diagnostic and treatment  modalities.

As on today ,  a cardiologist  can deliver a stent  anywhere along the coronary tree and even  implant  a valve percutaneously . A surgeon can put multiple grafts in a beating heart  with a patient totally awake !

A  person can live with an  artificial heart for months and a cadaver  heart can give  fresh lease of   life to a terminal heart failure patient .

Why such a glorious filed of cardiology  should often   evoke a pessimistic reaction  in the minds of  public and media ?

This is because  for a   simple reason , in the name of technology , we tend to  indulge in scientific excesses.

This article in Circulation is not a  surprise then . . . Click on the link, Thanks to AHA this  comes free of cost !

For pdf article click on  the image

Note : Non adherence , inappropriate therapy,  Class 2b  indications ,  are  simply semantics in stage  play !

Actually these terminologies are synonymous with

  • Guideline violations,
  • Unscientific ,
  • Empirical.
  • Unethical or  even quackery

Read Full Post »

What is off label prescription ?

Posted in Uncategorized, tagged on February 28, 2010| 1 Comment »

We generally  believe  drugs  and devices are prescribed  by  physicians with strong scientific basis .Unfortunately  it is  not  true  in many instances.  A drug which is approved for one disease is assumed to be useful in a similar disease  (But not tested in  clinical trials ) and it becomes  an unapproved  indication .This is often termed as off label use (A decent terminology for unscientific usage !) .But ,there are pros and cons to this type of physician behavior .

Pros

The best example  is  the role of sildanafil in pulmonary arterial  hypertension(PAH)  . A drug which was introduced for erectile dysfunction , was found to very useful in regressing pulmonary arteriolar pressure  (Mistaking pulmonary arteriole for penile vasculature  !?) .  A new therapeutic concept was born  for a  hither to difficult problem of PAH. This  successful  discovery  was  attributed   to off label  usage  of a drug .

Cons

But this is a rare  success story of off label therapy.  In real world , we  tend  to  overuse this in many situations and harm is anticipated.

Drug eluting  stents was used extensively in off  label situation ( Acute MI in a thrombotic milieu, very small vessels , in close proximity  to bare metal etc all these are non label or off label  use of coronary stents   which  resulted in many deaths )

Who gave the freedom and liberty for the physicians to use a drug or device off label ?

No body gave  it , we assumed ,  we have it .

When somebody uses a drug for an unapproved indication is it not unscientific  and guideline violation ?

It is a violation , but we can afford to do it because every body does so !

Is there any scientific  body to sanction and desanction off label  usage ?

Unfortunately  not !

So what  is the solution ?

Self regulation  . . . Can it  be  a  fool-proof method  ?

or  Is it foolish  to expect it so  in this   era of commerce  ?

Related video in youtube hosted by me.

http://www.youtube.com/watch?v=d2WfLrTiUks

Related article

Guideline violation in cardiology practice

Read Full Post »

What is the mechanism of deafness in Jervell and Lange-Nielsen syndrome ?

Posted in Uncategorized, tagged , , , , , , , , on February 22, 2010| Leave a Comment »

The same channels , that  create the  deadly prolonged  QT interval  by  delaying the  repolarisation  in the heart  is  responsible in the for the deafness  as it interfere with inner ear

Mechanotransduction of sound into neural signals .

For proper auditory function  , the cochlear hair cells   needs  a continuous flow of endolymph which  maintain a voltage gradient for  nerve  signal  transmission  .The lymph secretion is  is regulated by potassium channels  KCNQ1 and KCNE1 . Mutations of this gene impairs  the K + content of the endolymph. It results in  a compromised  endocochlear potential (Difference between peri lymph and endolymph potenial )  .This result in irreversible deafness .

Link to   a good   illustration from Medical physiology

Read Full Post »

What is a cannon sound and what is a cannon wave ?

Posted in Cardiology - Clinical, cardiology -ECG, Clinical cardiology -JVP, Infrequently asked questions in cardiology (iFAQs), Uncategorized, tagged , , , , , , , , , , , , , , , , , , on February 21, 2010| 1 Comment »

Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.

//

Read Full Post »

Lesser known cardiology journals . . . but with excellent content !

Posted in Uncategorized, tagged , , on February 21, 2010| Leave a Comment »

There are many  cardiology journals we read , trust , and celebrate  . . .

Many of us are not aware of   few other excellent journals

This is one is different

It is  from  Scandinavia &  deserves a special status.

Read Full Post »

Can we diagnose unstable angina in a patient with normal ECG ?

Posted in cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, Uncategorized, tagged on February 15, 2010| Leave a Comment »

It is said every clinical diagnosis needs to be substantiated with  documented objective  evidence .

Probably,  the commonest cardiac emergency , that can be  diagnosed purely by history is UA.

Yes , unstable angina is a symptom not a  disease entity !

By definition UA is

  • Any  new onset angina  of severe grade
  • Progressive crescendo angina
  • Angina with radiation to new site
  • Angina not controlled by nitroglycerine
  • Any angina after a PCI /CABG

If you read the definition again, you will realise ECG or enzymes never come into the  diagnostic picture .UA can be diagnosed even before one has a look at  the ECG ! So, it is too obvious one can diagnose UA irrespective of whatever is recorded in the ECG. Normal ECG is one such possibility.

When a patient is having severe  compromise  in the  blood supply to his / her heart  , how  on earth ,  it  is possible to have a normal ECG ?

It only tells us,  ECG is not a fool proof method to exclude ongoing ischemia . When we know , ECG can miss even a STEMI  it is not a big deal it misses a UA.

Apart from  the electrical blind spots of conventional 12 lead ECG, following are the other  explanations offered for a normal ECG in UA.We know UA occurs with ST depression(Classical ) , T inversion,  rarely ST eelvation

So UA can occur with

  • Pseudonormalised t waves
  • Pseudo normalised ST depression
  • Cancellation effect of two  opposing  subendocadrial ST segment vectors ( As in multiple active plaques PDA   and LAD lesion )
  • Even Ischemic cascade

Final message

Even though  UA  CAN  occur with normal ECG  , we are uncomfortable to   diagnose  UA without   documenting ECG changes . We should realise this fact , as missing a diagnosis of UA , just beause the ECG is normal  could have very costly consequence !

Read Full Post »

Learning from the “Dead” and “Dying” : Coronary care unit secrets !

Posted in Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -ECG, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology-Arrhythmias, Cardiology-Coronary artery disese, Infrequently asked questions in cardiology (iFAQs), tagged , , on February 14, 2010| 1 Comment »

STEMI is the commonest cardiac emergency . Many believe , we  are close to  conquering  it .  It is hardly the truth .

  • The  mortality is  up to  30 % out of hospital and another 6-8  % within CCU  and another 2 %   at  30 days due to recurrent ACS   .This  is followed by an   annual attrition rate OF 25  due to progressive LV failure  .
  • The commonest mode of death is electrical,  ie primary VF.
  • Mechanical deaths are also equally important. Free wall rupture carries 100% mortality . Ischemic MR, Ventricular  septal rupture (VSR ) may also result in deaths.

Here is a case history and ECG of a  patient with STEMI .

After thrombolysis , the paradox happened . ST elevation  increased by 4mm and soon the patient became restless with worsening pain and became silent instantaneously ,  with monitor showing EMD and asystole .A diagnosis of free wall rupture was made.

What we used refer  in our CCU (Madras medical college Chennai .One of the oldest CCU in  South Asia )

as   “Action pontentialisation”  of surface ECG . This ECG finding has  great  clinical significance .

Here is a zoomed up view of a qrs complex of  the patient , which is very

closely resembles an action potential

Picture courtesey  http://ocw.tufts.edu/Content/50/lecturenotes/634488/634591

Pathological basis of  “Action potenial”  Like ECG

  • When the ST elevation is huge and wide it mimics  an action potential .
  • Myocyte action potentials are normally recorded epicardially in physiology lab where a  micro electrode with glass pipettes directly enter the myocyte.
  • A giant ST elevation and a sustained dome indicate , the quantum of  electrical injury is  very large and the  ECG electrodes is picking up the myocyte electrical events like that of a intra cellular electrode.
  • It is to be recognised  ,  ST elevation in chest leads is substantially taller than limb leads   because the exploring electrode  is located just above the myocardium . But,    when a  huge  ST elevation  is recorded  over a limb lead (as in this patient )  one can imagine ,   how intense the electrical  charge  of  the myocardium  should  have been  !

This heavy downpour of electrical energy that  emanate from the myocardium   means two things

  • The area of infarct is very substantial
  • The tissue in question is  very unstable .

Clinical correlates of  action potential ECG

  1. Damage is transmural , the   infarcted area is soft, friable and often hemorrhagic .
  2. The pericardium is also  likely to get involved in the injury process .
  3. The myocardium is  rupture prone or already torn .
  4. Even minor hemodynamic stress can be fatal in these patients
  5. An episode of vomiting, a fall in blood pressure,   an episode of  LVF or a short run of VT is suffice  to result in a fatality.

The death happens by a sudden rupture ,  EMD and asystole .

Can a life be saved  by the much fancied Emergency PCI  ?

Not really. The PCI  can not reverse the myocardial damage ,  so it’s role is little . But , any way it should be done and  .  .  . it  will  be done  in most institutions to give the benefit of doubt (Of course , with  a definite the risk of doubting  !)

What is the risk  of  PCI in these situation ?

The infarct related artery * if opened up can convert a bland infarct into a  “angry red”  hemorrhagic  infarct .This   is as good as  giving  the patient ,  a  farewell  party for his journey to heaven !

Note : Primary PCI  definitely  saves life in STMI . The  * is applicable only in persistent ST elevation , late after an acute MI.

How could  have the above death prevented ?

As one of the comments to this article  suggested, we need to have methods to identify impending rupture early and accurately .This should  followed by a prophylactic  surgical intervention (Reinforcing the friable myocardium – with a patch or mesh  )  .This is again not  a easy decision to make .

Final message

When the ECG  assumes  a shape of an  action potential ,  it is often a sign of  imminent  death  . Even though it may sound a pessimistic  view  it is often the truth  . Of course , an  emrgency PCI or  CABG  are  the only options available , we have  to be remember the above truth  ,   as we   play  those sophisticated  games  within their coronary arteries.

Read Full Post »

« Newer Posts - Older Posts »