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Regional wall motion defect( WMD) is the hall-mark of myocardial infarction.It can vary between complete akinseia to mild hypokinesia.

The wall motion defect is a gross terminology which is used  to describe any abnormal motion of the ventricular   segments.Technically,  hypo,   hyper , dyskinetic , akinetic  ,  even any vigorous  movement of LV segments will also come under the general category of  wall motion  defects. For example in extensive  anterior MI   the posterior segments show vigorous  contraction.Though . this compensatory motion  benefits many , it has a potential to adversely stretch the  scarred myocardium and promote aneurysm formation

What causes the regional wall motion defect ?

  • Infarcted segment
  • Ischemic segment
  • Adjacent normal segment behavior (Piggy pack effect, )
  • Loading conditions
  • Heart rate

Finally ,  and  most  importantly the timing and arrival electrical signal to these ill-fated segments determine the sequential activation fronts. Wall motion defect is a more complex phenomenon than we would tend to believe.

What are the  the classical examples of electrical wall motion defect ?

  • LBBB
  • Pre excitation
  • Some forms of VPD

*LBBB causes a paradoxical septal motion with  reference to lateral fee wall contraction.It is still a mystery ,  this paradoxical motion does not cause any  mechanical  disadvantage in structurally normal hearts  .

WMD  in combination  of  LBBB  and  STEMI

We know ,   LBBB   due to ischemia or infarct carry a  sinister prognosis .

Here , there  is  “Double wall motion defect”  . One electrical and two ischemic .  We do not know , how LBBB influences the ischemia/Infarct related wall motion defect and vice versa. .  This is the reason ,  there is a large chunk of  poor or non responders  for cardiac resynchronisation therapy.

Can peri infarction  blocks and other non specific   intra  ventricular  conduction defects alter the sequence of  ventricular  contraction ?

We do not know .It is distinctly possible.Tissue doppler studeis have indicated this.

What is the influence  of  heart rate on the  of Wall  motion defect ?

An  otherwise insignificant regional wall motion defect  could be  amplified with tachycardia . Paradoxically , (as in a biphasic response to dobutamine stress test )  a significant WMD may be attenuated at a particular heart rate.  So, the influence of  HR on  WMD is  as simple as  it could be  ! ! !

Which  is the best time to assess  LV  function  after  MI ?

Considering these issues , LV function  assessed  at discharge ,  may not give us the exact quantum of  muscle damage.  4 weeks may a  reasonable  time frame . This is important in the current era  as presence of  significant  LV dysfunction  becomes an indication for revascularisation  .We  can’t be offered,  to err on this vital LV functional parameter.

Final message

WMD  is a combination of  electrical, mechanical , structural,  alteration in response to variety of myocardial insults.It is very hard to assess  individual components contributing to the net WMA. The easiest and surest way to  quantify  WMD  due to  muscle damage is to  do a deferred echocardiography , when all time related WMD ( Ischemic  stunning , perinfacion block )  disappear.

Coming soon

Diastolic wall motion defects .Is wall motion defects exclusive phenomenon of  ventricular systole ?

No , definitely not. Regional relaxation abnormalities are quiet common .it is poorly recognised .

Bradycardia is a common cardiac arhythmia. Sinus bradycardia  is  often considered an arrhythmia from a disciplined heart. It denotes high vagal tone .  A  heart rate  of  40 , some times even 35 is well tolerated . But bradycardia due to heart blocks are dangerous.

Sinus bradycardia can not get lower than 30/mt or so , as invariably either the  junction or the  ventricle , escapes with its own rhythm. Near syncope, dizziness , giddiness followed by  syncope  occur as the  heart rate  slows progressively below this level .It is often taught humans can not survive  when the heart  rate  goes below 10/mt .

Case report :

Here is middle-aged man who  presented  with a history of  recurrent syncope over a period of  3 days . He has no  history of CAD.

As he entered  the ER, this ECG was recorded.

At this pint of time  , when the ECG was recorded,  he was  conscious and talking ,  only to complain  of  little dizziness. After seeing this ECG , he was immediately put on a  temporary pacemaker.

Note : The ECG shows a single qrs complex per tracing of 10  sec duration .Ie HR of 6 /mt.One qrs complex for 50 large squares !  .Divide  300/50 and HR is 6 . Note also the p waves fire at 150/mt due to atropine effect .

The procedure  took 15 minutes to perform  , he was comfortable  and was administered atropine , and isoprenaline *, which increased his heart rate  from  6/mt to 10/mt .

Later he went on to receive a permanent pacemaker a week later.

* Temporary trans-cutaneous pacing using paddle stickers  is  an another  modality available in such situations where trans-venous pacing is  likely to be delayed  .

Message from this case

Cardiology’s  ultimate  moment of glory and truth  is experienced  when a  life  is saved with  a pacemaker.

Extreme bardycardias are  often  fatal , but here is a patient with  dangerously  low heart rate , still not resulting in asystole  or brady induced VT/VF . We had adequate  time to plan a strategy . Severe bradycardias  need not result in cardiac  arrest always.  Some hearts  have amazing capacity   and their  fighting spirit   amazes  us !  .It should be noted that , the above example may be  an exception than a rule .

Anemia is one  of the earliest human diseases  that was identified. Traditionally  heart disease and anemia have a  close relationship.(Is it a true relation ?)  .Most of  us  are made  to  believe so, by meager speculation !

In what way anemia is linked to heart failure?

The answer is explicit  in the definition of cardiac failure . There are two components to cardiac failure

  1. It is  the  inability or reduced capacity to pump  that affect the tissue oxygenation.
  2. Or able to do so only at the cost of elevated  filling pressure.

Do they  happen in severe Anemia ?

Even though anemia partially and indirectly   fulfills    first  half of the definition , it fails to result in elevated filling pressure of the heart. Hence anemia per se ,  may never* result in cardiac failure by definition.  

*Is there an exception to this ?

Severe anemia( Hb <  5 grams ) is often  thought to result in cardiac   dilatation .At this point of time ,  some consider cardiac failure to be present.

When does anemia produce a hypoxic injury to myocardium ?

Hypoxic injury to myocardium due to extreme anemia is possible .In clinical practice it is rarely experienced.

What is the effect of anemia on ECG ?

Anemia is probably the commonest cause for the so-called non specific or( non ischemic) ST depression and T wave inversion. These changes are more pronounced in females. When sinus tachycardia also co exists (Usually it is )   ECG can perfectly mimic an acute coronary  emergency.One should watch out for this possibility.

Anemia and  echocardiography.

  • Anemia causes mild enlargement of all cardiac chambers.This is  first seen right-sided chambers.
  • The ejection fraction is  in the   higher ranges of normal ,  often hyper functioning  and super normal EF (75%) are recorded.(Anemic heart contracts vigorously  ! where is the question of failure ?)
  • Diastolic dysfunction is almost unheard in  anemia .As quick relaxation must be there to augment  the next contractile beat.
  • Anemia can cause high velocity turbulence across LV outflow( or even in the AV inflows.) This turbulence is seen as color variance in color doppler. But , since it is physiological , the flow velocities are not elevated much .

Anemia and coexisting CAD .

This is a distinct possibility , as both entities are quiet common in general population. In fact, anemia  will worsen the underlying CAD. Anemia is an important  cause of   secondary unstable angina.Here, one should realise it is almost impossible for anemia alone (without CAD )to produce unstable angina .Even stable angina is rare in isolated anemia .If it occurs, anemia unmasks silent CAD.

Anemia and associated cardiac failure.

This has probably confused us a lot. They are often associated but the former plays an amplifier role  than an etiological role.

Cardiac failure triggered anemia

It would be a surprise , when the discussion here is “Anemia causing cardiac failure”  the reverse situation   could be much  more common. ie  “Anemia occurring due to prolonged congestive failure” .  The bulk of the knowledge we have is related to this question . It is  similar to  anemia of chronic disease (Hypochromic , microcytic )  as in rheumatoid arthritis,  CKD etc. This fact is  being  exploited by the industry  for quiet  some time now  (Oh , a mouth watering role  for erythropoitin in CHF ! ) .It (Amgen EPO )  miserably failed according to  available inputs.

Anemia begets cardiac failure and cardiac failure begets anemia

There could be some truth in this conceptualization  even though anemia can not make a myocardial contraction directly.

Final message

Anemia  with cardiac failure is not a  true cardiac  failure . In fact , it is not cardiac failure at all in many  situations. Only in terminal state , the heart begins to dilate .Till that time the heart is actually in the hyper functioning mode.

So , to call anemia as cause of cardiac failure is a misnomer . Ironically, in patents with  isolated severe anemia the heart   more often succeeds in its  assigned job of  supporting  the  heamic system in it’s  hour of crisis.

Reference

1. Anemia in heart failure :A review

Stable angina is graded by Canadian cardiovascular society classification ( CCSC ) by 4 grades. Angina at rest  usually  denotes unstable angina. But,  patients with stable angina  may also experience rest angina according to CCSC ,  still this is   not considered as  unstable angina by many . Post prandial angina is one such  example.

Few consider post prandial angina as unstable angina . This sort of reasoning can not be faulted .

In  the logical sense ,  we are dealing with varied  categories of unstable angina.  The importance of diagnosing unstable angina is to intervene early ,  so that we can avoid  major adverse outcome .

The problem in CAD is , often , the plaques and angina do not  obey the conventional  rules  !

.The following permutations and combinations could be  observed in any coronary care unit .

  1. Unstable angina –  stable plaques  – stable ECG – stable patient
  2. Unstable angina – unstable plaques  –  unstable patient
  3. Unstable Angina  – unstable plaque  –  stable patient
  4. Stable Angina –  unstable plaque  –  unstable patient
  5. Stable angina  –  stable plaque  –    stable patient
  6. Stable angina –  unstable  plaque  – stable patient

Among the above 6 categories  2nd  is   probably  the most dangerous group and category 5 is most benign.

Post prandial angina is a serious  form of angina.It implies  , even   diversion of  little blood to GI system immediately after a meal can provoke an episode of  ischemia  .This infers a  very tight  lesion somewhere in the coronary tree,  very often it could be the  left main or proximal LAD.

Of course ,  there is  another mechanism for post prandial angina, namely GI neurotransmitters  like gut peptides acting as a coronary vasoconstrictor.

Snippets on  post prandial angina  .

It is also recognised , post prandial angina occurs more often during dinner, followed by lunch and breakfast. Carbohydrate foods are  more likely to precipitate it .

Does PPA cause ST depression ?

Logically it should .In reality It happens in few .

How to manage it ?

It is very important to recognise , even though this article  argues  for including  PPA  as UA, there is no acute thrombotic process during  an   episode of  post prandial angina . In fact , it is  more of a secondary UA due to altered  blood flow pattern.

So , do not admit these patients  in CCU and administer  heparin or 2a 3b blockers.  (Unless of course ,they have other forms of rest angina )

Link to reference

1 PP angina angiographic correlation

2.Effect of carbohydrate diet on postprandail angina

3.Hemodynamics of eating !

Final message

Post prandial angina has all the characters  of a severe form of angina  .There  is every reason to label it as UA .It is suggested , ACC,ESC, AHA  should consider including  post prandial  angina as  UA or at least  UA equivalent .This would help intervene this entity early.

When the concept of acute  coronary syndrome was at infancy, when there was no echocardiography , when there was no coronary angiogram   when there was no coronary care units either , this man was able to identify a group of patients who are high risk to develop acute MI

These pateints are now refered to as  famous entity  unstable angina !

Serving in  Goverment institution of KEM hospital Bomay , he was instrumental in isolating reserpine which was a powerful anti hypertensive drug those days.

Realise , He is not a official cardiologist as the much hyped DM degree was not there  those days.His life is an strong evidence that , meticulous observation and documentation of simple facts from the bedside  is the many times greater than research done in  sophisticated laborataries !

Life history of Dr.Vakil (1911 -1974)

http://medind.nic.in/jac/t02/i1/jact02i1p100.pdf

His famous article on Intermediate coronary syndrome

http://circ.ahajournals.org/cgi/reprint/24/3/557.pdf

What will be the pulse rate in a patient who has ventricular bigeminy in ECG with a heart rate of 90 ( 45 sinus beats 45 VPDS/minute ) ?

A.Exactly Same as HR , ie 90/mt

 B.Exactly half of HR , ie  45/mt

C.Can be anything between 45 to 90/mt

D.Any of the above can be true

 The  answer is D . 

I have  noted  ,this simple question in cardiology resident examinations cause great anxiety among students .

Why is it difficult to arrive at an easy answer to this question ?

Traditionally , ventricular ectopic beat were also called extrasystole , implying every ectopic beat shall produce a peripheral pulse .Since ,  we learnt this is not true , we started refering them as VPDs.(Simple ventricular depolarisation which may or may not have a mechanical activity ) So , in a patient whose alternate beat is a VPD  , things become little complicated.

What determines a VPD to acquire  mechanical  energy  or simply  remain as an  electrical event ?

  •  Timing of the VPD* .
  • LV residual volume(LVEDV ) at the onset of  VPD
  • Force of contractility of LV( Of course ,  it is directly related to LVEDV)
  • Temporal relation to  aortic valve opening**

If  the VPD is too early or too late it can not have a mechanical activity . It should be optimally timed midway between two sinus beat to have a good mechnically active VPD. Some refer this as an interpolated VPD .Here, the VPD  becomes a  true extra systole for that individual. So , in patient with ventricualr bigeminy in ECG the pulse rate is usually half , can be same as HR when the coupling interval is optimal or it can be totally irregular as someof the  VPDS gain a mechanical activity and some do not (as often occurs multifocal VPDs. )

* Among the above  four factors timing of the VPDS is the most crucial as it can influence all the other three factors.

** Whatever be the timing or force of contraction aortic valve should be opened to generate a pulse wave. If for some reason this does not happen  there can be intermittent mechanial activity what  we refer to as pulse deficit .

Read a related phenomenon:  Ventricular  paired pacing

              Recently in a  southern Indian state  a big  cleansing  action against   fake  , spurious and expired  drugs  were carried out .There was  much hue and cry over the issue .  It was found , millions   of such drugs where in circulation and  The Govt has initiated a blanket ban on  all these drugs .Intriguingly it  was the mainstream  pharma  industry that was  indirectly driving  the  whip against these  fakes.

Unless the medical professionals know what is really fake  our   patients  can never  be protected against the fake !  At the outset ,  let us recall the definition of  the word fake

Courtesy  http://www.thefreedictionary.com/fake

Fake means

  •   One that is not authentic or genuine; a sham
  •   Having a false or misleading appearance; fraudulent
  •   To simulate,  feign.
  •  To cause  something inferior or not genuine .
  •  To appear more valuable, desirable, or real by  fraud or pretence

Applying the above definition  , all  the following  will fulfill the criteria  for a  “Fake drug ”

  •  A fake drug can be defined  as a drug which is projected  to have a one action   but does not have that action.
  • A drug which is claimed to have an  action  which is  futile   ( Eg : Antioxidant action of coenzyme q10)
  • A drug which is supported by fake studies.
  • A drug which is  just  better than a placebo but not better than a drug of it’s own class
  • A drug prescribed with a sole intention of  reciprocal benefit with pharma industry
  • A drug which is never tested in the local population.
  • A approved drug  for an  unapporved indication . It becomes  fake for  that  group of patients.(Eg Statins for Aortic stenosis !)
  • A drug or device  which has a class 2b indication as per ACC/AHA has a very high chance of  getting labelled as fakes.

*In simple terms , it is estimated the bottom half or  ( at least  one third)  of any long prescription  in an average Indian prescription  is occupied by  the fake drugs .

(A unnecessary Vitamin, a cardiotoner, a catalytic enzyme, a mitochondrial stimulator, a metabolic juice, a mood enhancer or depressor etc etc . . . )

Final message

In this era of  glorious medical industry   mankind  is  on a futile journey searching for the  elusive kindness and  truth from the industry . The easiest job  in today’s world  is  , fooling around the public. The victims are not only  the patients  but also the medical professionals . The later often do a role of perpetuators as well .

As we  realise , there are  thousands of   fakes  masquerading as true drugs , let  us pray the God  to  give us the strength to identify them  ,   the courage  to resist  the   temptation  . (To  prescribe)

Coming soon  “The greatness of fake drugs “

Heart is one of the unique organs , that a physician can touch and feel before diagnosing a disease .The fact that ,  the heart is located superficially within the thoracic cavity makes tactile examination possible . The current generation cardiologists should realise cardiac palpation was a huge scientific specialty by itself centuries ago . Apical impulse demonstration  in class rooms  would go on for hours together in the days of Leannc and Dressler .

It is an irony , when we are able to see and feel many areas of the heart in the direct vision ( RV parasternal impulse, pulmonary arterial pulsation, contractility of LV ) we got addicted to imaging modalities now.

This article tries to extrapolate the  morphology of  apical impulse  with that of ehocardiographic LV function . A normal apical impulse is a very subtle impulse often absent in a third of population.Some times it is called tapping impulse .The  two common abnormalities  of apical  impulse are hyperdynamic and heaving .

Read the link for normal apical impulse

A hyperdynamic apical impulse

The  hyperdynamic apical impulse is diffuse (Occupying at least two rib spaces >  3Sqcms) and very active  with brisk motions visible to naked eye .This implies the leftventricle is dilated significantly and the wall is not much hypertrophied. This is eccentric LV enlargement . It also tells us the LV function is well-preserved as the term hyperdynamic infers very active LV .It is obvious , a dysfunctional LV can not be hyperactive. A hyperdynamic LV apex in a patients with AR or MR indicates they will do well after surgery for the simple reason their LV function is preserved. In the same logic a patient with hyperdynamic apex often complaints of palpitation as the apex hits the chestwall . Which is a good sign with reference to LV function .

Note :A patient with heaving apex rarely complaints of palpitation.

Hyperdynamism occur in systole or diastole ?

Logic would say apical impulse would be palpable only in  systole .But in a hyperdynamic LV diastolic phase is also palpable (A palpable S3 is common associate of hyperdynamic apex)

Heaving apical impulse

The term heaving apex by definition indicate there is a brief localized sustained LV apex lasting at least 50% of systole.

  •  Aortic stenosis with normal LV function
  • Any dysfunctional and dilated LV which increases the after load

The sustained lift may disappear with very severe LV dysfunction , apical impulse is barely perceptible in failing hearts . A sustained LV apex suggest reduced dp/dt of  LV contractility .

Relationship between apical impulse character and LVH ?

Hyperdynamic LV apex is rare to be associated with LVH .Except probably in HOCM where the LV systole is interrupted very early in the ejection phase.

Heaving apex can be a marker of LVH .But, the onset of LV dysfunction can confound this finding.

Can a hyperdynamic and heaving characters occur together in apical impulse?

We have been taught cardiology with a black and white learning concept but unfortunately science more often exists in shades of grey An apical impulse can indeed have characters of both . A diffuse apical impulse with a heaving nature is common in regurgitating lesions with the onset of LV dysfunction Such situation can occur in LV apical aneurysm

Final message

Looking for apical impulse in current cardiology practice  may be considered as  the most foolish job  a physician can indulge !

Ask the secretary to record the history ,  take an ECG, do an Echo  , send both deserving (and of course  many undeserving patients too !)  to cath lab at the earliest  . . . This is the  modern-day cardiology mantra !

This article , does not vouch  for the accuracy of   what  some may consider as  a  “medieval clinical sign” . But , it  confers the patient  a better rapport  strightaway   as  the physician  puts  his or her hand on the patients heart  . Some  call this  as a healing touch ! It work  wonders in many !

Let ventricle is an elliptical or ovoid chamber .The pattern of LV enlargement can vary considerably in different pathologies. We know a dilated , globular heart is the typical feature of terminal congestive heart failure. But in the early stages of cadiac enlargement there are some distinct differences in the contour. (Aortic stenotic lesions retain the ellipitical shape till late in the course )

LV enlargement due to mitral regurgitation is somewhat different from aortic regurgitation. A globular configuration occurs more often in severe MR than AR. This is due to the fact, the long axis and short axis ratio of LV  is maintained till late in the course  of aortic valve disease . Cardiac long axis enlargement is more pronounced in aortic valve disease than in MR. The AR jet reaches LV  at a higher pressure gradient (Diastolic pressure of aorta) than mitral inflow velocity . (Often mimic physiological flow with an S3)

For a given degree of regurgitant volume AR will cause more cardiac enlargement than MR. In the same note , one should realise  the LA becomes huge in MR which receives high pressure regurgitant jet . Further ,mitral valve disease is more likely to result in early PAH and that results in right sided chamber enlargement giving the cardiac contour a more globular configuration

Is the cardiac contour different in rheumatic and degenerative(Myxamatous) mitral regurgitation ?

Yes , rheumatic MR results in less enlargement of the base of the heart as the fibrotic process restricts and restrains LV and prevents uncontrolled LV dilatation . In fact , giant LV are often  reported in mitral regurgitation due to mitral valve prolapse than rheumatic MR.

Why the configuration of LV important in the management of cadiac failure ?

The globular configuration of LV implies , the papillary muscles are attached in a disadvantaged angle and keep the free wall stress high. Specialized procedures are required to restore the LV shape especially in secondary to mitral annular dilatation. Isolated aortic valve disease rarely require LV remodeling surgeries , even if AVR is done late stages.

What is the maximum dimension of LV reported in cardiac failure ?

The upper limit of normal for LV diastolic dimension is 5.6cms. In MR it often reaches 6-7 cms . The maximum of 10cm has been reported with AR. An LV beyond this level looses it’s elasticity and likely to be incompatible with survival unless LV reduction surgeries like Batista are performed.

Is secondary valvular cardiomyopathy an accepted entity ?

 The  term cardiomyopathy when originally defined decades ago ,  required exclusion of all known cases of cardiac enlargement. But now we have a more liberal working concept , if the LV enlarges disproportionate to the loading conditions of the valvular lesions  , secondary cardiomyopathy is said to be present. If cadiomyopathy sets in,  the cardiac shape invariably takes in a globular configuration irrespective of the valvular lesions. So, the simple parameter of shape of LV in X ray chest can give us a clue regarding the outcome in valvular heart disease.

Further reading

Also read sphericity index by echocardiography A spherical LV can be easily quantified by echocardiography

Ego can be a  great  motivator and destroyer as well. It has the  potential not only  to damage the self  but also the people in the near domain .This has been proven in all walks of life. Medical practice is no different . In fact ,it can have the more devastating effect as the victims are often the poor patients.
The medical ego can be individualistic,  departmental, institutional, etc.

Often in the dormant  form , can raise to gargantuan  levels when stimulated or challenged.  In its mildest form it occurs every day in the office practice. A physician  often thinks he is always right and fails to get a second opinion even in difficult  cases . Some where  along  the medical  curriculum  ,  doctors have to be taught that ,  what we know is only a fraction of what we are supposed to know ,  and  the importance of self auditing. This never happens in most medical schools.

Individual Physician ego

This exist in several forms . Ego with fellow colleagues is the most common type . Failure to accept a error in diagnosis is the most  frequent form injured physician ego. There are many instances doctors carry on with the wrong diagnosis tag (On their patients)  even after some authentic documentation is available against it. This especially happens when the correct diagnosis is made by  a junior colleague . Eg : “I still think it is a pheochromocytoma let us do the scans again”  Same tests  are repeated . In the intervening period  involves  treatment delay  and  financial costs for the patient. It is obvious , such an  ego in emergency rooms can be  disastrous .

Few doctors have a habit of asking for fresh set of investigations even if the patient has recent records of his illness . This is because many  feel interpreting   investigations ordered by other doctors is an inferior job .(Of course ,  financial incentives for repeating the  tests  could also be a motivation  )
Ego with paramedics and fellows

This is also quiet common. Doctors expect  their orders to be carried out at any cost.  They take it very seriously , if a nurse or a junior doctor behaves independently . This is understandable as it raises the fundamental question  who the  boss is ? !  But ,  the problem here is, even a smart move in the interest of patient is  not always relished  the physicians . (Because it is  perceived as an  insult to the consultant ) . You can’t act smarter than me !

We know the major responsibility  of caring a patient lies with staff nurses and  junior doctors .(It is a universal medical rule the consultant will be remote from the patient care unless of course it is needed).If the specialist exerts an  academic ego on them , there is every chance for the patient to suffer as  even vital interventions could be delayed.

(Eg :   Sir , I withheld  the beta blocker in  this  patient  as he  had a  bradycardia ! I thought it is  better to remove the urinary catheter as the patient was struggling with it  etc and etc )

I have observed  , even  some of the shrewd  directives  from the residents and junior doctors have elicited  big hue and cry from some of the renowned physicians of our region.While many   recognise the good work done by the junior colleagues  , still  their  ego does not allow to  appreciate and complement them . This is not a good sign for the  medical professional .

Specialty ego and departmental ego

This is new phenomenon . Traditional ego was between surgeons and physicians. Now , with medicine growing leaps and bound there is probably a medical and surgical specialty for every human organ . This helps the physicians ,  to shrug of the collective responsibility . It  has become a  dangerous trend in many institutions.

God created  human body as a single entity  . Specialists  share their  organs  , convert a  human body  into a commodity (Has to  make a living out of it )  As the medical science is branching out at a phenomenal rate  it becomes   a difficult task for them  to come to the rescue of the patient when they need a collective intervention  . Further , conflicts of interest and ego clashes take a front stage.

Even in an  academically and ethically superior medical center it is a  herculean task to arrange   for . . .example
An ENT surgeon and neuro surgeon to operate a nasal tumor together.

A hybrid procedure of PTCA and CABG (Could be very useful in many situations)  can not be practiced  that easily .

The issue here  is not simply logistic .It goes beyond that . . .

(Why should I  sweat for some one else’s fame ?)

Institutional Ego

It has a peculiar issue .The  admitting  physician is  vested with supreme powers – he becomes  the sole caretaker  for the given  patient .Though it fixes responsibility , it has a potential  risk , as this  patient automatically  becomes untouchable for other consultants . There are centers in which even intra departmental  consultations are lacking .I know at least a handful of cardiologists who  do not talk with each other  even at times of crises in cath lab. This is more prevalent in fully commercial institutions .

In this regard  group practice with fixed financial remuneration may be a  lesser breeding ground for ego clashes.

Another form  egoism may be financial  discrimination , which  is seen in some of the big corporate hospitals . There are instances some doctors and institutions  shy away poor or relatively poor  patients .There are institutions which feel allowing entry to   less sophisticated public  inside  their premises is detrimental to their reputation and ambiance.  

Ego issues with patients.

Generally doctors show great respect for their patients. Information sharing is the major issue. What to tell and what not to,  can  some times reach really difficult proposition. Does the patient have a right to criticize the treatment ? Whether you like it or not some patients do it .

Few suffer from a  worst  form of physician ego , that is directed  against their own  patient. Doctors are  rarely  comfortable when patient ask probing questions.This is acceptable in few instances. The root of the problem is doctors rarely accept their ignorance .

There are many instances  where a consultant   refuses  to see  his own patient  once he  gets  a second opinion from another doctor . It need to be realised  this is actually the fundamental right of the patient he is executing .No need to get offended .

Why this ego ?

It is the  part of normal human psyche. There is no reason to believe doctors  are different . But the following could be unique factors .

  • A subconscious feel of  ” demi god” status  conferred  by the patients .
  • Failure to have an open mind approach .
  • This translates into fixed ideas about a patient and his illness.
  • This is especially common in countries  where , single doctor or a family of doctors run nursing homes .

The other substrates  for ego growth among physicians are

  • Academic  excellence
  • Practical skills
  • Popularity in the society
  • Financial superiority

Negative ego : A feel of inferiority also creeps in for many physicians  who  find to hard to acquire the above .And this  can  have  a serious effect on  the patients .It is  shocking to note many of  the academically incompetent  have a strong  dose of ego .This is most dangerous for the society.   A deadly combination of  incompetence  and arrogance

What is to be done ?

  • Containing  the  physician egoism  could be more important for doctors  than attending to  sophisticated CMEs and conferences and workshops .
  • Counseling is required for many .
  • Behavioral science with the specific tips for  self-regulation is to be included in the basic undergraduate medical curriculum
  • Courage to tell the truth to their patients to be imbibed.

Final message

Hippocrates said some 2000 years ago the fundamental quality of a doctor  is  to accept his limitations and ignorance .Every action of his or her, should aim  only at removing the suffering of the patient .

Now we are in the era where , market force  have literally hijacked the medical filed  . A  medical degree  can be bought in a weekend university shopping (At least in India it is possible ! )  .

In this scenario  if our students grow with one more wise  ie “hyped up ego”  one can imagine  where our profession is heading for !

We need to initiate a debate on the issue . And there need to be a movement to cleanse  the contaminated profession. It should be  in the league of nuclear  treaty ,  war on terror or the global environmental protection.