Archive for the ‘Clinical cardiology’ Category

Exertional dyspnea disproportional to the effort is the most common (cardinal)symptom of heart disease. Whenever we discuss the mechanism of cardiac dyspnea , we primarily attribute it to left heart disease, elevated LVEDP and the resultant pulmonary congestion.Conventional teaching in the past (may be in the present too !) doesn’t implicate raised RVEDP in the genesis of dyspnea.

It’s good to recall , the sensation of dyspnea is felt at the peri -Amygdala nuclear zone after complex processing with various cortical and sub-cortical level .It is subjected to as many afferent triggers other than J receptors in pulmonary micro circulation. (Eg Exercising skeletal muscle). It is believed, mechanical stretch receptors exist within the walls of heart along  the sub-endocardial aspects of chamber.

(Muscle spindles which are the sensors of muscle tension are extensively noted in skeletal muscle that contribute to the origin of dyspnea .We are not yet accruing enough evidence  whether cardiac muscle do have the same muscle spindle or it’s equivalents to cause dyspnea when stretched. However, we clearly witness in the practice of clinical cardiology , isolated elevation of RVEDP ( also RVSP ) to cause significant dyspnea in specific clinical situations.

Potential causes for Isolated Right ventricular dyspnea

  • Pulmonary hypertension  (COPD included* where in it could be a combination of lung and cardiac dyspnea)
  • Acute pulmonary embolism
  • RV Infarction
  • Acute rupture of sinus of Valsalva aneurysm (RSOV) Here RVEDP is often > LVEDP and dyspnea is due to the acute stretch of RV
  • Isolated normal pressure TR(RVEDP is low still cause dyspnea  due to volume related RV triggers)
  • Any RVOT obstruction (Classically valvular pulmonary stenosis)
  • Does RV dilatation without elevated RVEDP cause dyspnea ?  Though right ventricle is developmentally and hemo-dynamically better suited to handle volume , still, it  struggles to manage sudden increase in volume .(Another clinical example is seen in patients who are on dialysis)

*RV diastolic dysfunction is still a Infantile hemo-dynamic concept .Whether it can raise RVEDP significantly during exercise and Independently contribute to dyspnea is at best a hypo-science.

Role of muscle spindle and mechno-receptors


Muscle spindle

structure of skeletal muscle spindle. Though we don’t have a highly developed spindles in smooth muscle and cardiac muscle we have evidence to suggest cardiac neural ending do have mechano-receptors with afferent connection through visceral neural plexus that can trigger both heart rate and respiratory centers Further reading : Neuroscience. 2nd edition. Show details Purves D, Augustine GJ, Fitzpatrick D, et al., editors. Sunderland (MA): Sinauer Associates; 2001.

Bain-Bridge reflex: The hidden link in right heart dyspnea

Bain-Bridge reflex is a 100 year old concept. still helping us to understand the basics of right heart hemodynamics and how adjustments with acute volume loading take place.He proposed that  veno-atrial stretch receptors are located  primarily in great veins as it enter ,right atrium (RV as well).

This gets activated through vagus and stimulates  in brain-stem sympathetic system and increase the heart rate to handle the excess blood reaching the heart. How often we feel the symptom of palpitation  whether due to this reflex ( when it is operating) is not really tested. But, what we can infer is , the surge in sympathetic tone perceived can be perceived as  dyspnea.

*Clinical Relevance of the Bezold–Jarisch Reflex and its possible interactions with Bain Bridge reflex is a different topic.

It is interesting to note many of these reflexes cause hypo-tension, bradycardia and hypopnea (Even near Apnea.) The word dyspnea is surprisingly not used .It is highly plausible many of the unexplained dyspnea we see in otherwise healthy population is attributed to acute or chronic volume overloading or under-loading of right heart.

Role of PFO in right heart dyspnea

PFO is a natural decompressing orifice in the IAS guarded by a flip-flap safety valve which is a remnant of septum primum .Though it can flow either way , since the flap of the valve is larger in LA side,  it gets closed when  LA pressure raises but opens up , if RA pressure raises making it more often a right to left shunt at times of elevated RA mean pressure. In isolated right heat pathology , this communication shunts  right to left and  adds a new dimension to cardiac dyspnea (Now, It becomes a hypoxic /biochemical dyspnea over and above the right heart stretch related dyspnea )

Other mechanisms in right heart dyspnea

Pulmonary arterial stretch and altered QP : Role of ventilation perfusion mismatch should also be considered as a cause for dyspnea in isolated RV pathology. The term V/Q mismatch is a poorly understood term fro me. My Inference is, since RV contraction  provides the Q in the equation V/Q .Whenever Q falls V has to fall to maintain neutrality causing net hypoxia and dyspnea.

Final message

Dear fellows, never hesitate to attribute the origin of dyspnea,  to elevated RA mean pressure /RVEDP. It is due to RA/RV stretch secondary to volume and pressure overloading with a perfectly normal pulmonary capillary wedge pressure or LVEDP. As in the left heart ,this occurs both in pathological as well as perfectly exaggerated physiological times.


1.Bainbridge FA. The influence of venous filling upon the rate of the heart. J Physiol. 1915 Dec 24;50(2):65–84. [PMC free article] [PubMed[]

2..A J Crisp, R Hainsworth, and S M Tutt  The absence of cardiovascular and respiratory responses to changes in right ventricular pressure in anaesthetized dogs. J Physiol. 1988 Dec; 407: 1–13(This paper actually undermines the importance of RV receptors. It is still perplexing to note both the inflow into RV (ie RA  and the out flow  pulmonary artery circuit has richly innervated by receptors , its difficult to accept why we  have failed to get much evidence for RV stretch receptors) Its potentially great area of research for cardiac physiologists. That will be a tribute to the greats like  Bain Bridge and Bazolds Jarich.)

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Not every one feels the palpitation during tachycardia / Bradycardia /VPDs , Why ?

Palpitation is awareness of one’s own heart beat. It is a complex perception of sensation at cortical level (like dyspnea) . It can occur during physical and mental exertion.However , if it occurs without any physiological reasons , it becomes abnormal. It can mean an abnormality  in heart rate , rhythm or  raise in stroke volume. The first rule of palpitation is both tachycardia and bradycardia can cause it. Tachycardic palpitation is due to valve motion and bradycardic palpitation is due to both motion and increased stroke volume.

The most common mechanism proposed for palpitation is hyperactive anterior mitral leaflet

How and where  does the sensation of  palpitation felt ?

Does  it originate in  the chest wall ?  or Is it the vibrations spreading along  the flow of blood in great vessels ?  or Simply  represent  the vigorous valve motion  sensed by Intra cardiac receptors ? How it is  transmitted to spinal cord where it’s felt at cortical level  ? We are not clear yet. Paccinian corpuscles is thought to sense these vibrations and hand over as electrical signals  to spinal cord either directly from cardiac valves /walls or indirectly from chest wall.

Paccinian corpuscles are predominantly present in sensory nerve fibres located in the dermis of skin. It is also observed in nerve ending to joints, Chestwall, blood vessel and also heart .They act like pressure as well as vibratory receptors * The exact reference for Paccinian corpuscle to be present within the heart is not available to me. Readers may contribute,

Importance of age and gender and IQ

Palpitation is primarily a symptom of young age where the heart is supple and more dynamic. Women tend to perceive more for some unknown reason. Elderly people rarely complaint about palpitation .It could imply aging  with or with out autonomic dysfunction which suppresses transmission of palpitation signals to brain.Chest wall thickness also matters. My guess would be, Chest wall thickness, epicardial fat pad could absorb the vibratory  energy  and chest wall receptors fail to recognise it. One curious observation is,  palpitation is described in a succinct manner by certain patients only. Since , it essentially involves  higher cortical senses , we believe spatial intelligence of the patient  may also be important.

Why Irregularity in heart beat is well recognized?

For the given heart rate , irregular rhythms are felt  more often as palpitation than sinus tachycardia. This is the reason single ectopic beat is easily felt than  sustained tachycardia. A common sequence of  palpitation due to ectopic beat is , a suddenly  missed beat, subsequent pause and forceful post ectopic beat.

Valve morphology and impact on palpitation

Mitral stenosis patients can feel their loud first heat sound (S 1)  or varying  S1 during atrial fibrillation as palpitation; Mitral valve prolapse with redundant , hyper kinetic motion is probably most common cause of benign palpitation.

Sclerosed  and calcific  valves attenuates palpitation. Calcific mitral valve in mitral stenosis make both S 1 intensity and opening snap feeble .These patients are less likely to feel palpitation .

Individual valve pathology can generate palpitation as in Ebstein anomaly , which has a the large sail like septal leaflet that flutters to create palpitation(Apart form pre-excitation syndrome common in this condition) As a general rule ,It is possible semi lunar valves are less likely to cause palpitation than AV valves as the latter only exposed to direct contractile pressure of ventricle.

Right vs left heart origin and localised palpitation

I am not sure one can differentiate left heart from right palpitation. But.palpitation arising from right ventricular  volume overload and increased pulmonary flow like in ASD  are associated with direct local sensation over pericardium . Mitral valve motion can not be localized by  patients .However apical impulse can be felt.Neck pulsations invariably mean high flow states. Venous cannon waves due to high pressure tricuspid regurgitation can be felt with each heart beat (RV systole)

Exertional vs Non exertional palpitation 

Palpitation occurring during exertion often imply its due to excessive handling stroke volume or (Pathological regurgitant volumes) Stenotic lesions are less likely to cause palpitation during exertion it’s never an absolute rule. Exercise Induced arrhythmia always happen in any valve lesions.

Relation with LV function

A dysfunctional ventricle cannot  generate forceful contraction and hence palpitation is uncommon symptom. Cardiomyopathy presents with more of dyspnea rather than palpitation .Even,  an episode of AF do not cause palpitation in such patients .They simply feel breathless (Dyspnea ? Or is it a palpitation equivalent ?)

New age palpitation

With so many foreign bodies and accessories entering the heart  it’s not surprising for patients to feel amusing sounds and vibrations hitherto unknown in human body.

  • Prosthetic valve clicks (Sounds from mechanical valves can be  annoying .Tissue valves, TAVR are more quiet)
  • Abnormal electrical activity  from pacemakers and ICD coils.(Apart form pacemaker mediated muscle twitches)
  • Now, we have entire mechanical LV assist devices  working inside the heart with a 24/7 motors .(LVAD hum its called) Very soon heart is going to become a noisy place and patients would learn to ignore these abnormal sounds

Pleasant physiological palpitation

What brings the unpleasantness during palpitation? (applies to dyspnea as well). It is purely state of mind. While, palpitation due to extreme fear is unpleasant , palpitation due to pleasant emotional arousal (Often referred to as flying butterflies ! (Is it the wings of AML ? ) within the chest  as we hear from some of young  women & men ).Since they know the reason why they get it, cortical input welcomes it ,converts them to pleasant  beats .The Non-academic stuff  is intentionally made to understand how the limbic system and Hipocampus  areas of brain can modify the incoming signals of palpitation that comes from down under.

Thoughts to ponder 

Does post heart transplantation (De-nerved heart) patients experience palpitation ? Again, I am not sure .If palpitation is carried by cardiac nerves it should disappear. Of-course , 30 % of transplanted heart do get re-innervated. When you get a chance to meet a heart transplant patient you ask yourself and find the answer.

*Please be reminded Anginal pain almost vanishes  post transplant.In fact ,there have been instances of cardiac auto-transplant for refractory angina in the past.

Final message

Though all of us can list causes of palpitation without any difficulty , we rarely dwell into exact  the mechanism of genesis of this symptom and  its perception. As we enjoy flying in an exotic world of cardiac  interventions  . . .  the principles of  practice of medicine also expect us to take adequate efforts to understand fully the cardinal  symptoms of our patients . After all , they are the true teachers of Medicine. It is because of their pursuit for explanation for their symptom (Often vague though)  we make our professional progress.

Further  reading

John T.Shepard  The Heart as a Sensory Organ JACC Vol. 5, No.6  June 1985:83B-878

(The heart has variety of sensory nerve endings , still to be explored)

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We know pleural effusion (hydrothorax) is disproportionately more common on right side in cardiac failure.Though its a well observed phenomenon, the mechanism of which  has not been clear to us. It could be due to multiple  anatomical , physiological factors.


*The are  right and left lymphatic (Thoracic) ducts that drain the corresponding lungs and pleural space . There can be overlap and contribute to the differential occurrence of pleural effusion



A meticulous paper written some 75 years ago (1946) from Harvard medical school teach us some important points in this phenomenon.

There is still lot, to be understood about pleural effusion in cardiac failure. We need to know why some pleural effusions tend to occur independent of hydrostatic forces.  It is also noted long-standing transudative effusions can become true exudates. Role of local pleural capillary hypoxia resulting increasing permeability is underestimated.Hepatic congestion and trans-abdominal seepage of fluid is a distinct possibility.

One more area we are not clear is  the relationship  between the  genesis of  pericardial effusion in cardiac failure and concomitant pleural effusion. Post operatively , after univentricular repair (as in Fontan ), pleural effusions can be much problematic with high venous pressure interfering with  pleural drainage.

Impact on symptoms

Finally, even mild pleural effusion can increase the work of breathing and result in dyspnea which is out of proportion to cardiac dysfunction.While we expect the diurteics to clear the effusion of cardiac failure, it doesn’t happen always arguing for a non transudative mechanism in at least some of them.

Further reading

Discerned readers are advised to study the pleural space dynamics in detail.

Link to the original Article of Edgar Mcpeak and Levine 1946




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Syncope and seizure are most dramatic symptoms that rarely fails to call the attention of the patient and family.Syncope is primarily evaluated at medical or cardiac units. However ,when syncope presents as convulsions (often It is ! ) the patient lands up in a Neuro unit as a case of epilepsy.Some how, many of them are prescribed anti convulsants without being evaluated for what triggered the seizure.


Cardiac seizure and Neural syncope : Require a balanced approach ! (Image courtesy http://3.bp.blogspot.com)

Real life experience now suggest, a bothering  number of patients in epilepsy clinic might harbor a primary cardiac disorder in the form of either brady or tachycardia which is often inherited due to defect in ion channels of cardiac cell.

The issue is two fold. 

  • Cardiac patients mis-diagnosed as seizure
  • Primary seizure patients suffer a cardiac death (as seizure induced arrhymias or acute pulmonary edema )

Incidence of sudden cardiac death in patients with seizure disorder though rare is being increasingly recognised. Mechanical problems like valvular Aortic stenosis can also result in syncope followed by seizure.

Final message

Cardiologists do have a major role these situations.It may be wise to advice basic cardiac work up in  every seizure disorder.  As we are beginning to understand the neurogenic triggers in sudden cardiac deaths , the need for Neuro-Cardiac units is real.(Some of big university hospitals do have such departments)


1.Zaidi A1, Clough P, Cooper P, Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol. 2000 Jul;36(1):181-4.

2.Leestma JE, Annegers JF, Brodie MJ, Brown S, Schraeder P, Siscovick D, et al. Sudden unexplained death in epilepsy: observations from a large clinical development program. Epilepsia. 1997 Jan. 38(1):47-55.

3.Kloster R, Engelskjøn T. Sudden unexpected death in epilepsy (SUDEP): a clinical perspective and a search for risk factors. J Neurol Neurosurg Psychiatry. 1999 Oct. 67(4):439-44

4.Leestma JE1, Walczak T, Hughes JR, K A prospective study on sudden unexpected death in epilepsy.Ann Neurol. 1989 Aug;26(2):195-203.

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effect of inspiration on jvp and bp pulsus paradoxus bernhiem effect ventricular interdependence

Image  modified  from  http://www.anatomygallery.info

That’s  normal . . . what happens during pathological states ?

There are important diseases  that  restricts entry of blood into right heart chambers. They can occur either in an acute  (Tamponade) or in chronic  fashion like constrictive pericarditis  and restrictive cardiomyopathy.These entities  show distinctive impact on JVP and systemic pulse.

The two pathognomonic signs are Kussmaul sign and pulsus paradoxus* that go hand in hand in most  situations.Inappropriate elevation of JVP with inspiration is termed as Kussmaul sign , while exaggerated fall in systemic BP with inspiration is called Pulsus paradoxus.The later is the  arterial counter part of  Kussmaul sign in JVP .However, there can be dissociation between these two signs occasionally.

* Pulsus paradoxus is a term originally  used by Kussmaul when he noted heart sounds were  retained while pulse dissappeared  in  patients with cardiac  tamponade .Later we realised the loss of pulse was linked to inspiratory cycle  of respiration. To make  this sign objective  sphygmomanometery  criteria was formulated which measured the difference between inspiratory  and expiratory korotkoff’s  sounds .

Coming up next 

Why Kussmaul sign  is often absent in Tamponade while  its arterial counterpart pulsus  paradoxus may still be conspicuous ?

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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 !


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This  query often  evokes  confusion  among fellows and General physicians .

              The answer is simple .Yes ,  you can.(With few conditions)

  • Thrombolysis  or PCI  is  done  with reference to  the  presence  or absence of ST elevation and chest pain.
  • If there is ongoing chest pain  and  significant new onset ST elevation  thrombolysis or PCI is indicated whether there is associated q  waves or not.

Clinical situations 

 Ischemic  q waves: Q wave can occur  with transmural ischemia which result in electrical stunning and loss of R waves . (Many of them  regenerate this R within few days after STEMI ,  indicating the q  waves can be  ischemic  in origin)

Reinfarction : Patients with  old  MI can develop fresh ST elevation  in q leads due to tachycardia and dyskinetic infarct segment .This group  of patients  should be carefully evaluated before labeling them as  re-infarction

* q RBBB in early hours of  anterior STEMI is fairly common which  may revert later. qRBBB is not a contraindication for re-perfusion .

Final  message

Presence of q waves does not  imply one should not  entertain  thrombolysis or PCI .The decision  to reperfuse  , rather  goes with  presence of  chest pain , ST elevation and  of course  within the  acceptable   time window!

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Can we close an  ASD in a  25 year old women  severe  pulmonary hypertension ?
Volumes of literature has been written  on the subject.Dedicated cath studies  have been done with multiple parameters .
Still , there is a lingering doubt !
Here is  a  3 minute  practical solution  based on 5 easily available parameters. (* Also referred to as  unscientific  in medical parlance !)
1.  O2 saturation
2. Pulmonary artery diastolic and pulse pressure
3. RV function,
4 .Systemic pressure
5. Functional class
  • If O2 saturation is > 90 % consistently  there is likely to be significant  left to right shunt  .Closure is to strongly considered
  • If 02  saturation is near 95 % there is absolutely no contraindication at any level of PVR.
  • Systolic pulmonary artery pressure derived by TR jet is least useful index.Pulmonary artery diastolic pressure reflects true vascular  reactivity of the pulmonary  circulation.A wide swinging pulmonary arterial pulse indicates dynamism in circulation and hence operablity.
  • If pulmonary artery  pulse pressure is  wide (>50)  , or PA diastolic BP is < 30 one can safely presume irreversible damage to pulmonary vasculature has not occurred and these patients would  benefit  from surgical closure .
  • RV  function should be assessed carefully in every patient.This is as important as PVR .Significant RV dysfunction is an absolute contraindication.
  • Never close the shunt in patients who is in class 4  symptoms.
  • Never close a shunt if the systemic blood pressure is low( 90mmhg)
  • Some believe  PDA may be closed at any given PVR , while  worst outcomes occur with ASD as supra-systemic pulmonary pressure is possible.
Always monitor these patients meticulously especially  in the initial days following surgery  for deterioration .Most patients will do well if they cross the first 30 days. The RV  learns to adopts with  new  pulmonary hemodynamics !


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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 !


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)



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