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nobel prize in medicine 2

Why not Nobel prize for clinical  science ?

 

nobel prize for medicine

Nobel prize was constituted  to reward people or organisation  who make a  huge impact on the welfare of man kind. It is given in various categories  for  outstanding contributions in Physics, Chemistry, Literature, Peace, Physiology or Medicine, and Economic Sciences

Unfortunately,  there is a strong bias towards  raw basic science when it is given in the filed of medicine.Do you know  ,there is no Nobel prize exclusive  for medical science ? It shares with human physiology the only field included for Nobel prize in medicine.

Evolution of human  history reveals it is not the stunning  scientific discoveries that impact the mankind . It is  largely dependent  on how we  use them . It is true and natural ,invention of  sub atomic particles , decoding  quantum mechanics  and  trans-cellular  signals always generate great interest  than others.

In medical science, time and again we have seen problems arise in  applying fruits of scientific  research into  practical  usage in the patient domain  in the bedside.

What is use of rewarding inventor of  nitric oxide with a  Nobel prize , when billion-dollar nitrate  industry is thriving on a non existing  life long indication of  stable angina .

It is  surprising  to note ,  Nobel  committee does  give credit to wisdom &  intellect  while awarding  prize in  peace,  literary  or  economic sciences. For some reason it lacks  such a vision when it comes to medical sciences !

We have seen Nobel prize being  awarded to organization that strive for peace and welfare of society and community like UN ,EU  etc.The world health organization is the premier power supposed to provide and  regulate the health in this planet.I do not recall any time WHO  was close to  considered for the  Noble prize in medicine  !

Nobel Ironies

Nobel committee rewards  economists who point out lacunae in vital world macro and micro economics  theories.

Dubious men(Heads of state )  are decorated with Noble peace prizes  for preventing a war in  one geographical area while doing exactly the  opposite elsewhere !

In this modern  millennium  where scientific pursuits are contaminated and  many of the  research questions are misdirected or irrelevant , Nobel committee needs a through rejig in the manner in which  medical  Nobel prize is  being awarded. We know ,Noble’s death wish was to award the brightest mind with highest scientific  breakthroughs in those world . . . but

I guess Alfred Nobel if alive would have changed his rules .He wouldn’t  have imagined modern science would systematically devalue common sense and reinventing it would also deserve an award equivalent to Nobel !

Some of the medical  discoveries that deserve noble medical prize

  • States which excel in   school health nutrition and  other basic health programs  for the downtrodden
  • Doctors who promote bed side clinical skills
  • Tobacco eradication networks
  • Organisations like medicine san-frontiers which strives for basic life saving medication for all
  • Journal houses that specialise  on Medical ethics and clinical sciences
  • Medical professionals and institutions provide value education
  • Medical economists who expose the wasted financial resources that  widen the gap between sick and rich

How about    Nobel prize in cardiology  for preventive cardiologist  who successfully terminates a million statin prescription and restoring natural exercise directed lipid regulation in them  ?

How about  Noble prize for a noble  physician sitting in corporate hospital infested with all commercial ingredients who could resist and argue successfully  against   inappropriate tonsillectomies  and appendectomies ?

I am sure , such a man will be a  laughing stock  for most of us !

An appeal to Nobel committee

It is a wish , Noble prize  in medicine is to be included for people who do yeomen services in preventive and  clinical care and professional who carry forward the legacy of  caring for the sick with  clinical application of available scientific wisdom !

In this scientifically obsessed world , It will be a new beginning in the  way future medical research will be directed and nurtured ! Only then the true power of Noble prize in medicine will be  realised !

Reference

Link to Wikipedia Nobel prize in Medicine

 

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What happens to diastolic blood pressure in severe Aortic stenosis ?

Traditional answer: The diastolic BP remain unchanged. Only systolic BP falls as it is related to LV  stroke volume .(What we refer to as systolic decapitation of BP  )

Reasoning :Diastolic BP is related to peripheral vascular resistance , hence aortic stenosis has  little impact on diastolic BP .

 Further analysis

If we assume only the systolic blood pressure  is bound to decrease in  AS , at one  critical point of time*  systolic BP  should  approach  the diastolic pressure and pulse pressure should approach zero .This can not happen , hence at that point  diastolic pressure will also fall.

*What is that  point ?

No one really knows !

Correct answer

In severe aortic stenosis  both systolic and diastolic pressure falls , but the fall in systolic BP is more striking .

* Though it is customary for clinicians  to discuss them in isolation both systolic and diastolic  blood pressure are closely coupled parameters..In the absence of peripheral run off one of the  strong determinant of diastolic BP  is . . .  systolic BP !

Complex concepts

1. What happens in combined aortic stenosis and regurgitation ?

In  combined AS and AR   we get  pulsus bisferiens. implying  AR will  elevate the systolic blood pressure in spite of obstruction.

2.What happens in associated systemic Hypertension  and aortic stenosis . (Which is very common combo in elderly )

Since HT will increase the  aortic pressure , the LV-Aorta gradient tend to fall.

However ,this  does not happen always as if the original cause for HT was  dependent  more on the stroke volume rather than peripheral mechanisms .

3. Aortic stenosis with aortic  atherosclerosis .

A stiff aorta augments the percussion wave amplifying the symbolic BP and blunting the  classical anacrotic pulse of AS.

4.What happens to BP  during exercise in  severe AS ?

Exercise demands raise in systolic BP and temporary reduction in diastolic BP due to peripheral  vaso dilatation in exercising muscles.

If a fixed  crtical AS does not allow the systolic BP to raise  as required , diastolic continue to fall pulse pressure should still become wide .

Excercise testing is a tricky business in AS. Some have attempted it to assess the functional capacity.(Read below)

Reference

 

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Learned physicians will agree, BP recording by classical auscultatory   method  is  not always an  easy task !

Such an important clinical sign is left to the whims and fancies of human ear’s ability to detect  of low pitched vibrations emanating from deep seated brachial artery .(5 phases of Korotkoff )

Since  Korotkoff sounds are low frequency sounds , it is best heard with bell of the stethoscope ? How many of us do it ?

There is little surprise , two BP  recordings  rarely  match even if it’s performed minutes  apart  !

korrotkoff sounds

While phase one is easily identified , the gap between phase 4 and 5 can be very  narrow and  differentiating  them is often an auditory illusion.

Korotkoff sounds is  subjected to severe tissue plane damping esepcailly in low flow states and obese arms.

So is there an alternative  method to measure diastolic BP ?

Most will agree , systolic BP can be  well measured by palpation ,

What about diastolic BP ?

In this technological era , it may appear foolish to depend on a tactile measurement . But as these articles suggest , it is worth a try!

 

diastolic blood pressure by palpation korrotkoff

In certain population  we know the kortokoff sounds are low quality .Auditory interference can be more than tactile sensation. In those hands ,Korotokoff  equivalents  can be felt by sensitive fingers.

After thought

How does automated BP recorders  sense systolic and  diastolic BP ?

Does it sense the sound or feel the vibrations.

Reference

measurement of diastolic blood pressure by palpation

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Recently , I came across a   young women  who underwent the following three tests for one episode of syncope after witnessing her pet dog bleeding with  an Injury !

  1. Carotid doppler
  2. Holter monitoring and event monitors
  3. Brain MRI /MR angiogram

This was followed up  by Head up tilt(HUT)  in a premier hospital

After 1 week of investigation ,a diagnosis of  Neurocardiogenic syncope was made and she was reassured and no drugs were prescribed.

(The collective yield of the above three investigation in fixing  a specific diagnosis is  less than 10 % of all known causes of syncope )

Syncope  approach  evaluation

To diagnose  common syncope . . . we need common sense !

Syncope is a dramatic  symptom.It is one of the commonest symptom in ER as well . Life time incidence of syncope is at least one episode in 50% all human life ! The definition  of syncope until recently , was liberal .Any transient loss of consciousness with spontaneous recovery  was termed syncope.

This includes

  1. Hypoglycemia
  2. Anemia
  3. Siezure disorders
  4. Structural  neurogenic (Including ,  brain tumors , Dural hematomas etc )
  5. Panic attacks (psychogenic)

Cardiologists wanted to fix syncope as an exclusive disorder of  circulatory insufficiency.By bringing in a modification in the definition  , ie  syncope is  now defined as a transient loss of consciousness due to   reduction in cerebral perfusion  .

This definition helped cardiologists  to exclude the above entities . Still many would include all in single basket as patient should be seen as a whole and we can’t expect them to  land according to our convenience and classification.

Here is an incomplete* list about causes of  syncope (* 99% complete ?)

Vascular

  • Vaso- vagal syncope in young ( Neuro-cardiogenic , Common , Benign)
  • Autonomic dysfunction of elderly ( Including postural hypotension )

Cardiac

Arrhythmic ( Sinus node dysfunction /CHB/Idiopathic VT/Long QT syndromes)

Structural heart disease

  • Valvular  heart disease  (LVOT/RVOT obstructions)
  • Myocardial disease
  • Rarely ischemic heart disease

Miscellaneous

  • Severe pulmonary hypertension (Including PPH ,  pulmonary Embolism )
  • Paradoxical embolism.
  • Aortic arch disease -Takayasu related arteritis .

Investigation

We have a sophisticated array  of investigation for syncope .It can be a never ending exercise , ranging from  spinal cord evoked potentials to diagnose Shy-drager syndrome ,   . . .  to implanting long-term loop recorders to decode  heart beat behavior.

However , evaluation of syncope is the ultimate wake-up call  to all current generation cardiologists  . . . Why clinical cardiology  should  never  be allowed to die (and  it  will not ! )

Common sense begins with answering  few simple questions . Is it really syncope ?

If  you ask this question three times and with  specific leads to the patient  and the witness ,  truth will come out  . 90% of times it may not be syncope at all (Near syncope, accidental  fall, dizziness ,extreme blurred vision, drowsiness  etc)

If it is syncope , Is there a non cardiac cause ?

It may related to the Hypoglycemia / Anemia /Panic attacks.Get a neurologist opinion , it would be terrible mistake if you miss a space occupying lesion  within the brain. (Missing chronic silent sub dural hematomas is  frequent   in the evaluation of syncope of elderly !)

Ruling out  cardiac syncope is relatively easy

In the remaining  patients  basic investigation like routine blood tests,ECG, ECHO   will help us  rule out most serious cardiac disorders.Similarly  bulk of the electrical cardiac syncope can be diagnosed.(Holter , carotid study in selected few )

Need for neurologist -cardiologist interaction.

Syncope due to VBI,  transient Ischemia attack , Senile vascular dementia  is a grey zone . Many have complex neuronal -vascular mechanisms . What is Consciousness ?  and  What is LOC ?  :Is it the lack of blood or severely depressed nerve signal in the reticular activating system? Lots of interaction between cardiologist and neurologist is required to clear our ignorance.(I  have one such  elderly patient who is intermittently awake ! I call this chronic syncope !)  .

Undiagnosed syncope is not  a crime

Realise the most important lesson in Medicine . If you  have ruled out all serious  causes of syncope you should have the courage to be satisfied with that !

Scientific pursuits has a limit. Searching for the mechanism of a psychogenic  fainting attacks with intra cerebral electrodes is a clear case of  physician acquiring a psychotic  behavior !

Final message

Syncope is not only a dramatic symptom for the patient , it also unfolds a drama of costly  investigations  . .  . many  with  dubious value.

Talk to the patient personally for  10 minutes in a quiet room, try to apply that elusive  clinical sense  . . .   it would rarely let you down !

After thought

What is the true clinical value of * Head up tilt Test (HUT)?

Will be posted soon

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We know LVH and SHT go together . Mind you , this is not an Intimate relationship.

Widespread utilisation  of echocardiography  has revealed  , definite  LVH occurs only in about 20% (A guess !) of  HT . (Do you know in the Famingham study the incidence of LVH  after 12 year follow up was a paltry 3 % .Will you agree with that ? Mind you , It was in 1969 when Echo was not there )

What determines LVH ?  The clear answer is elusive. It is easy to escape  from the issue by calling it  multi factorial !

Why don’t you try this question .

My guess would be ,  magnitude ( or  even duration of HT !)  is  less important than genetic predisposition  or  associated diabetes ,  renal involvement.Our analysis from  hypertension clinic reveals LVH is many fold common in secondary HT  when compared to primary HT !

I often used to provoke the students by saying if the LVH is gross in HT it can not be primary , 9/10 times  ! Invariably  we find some  other  association or reason for the HT !

Link to related topic in this site

Why-lvh-does-not-occur-in-all-patients-with-systemic-hypertension ?

How-diabetes-modifies-lvh-due-to-hypertension ?

incidence of lV left ventricular hypertrophy framingham study

Next  . . .

How does LVH regress with treatment ?

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Right ventricle is a passive venous component of the heart .It simply acts a  transit pump for blood to reach the lungs.

It  is true  , RV is dispensable in many complex congenital heart disease as we  can connect the great veins directly into the pulmonary artery  by  Fontan , Glean and it’s clones  bye passing this chamber . Still , by no means the importance of this chamber is to be underestimated.  RV dysfunction and failure  is the key to survival  many  disorders.RV shock is is cause of sudden cardiac death in acute pulmonary embolism and RV infarction .

RV is an unique muscular chamber .It is more of a triangular shape. It has  three different parts connected by three different angle .There is no true  apex  for RV , it is   connected  to Inflow and outflow in peculiar fashion .

In the  following table I have  tired to  describe  of how different parts of RV  behave in various disorders.

what is the morphology of  RV enlargement RV inflow outflow body sinus portion of RV

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I know ,there is a VSD out there !  but I am  unable to  get the gradient across it.This situation can be quiet  common .The reasons could  be technical, anatomical or  hemodynamic.

As a rule ,  if we hear  a  pan-systolic murmur clinically ,   one must be able to catch  a good  Doppler spectrum somewhere by  echocardiography . However , If  the murmur is restricted to  early or mid to late  systole, VSD  jet is often attenuated in echocardiography .

In the  following situations ,  VSD  jets  may not  record a distinctive Doppler spectra. Invariably the velocity is low , spectrum is short,  less intense ,  lacks good shape and borders are hazy !

  • A closing  VSD
  • A Small muscular VSD
  • VSD with  Severe pulmonary hypertension
  • VSDs with muscle bundle criss crossing
  • Double chambered right ventricle (DCRV, where VSD usually drains to high pressure chamber.)
  • VSD  associated RVOT obsruction  (Note: classical TOF VSD will never generate a murmur)
  • VSD with sinus of valsalva aneurusms (  Doppler  jet  can be really  difficult to record )
  • Inlet VSDs are missed because  convectional  views of echo are perpendicular to these inlet jets.(Short axis better  )
  • Another common situation  is post STEMI VSR.Both a small apical VSD or multi tract  VSD associated with  infero posterior  STEMI   gradients are  difficult to obtain.

What is   inference ?

Doppler spectrum will help detect  small VSDs and color doppler will not miss even a tiny VSD.Doppler spectrum across VSD  is dependent many  factors other than the presence of VSD. However some large VSDs are detected better by 2D echo rather than doppler signals.

Final message

Presence of a Anatomical  VSD does not  imply it should generate a noise.The murmur as well as Doppler signals  are  primarily  determined by the pressure difference on either side of VSD. After all , one of the  largest VSD  that  we encounter

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