Feeds:
Posts
Comments

Archive for 2010

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 !

Read Full Post »

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

Read Full Post »

 Excercise physiology has been studied most extensively in the last century.The hemodynamic impact of excercise in various disorders of heart has been well established.
Dyspnea on exertion is the commonest symptom in clinical cardiology practice. It is well-known pulmonary stretch receptors located in pulmonary vasculature is one of the  major mechanism of dyspnea.

Excercise increases the cardiac output manyfold.Transporting  up to 10-12 litres of blood every minute across the lungs with a narrow pressure  head (about 10 mmhg ) is not an easy job . It needs lot of lung discipline .

It is surprising to note, there is little data on excercise induced pulmonary hypertension in the evaluation of patients with unexplained dyspnea.

We know, excercise increases the systemic blood pressure ,we  presume it should not raise the PAP (however severe the exertion is 1 )as pulmonary circulation  is a  high compliant low pressure system. 

Is our presumption correct ?

Exercise induced PAH can occur in both   health and disease 

In patients with preexisting disease

  • Stress induced LV dysfunction and resultant raise in LVEDP-PCWP-PAP .This is the most common mechanism in valvular and myocardial  disease.

Apparently healthy population

  • Excercise  induced PAH as a  marker for silent CAD .
  • Transient Hyperkinetic PAH* (Note :Here PCWP is usually normal )

This is similar  to hypertensive response to EST in systemic circulation.Existence  of this entity , is controversial, But this may reflect  reduced pulmonary vascular reserve  or reduced pulmonary nitric oxide secretion.

*The main difference here is the PAH is more often an  isolated systolic PAH. While LV dysfunction induced PAH is  a combined diastolic and systolic PAH .
How to assess excercise induced  PAH ?
It is not an easy job. Invasive catheter derived pressure measurements have been done ,but it is not practical .

The simplest way is to look for the TR /PR jet in echo in both pre and post excercise phase.

Final message

Excercise induced PAH is an inadequately studied entity in cardiology , in spite  it’s great significance .
This phenomenon is observed  in both diseased and normal heart.

The quantum of excercise induced PAH  is  widely variable depending upon the cardiac  status especially  LV function and the  functional integrity of pulmonary microvasculature .

Read Full Post »

Ventricular septal defect(VSD) is one the commonest congenital heart disease . Right from the days of Gasul , Abbot, and Keith we have analysed the natural history for nearly a century . VSD is an intriguing congenital heart disease where a child can develop a florid cardiac failure within weeks of birth in one end to a totally asymptomatic adult with a benign cardiac acoustics defect (Namely a systolic murmur in the left parasternal area.) But for this murmur , the patient would be labeled absolutely healthy.

 In between these two spectra is the huge population of VSD that gets closed spontaneously. A rough estimate says 60 % of all small VSDs get closed by age 10 .

So ,what we are supposed to do once a child is diagnosed of VSD ?

Should we close or should we wait ?

The indication for closing a VSD is discussed elsewhere ( Read this link )

 What are the factors that determine VSD closure ?

  • The size
  • The site
  • Age of the child
  • The Rim morphology
  • Associated lesions*
  • Hemodynamic stress
  • Inherent tissue factors
  • Infection **

* Associated defects like PDA, RVOT obstruction are strong deerrants against spontaneous closure

General rules of VSD closure

 Size

VSDs <5mm have great chance of closing Large VSD > 1cm is rarely get closed .

Supracristal VSDs located sub arterially are immune to spontaneous closure however small the size is .

Location & Site

 VSDs that are located exclusively within the membranous septum rarely close . VSDs which are located in the perimembranous area (With at least 50% circumference is fenced by muscular or trabecular septum has the greatest potential to close by natural forces.)

Isolated muscular VSD if large can not get closed . Inlet VSD has anatomical difficulty to get closed.

Rim Morphology

 Small muscular VSDs have a potential to close , but it is believed differential cellular lining of VSD rims (Eg : A combination of muscle, membrane , is more likely to close .)

 Process of tissue growth As the child grows the it is expected the heart will outgrow the lesion . This is thought to be the commonest mode of VSD closure. As the IVS mass increases as he child grows it brings he rims together . But logic would suggest unless some degree of neocardiac proliferation occur a VSD may never get closed completely .

Some times even large VSDs try to close with the help of the neighboring structures like septal tricuspid valve leaflet . Indeed this can be the dominate mode of closure in many. This can induce a tricuspid regurgitation .

**Role of infection

Paradoxically an episode of infective endocaditis in the edges of VSD accelerate the process of approximation of tissue plane and healing .

 Relation with Pulmonary arterial hypertension (PAH)

 Once PAH sets in the VSD never gets closed spontaneously , This may be due to all VSDs that result in PAH has to be significantly large

 Can a VSD get larger progressively?

In physics and hydraulics a hole under hemodynamic stress is destined to progress In human biology this is thought to be rare .Post MI VSRs can behave in an unpredictable manner as he edges of the defect a often softened and prone for tissue plane dissection and extension .

Why some VSDs never close ?

It is clear , size and location matters the most , but there are other issues some of them may be unique tissue properties .

Why is it important to know the biology of VSD closure ?

In this era of interventional cardiology we are using mechanical devices to close VSDs and ASDs .It is fraught with many technical issues. If there is a biological glue or membrane that can be delivered by catheter to close small VSDs or ASDs .

 So for no therapeutic approach to hasten the natural closure of these defects has been practiced .Further research is required to explore the cellular adhesiveness and help accelerate closure of these defects.

Read Full Post »

Chronic total occlusion is the cardiologist’s  daymare .Here is an article that adds on to 1ooth technique to cross the chronic total occlusion within the coronary artery !

If only we succeed in  this  Arabin magic , in the cath lab we can open the doors of  all CTOs .

This technique is based on the principle  to push the hard plaque  into the adjacent side branch like a sliding door,   if the pateint has one !

The only isssue  with this  technique  could be the    “cave door”  may close again immediately  as it did for Alibaba    !

Reference

 http://www.ncbi.nlm.nih.gov/pubmed/20088015

http://www3.interscience.wiley.com/journal/122619470/abstract

Read Full Post »

Wide qrs tachycardia often  evoke a   OCD like reaction  among  many  cardiologists (Obsessive compulsive disorder).  Whenever we are given a strip of wide qrs tachycardia  we are compelled to initiate a  conscious or  subconscious debate , whether it is VT  or SVT . Tens of thousands of articles, seminars, CMEs , have been conducted for over 30 years  for  decoding  wide qrs tachycardias  . The fact that the confusion  is still widely prevalent indicate only two things

  1. Either , it is not possible to arrive at a simple fool proof  bed side modality  to confirm either VT or SVT
  2. Or it is a too trivial  electrophysiological   issue  that   need  not be worried about  as we have broad spectrum antiarrhythmics (Like antibiotics ! , where we  rarely  bother about identity of the culprit  bacteria  )

The power of statistics and commonsense have never been applied  in the management this vital cardiac entity  .While a  75% sensitive  exercise  stress test (EST) has a huge following in clinical cardiology , a   99 % sensitive   clinical criteria*  for diagnosing VT is  not respected .

*All wide QRS  tachycardia  in patients with   with history of   CAD/STEMI would be VT

If only we had applied our mind to this article published in 1988 we will never ever have the need to split our hairs for decades.(That too without success !)

In  pursuit of  knowledge , are we often  chasing  an imaginary  issue ?

The cardinal  principle of medicine says

“Diagnosis should precede treatment  whenever possible

But there need to be a correction  in the above statement .  Time , effort , cost involved in arriving at a  diagnosis  should be meaningful .( Needless to say  . . . it should  a correct diagnosis  too ) And if the power of statistics far exceeds the  frivolous scientific data  , street sense can be applied  liberally even though current generation may call it un scientific .

The issue here is  not being  scientific or unscientific , but whether you are right or wrong  . The article  which is quoted here  has a great insight  about the philosophy of VT diagnosis.

The message form this article goes something like this . . .

In the diagnosis of  wide qrs tachycardia , If we apply  the so called scientific principles   the chances  for missing   a real VT is extraordinarily high , while  if you blindly apply common sense and logic you are going to be 90% right .

What a powerful  statement this !  even though it appears  absurd ,  it is absolutely true !

A young physician  should realize the importance of this . Scientific  decoding of arrhythmia  may be an academic  pursuit but in a given patient at bedside  diagnosing by experience and common  logic are  far more productive and accurate. Miss diagnosis of VT was not common prior to 1980s .  It has become a recent phenomenon .

Probably too much of electrophysiology haS  made a simple diagnostic pathway a complex one. When we relied only on commonsense the errors were less . I  have  often observed  fellows  making mistakes quite frequently  while  nurses  were too confident  to call a wide qrs tachycardia   as VT .

Final message

Medical decision making is an art , in fact it is  a “fine art ”   We keep saying this for centuries , still medicine as a  science  easily overtakes medicine as an art. Here comes the problem . Some times (or is it many times ! ) too much of inquisitiveness in the   name of  science  make practice of medicine  complicated and the victims are often the patients !

Let us simplify medicine  . . . let us accept an occasional  bad outcome  . . . for not being 100 % scientific  ! After all  , a million mistakes happen every day in the  pure  scientific  pathway .

Reference

http://www.amjmed.com/article/0002-9343(88)90008-3/abstract

Also read Knowledge disease

Read Full Post »

Like in neurological disease, one can locate the site of block in bundle branch blocks. Though it has never been thought ,  to be clinically important to localise a BBB . (Unlike coronary lesions)

Generally ,  RBBB can be proximal  or  distal peripheral type.The commonest site could be the distal  type.

It should be realised , for over 100 years in  electrocardiology , we have been using some inaccurate terminologies just because it is easy to understand or being traditional .It is difficult  to assimilate a fact , even today that   “An electrical delay in conduction and block are one and the same ”

In fact,  bulk  of  the RBBB is nothing but delayed conduction over this bundle. So whenever we say RBBB  , we imply an incomplete block  ie conduction still occurring   over the  so called blocked bundle.(This dogma applies for LBBB and AV blocks also to a lesser  extent)

Examples of delayed  RV /RVOT conduction

  • Any disease where  RVOT dilatation  occur can cause a RBBB
  • Atrial septal defect
  • Many cases of RVH
  • Pulmonary arterial hypertension

What is the benign rSr’ pattern in V1 ?

This is nothing but a relatively late depolarisation of  RV outflow or conus that produce a terminal RV activity .

Many of the ostium secundum ASD may show just this rSr’ pattern   confirming there is no organic damage to RBB in ASD .

Calling rSr’ pattern as incomplete RBBB is not advisable (As many ECG books may suggest ) .This is because , even full blown RBBB pattern may actually be an incomplete one .Further , the degree of terminal r’ in V1 or s in lead 1  does  not always   determine the completeness of RBBB.

Is there a totally blocked right bundle branch block ?

Yes , it is not common .

  • It can occur in extensive anterior MI .
  • Some cases of Ebstein anomaly.

It can be an working rule , complete RBBBs  locate the lesion proximally and incomplete  ones distally .

What is the other evidence for RBBB in ASD  is  only a simple   delay  in conduction ?

After ASD closure  in many of the patients the RBBB pattern may disappear.This indicate RVOT regression .

Can you clinically differentiate the proximal from  distal RBBB ?

Ironically ,what is difficult in ECG may some times be possible clinically.The classical description of wide splitting S2 occur often in peripheral RBBB.

It represents a delay in the closure of pulmonary valve due to delayed electrical activation or increased hangout interval as in ASD .Logically S1 should also be split in RBBB. But this is not often discussed.

This is because , the split in S1 is lesser in magnitude and is not influenced by the hangout interval .(Hang out interval is the time taken for the blood ejected from RV to fill the pulmonary circulation. Due to the low impedence of pulmonary circulation the the blood that is ejected into the MPA continue  to run off for about 100milli seconds even after the RV/PA pressure crossover .)

S1(T 1) occurs  immediately with the onset  of RV contraction . Similarly M1 occur with LV contraction.It should be recalled it requires hardly 5mmhg of RV pressure to close the tricuspid valve and about 10mmhg for LV to close the mitral valve.

If for some reason if  there is a delay  in RV contraction , as in very proximal RBBB the T1 is delayed and hence S 1 split.

Note in most of the peripheral or distal RBBB the bulk of the RV free wall contraction is not interfered with . So , in distal RBBB it is highly unlikely the S1 will be delayed or split while S2 will be delayed.

What happens to S2 in proximal RBBB ?

Logic would dictate both S1 and S2 should be wide split.

Final message

There is a simple way (Some would call this an futile  academic  excercise  !)to  differntiate proximal from distal RBBB.If the first heart sound is split wide , it fixes the lesion proximally. This may  indicate a more adverse outcome than a simple peripheral delay in conduction.

Read Full Post »

Echocardiography is an imaging tool . Can it  be used as a non invasive  EP lab ?

Heart is an  electromechanical organ . For every mechanical activity there must be a electrical event preceding it . So, when we analyse the cardiac contraction and relaxation it indirectly provide us clues how the electrical activity spreads across the heart.

The concept of using echocardiography for diagnosing cardiac arrhythmias have never been popular for the simple reason we have a cheap and best modality : The ECG.  But, it  does not give us the temporal relationship with the cardiac contraction. When these two are combined it can be a really powerful tool to analyse many cardiac arrhythmia.

  • In fact ,  for every brady and tachyarrhythmia there has to be an unique pattern of IVS motion and mitral , tricuspid valve movement.
  • Almost all bradycadias can be diagnosed with echocardiogram by virtue of analysing the timing of  atrial vs  ventricular  contraction.
  • We know echocardiogaphy is the only modality available to diagnose fetal cadiac arrhythmias.* (How can  this modality becomes useless when the baby comes out of the mother’s womb  !)
  • Apart from this there is an  unique use for echocardiography to locate accessory pathway in WPW syndrome

The premature contraction of LV can be seen in few as  an early systolic dip in IVS movement -Type B WPW.

Image courtesy :  Helmut F. Kuecherer Circulation 1992;85:130-142

Abnormal jerky movement of LVPW indicate left accessory pathway -Type A WPW

Newer modes of echo like tissue doppler will improve the phase analysis of tissue motion and may provide us accurate information about preexcitation

Final message

The future looks bright . Time is not  far off . . .  where ,  we shall  use ultrasound as an adjunct  EP  study .

Reference

*Fetal Echo  =  to  Fetal electro cardiogram

WPW syndrome

http://circ.ahajournals.org/cgi/reprint/85/1/130.pdf

http://content.onlinejacc.org/cgi/content/full/33/3/782

http://www.heartjnl.com/cgi/content/full/82/6/731

Read Full Post »

When every one is thinking bare metal stents are dead ,here comes  an ace  from Medtronic !

A breakthrough technology that make stent navigation into complex lesion as smooth as “knife in butter”

“If only you feel it ”  says the Medtronic ad

The smooth flowing metal inside the coronary artery

Read Full Post »

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.

Read Full Post »

« Newer Posts - Older Posts »