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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.

It is well-known sexual arousal and activity is a powerful hemodynamic stress .In the healthy persons it is never an issue .In fact there is data to suggest sexually active men and women live longer.

But , in patients with cardiac risk factors or an established coronary event unrestricted  sex can be a risk factor for CAD.

There needs to be a distinction  between a coronary risk factor and a coronary  trigger .Trigger is an  immediate switch  for a coronary event in a  patient with  baseline risk profile .It is highly unlikely triggers alone can  cause an ACS .There need to be risky substrate.

Extra marital sex could be such a trigger in some .(Both male and female)

  • The sexual activity performed with guilt  has  more powerful risk.
  • First time offenders
  • New  partners
  • New environment

All of the above are  supposed to increase  the risk .

The mechanism  attributable is  a   sudden adrenergic  surge  which inappropriately high when compared to marital sex . In conservative societies , the effort taken to hide the illicit relationship   is much more stressful than the event itself. And hence these men and women carry on their new-found coronary risk for longer periods.

Reference

http://www.ncbi.nlm.nih.gov/pubmed/20382352

http://drwes.blogspot.com/2010/04/extramarital-affairs-and-heart.html

Constrictive pericarditis(CP)  has been a fascinating disease   for the cardiologists  for many decades .  (Of course , not  so fascinating for  our  patients!) The reason why clinicians were thrilled to diagnose this entity is due to the unique clinical and echocardiographic and hemodynamic features. Further , it is  one of the few  curable forms of cardiac failure.
It is also about the  philosophy  , pericardium an inert  membrane  which is supposed to protect the heart , becomes a  villain  . When this innocuous layer  is insulted by  chronic   infection (Tuberculosis most common) , radiation injury or post cardiac surgery  it takes a dangerous avatar and  start invading   the organ which  it  guards .
The pericardium becomes thickened , (often > 5mm -2cm) calcified , behaves like a “shell of tortoise‘ and begin to constrict the heart . Once the process of constriction sets in it becomes relentless . It only   requires   , a 10 -15mmhg of constrictive  pressure to make  the poor heart  struggle to relax .(The maximum intracardiac  diastolic pressure ,12mmhg(LV)   .For the right side of the heart it is very low (0-5mmhg) .
So it is obvious the right side of the heart RA, RV gets compressed first .This is why the classical features of constriction with edema , ascites elevated JVP occur.The associated hepatomegaly some times mimic a chronic liver disease.  Of course  relying only  on the  classical findings to diagnose CP would be a crime now .
There are many atypical varieties of CP
  • Localised constriction
  • LV>RV constriction
  • RV>LV constriction
  • Transient constriction
  • Effusive constrictive

* Rarely  constriction is confined to AV groove .  This article  is about this entity.

It is difficult to imagine how a pericardium constrict a rigid fibrous skeleton of the heart namely the AV groove.
But what happens is ,  there  are some gaps in the ring  . The  posterior mitral annulus which  has a deficient  rim  and forms  the most vulnerable  zone for pericardial constriction
Further , AV groove  is located  in a relatively  gravity dependant portion  of the heart  . It facilitates  stasis of inflammatory exudate  in this groove .This may be  the reason  why the  AV groove  shows high incidence of   calcification.
Clinical features of AV groove constriction
It mimics  a presentation of valvular heart disease.
A mid diastolic murmur across mitral valve may occur mimicking valvular MS.
Synonym : Mounsey’s pericarditis
This type of pericarditis should ideally  be called as Mounsey’s constrictive pericarditis   for his
elegant description of this entity 5o yearts ago  even before    Echocardiography was invented.
(These are the days , we struggle to diagnose Mitral stenosis without echo is a different story !)

The LV angiogram that stunned me  !

See how a heart is encased within the pericardial shell , still fighting hard

Thanks to circulation for it’s greatness  to offer such great video free

http://circ.ahajournals.org/content/vol118/issue16/images/data/1685/DC1/CI191060.DSmovie2.AVI

The one and only journal for cardiovascular surgery from the subcontinent. Great to  know   full text articles are available from year 2003  , free of cost .Every cardiologists from India must read this journal regularly to update  about what our surgical colleagues are doing  in our country.

Thanks to the  National Informatic centre  for hosting this journal in their server .

http://medind.nic.in/ibq/ibqai.shtml

Which you think is the most important journal in cardiology ?

  • JACC ?
  • Circulation ?
  • American journal of cardiology ?
  • American heart journal ?
  • Heart rhythm ?
  • European heart journal ?
  • The Heart  ?
  • Journal of invasive cardiology ?
  • NEJM ?
  • Lancet ?

None of the above  . . . is the right answer !

Probably,  the best journal  that is going to have the  greatest impact in cardiology practice in the future  could be  this  . . .

 Unfortunately  most  cardiologists are unaware of   this journal . The need for this journal , that  too from most respected Circulation family , will vouch for its importance in the current era  of  cardiology  that is driven more by the market forces than by the academics.

Click here  to reach  journal

Journal  Highlights

  • This  journal is 3 year old , and most of the medical colleges   do not subscribe to this.
  • None of the 100  cardiologists  who were questioned , were unaware of such a journal.
  • Even those who read this journal often term as boring  , academic and not practical !

 

The Circulation team which  started this journal  with  only one purpose  . . .that is ,  auditing the uncontrolled  proliferation of  pseudoscientific literature without proper quality assessment and dubious outcomes. Three cheers to the circualtion team for publishing this journal and let us propogate the importance of this publication.

Human heart is a vital bundle of muscle  weighing  about 300-400 grams. The blood  supply of this muscle  mass  is highly variable . Some areas are abundantly  vascularised(  eg -IVS.) Some areas have a balanced blood supply with  twin blood supply (Often the  LCX and RCA in the  crux of the heart ). Certain areas have a precarious blood supply . They are  some time called as water shed areas or  vulnerable   Bermuda triangle of the heart – the  overlapping zone of   LV apex,  free wall and  the anterior surface.

When the blood supply is so  heterogeneous , it is  not surprising  to find  the neural innervation of the heart to have a  unique pattern as well .The cardiac  autonomic nervous system   is  mediated by the  cardiac plexus  . It  has a  dominant adrenergic  innervation in the anterior   aspect of the heart   that is  rich in catecholamines , while the infero posterior  aspect  of heart has a high density of  vagal fibres .

So , it becomes easy to understand , why  ischemia of inferoposterior regions often trigger  a vagal response and an adrenergic response  in  anterior ischemia  .Of course , overlap can occur especially in multivessel CAD with collateral dependent circulation.

The inferoposterior MI ,  generally  have  a better outcome as it imitates  naturally beta blocked heart . (Less heart  rate , less MVO2  more salvage ) Still  hypotension  can be  a worrisome complication in inferoposterior MI .

The following  factors contribute to hypotension in infero posterior STEMI

  • Heightened  vagal tone  due to Bezold  jarish reflex
  • Involvement of RV is known to occur up to 40% of all  inferoposterior MI. Loss of RV pumping action is the classical explanation of hypotension
  • Recently recognised  fact  : Infero posterior MI often have subclinical and subelectrical atrial involvement. This is a powerful trigger for  the atrial  naturetic peptide secretion. ANP  a water losing hormone explains much of hypotension in this situation. .It should also be noted atrial necrosis is not necessary for ANP release. Simple atrial stretch  or even RV stretch can be a stimulus for ANP .
  • Variable degree of LV involvement is  common in infero posterior  MI .This can have detrimental effect on LV pump function . It  can  be a independent  factor for  the hypotension.
  • Excess sedation with morphine may aggravate or precipitate hypotension.(Vagal  action of morphine )
  • Finally , and most importantly a common cause  is  hypovolemic  hypotension (Applicable for any STEMI – Severe sweating  and sometimes vomiting can  loose  up to  10 liters of body water )

How to manage ?

  • Correct hypovolemia
  • Water challenge in RVMI is a popular (Often abused) concept . Rule of thumb is , if 1000ml  of  rapid infusion  fails to correct the hypo it is  highly unlikely  it will  do it at 5 liters  ! Cases of fluid overload and dilutional hyponatremia have been reported.
  • Atropine (This is one of the rare situations  where vagal blockade increases the BP ) .Dopamine may be useful but logically we need to  reduce the high vagal tone  and bring autonomic parity  . (Increasing adrenergic tone to that of high vagal levels  for autonomic parity  is  a lesser logic !)
  • Temporary pacing may be needed if  blood pressure fail to raise because of  troublesome bradycardia.
  • And  of course  , rapid PCI and revascularisation  when Indicated

Final message

Hypotension in inferoposterior MI is often  considered innocuous. But , it can be dangerous in some , especially in the  elderly and comorbid individuals . It has  varied mechanisms  , that are distinctly different from anterior STEMI.  Recognising the underlying mechanism  hypotension  will aid us to correct it  rapidly.

It is  over a century old dictum , that  edema legs and elevated JVP is the hallmark of cardiac failure.In fact , these two  constitute  major criteria of Framingham  cardiac failure score.When these criterias were formulated the concept of diastolic heart failure was not in vogue. So we  do not know whether the same would apply for diastolic heart failure also.

In all probability these  conventional criteria may not apply to diastolic heart failure  .

But why not ?

We know diastolic heart failure  of the left ventricle  is less likely raise the  systemic  venous pressure  to cause the edema and raised JVP. But still ,  isolated LV diastolic dysfunction can increase the PCWP and PAP and RVP . Remember diastolic  septal dysfunction , may compromise RV relaxation also.(Reverend Bernheim like  effect)

We should  also realise , raised  venous pressure is not the only mechanism for edema legs.

Diastolic dysfunction can trigger  ACE genes  .IT can get activated and hence renal conservation of sodium.This neurohormonal activation can be dominant  mechanism of edema in few. This  prevails over  the hydrostatic forces. And  hence edema can result in isolated diastolic dysfunction.

What about RV diastolic dysfunction as a cause for right sided failure ?

This is a poorly  understood entity.Logic suggests  it may have clinical significance. Since  morphologically and developmentally LV  and RV share a common  sheet of muscle  , LV diastolic dysfunction can have it’s impact t on the RV as well.

Final message

Edema legs and raised JVP is a hall-mark of  isolated  systolic heart failure or combined systolic and diastolic failure   .It is not rare to find an occasional patient isolated diastolic dysfunction*  to present  symptoms of  systemic congestion .

*Of course ,  in this era of hi tech cardiology practice  it may be  inappropriate  to  depend on these  primitive clincal criterias  to diagnose CHF . (These  manifest very late in the course of CHF!)

Read also

Why  some patients with cardiac failure never develop edema ?

LBBB is probably the most important  conduction defect of the heart .When we say LBBB , we visualize a  strikingly  wide bizarre qrs complex .

Left bundle even though is considered  a discrete structure , the fascicles  make it a diffusely spread structure. Many varieties of LBBB with various degrees of involvement occur.

Talking about the basics of  LBBB  electrophysiology  is out of place for the current generation cardiologists,  who  have little spare time as  they sweat it out inside the cathlabs.

In early 1960s and 70s great articles came from pioneers regarding these defects. If we want get a good insight  read  this  articles from  Sodi palleres .Who  says LBBB is a dynamic process, where it can occur from mild functional  delay to a total block .

The conduction  properties of left bundle is very much influenced by heart rate.

Law of statistics would  suggest  for every complete LBBB  at least three to 4 times incidence of incomplete  LBBB

Then . . .

Why we are not diagnosing ILBBB often ?

  • We miss it
  • Mistake it with LVH
  • We know it  is there , but we do not  want  to diagnose it .

How to diagnose ILBBB?

See  Sodi palleres criteria*

What is the relationship between qrs width and completeness of LBBB ?

Surprisingly and contrary to the belief , the width of the qrs has no linear correlation between severity of LBBB. In fact incomplete  LBBB can occur with even 150ms qrs !

Then ,  what  exactly determine the completeness of LBBB ?

What  matters is , whether the down coming impulse gets blocked  and split in the  left side of the IVS or not ? This causes the  the septal vector to  change  it’s direction ( ie  right to left instead of the normal left to right) It  removes the initial small r wave in v1  and q in v6  in complete LBBB. In  incomplete LBBB these  r and q are  often retained .

What is the differential diagnosis of ILBBB ?

Type B WPW may mimic LBBB and vice versa.

LV hypertrophy .

Differences : See table in  the Barold’s article  linked above .

Unanswered questions

  1. How common is ILBBB in STEMI ?
  2. How often ILBBB progress to LBBB ?
  3. ILBBB in dilated cardiomyopathy : Is desynchrony an issue ? (Normal QRS CHF !)
  4. Is functional  rate dependent  LBBB in cornary care units  same as transient  ischemic LBBB ?
  5. Intermittent LBBB and Incomplete LBBB  aren’t they  synonymous ?

Final message

ILBBB is not that uncommon as one would  tend to perceive.

Reference

My humble tributes to  Barold, Sodi -palleres , and Leo  Schamroth . Probably  one of the best  article on ILBBB is linked below. Reviewed    in 1963 !  Not much data has been added  in the next 47 years as on 2010

ERS -Early repolarisation syndrome  is known as a   benign ECG finding  for  many decades  .Now it  is beginning to look dangerous as evidence is accumulating  it may have a link with ventricular arrhythmias.

ERS represents complex changes in  ionic movements during  cardiac repolarisation . (To be specific , it is due to a functional gain of  K + ionic channels during phase 3 of action potential).Generally this is a very benign condition. But , what concern us is ,  it can predispose to ventricular arrhythmias when these patients are confronted with ischemia .

When repolarisation occur early it indirectly shorts the QT interval .We know QT interval is a notorious period in human ECG as both a short and long (<320ms, > 460ms)  can be dangerous.

Is ERS a marker for potential cause for primary VF ?

Read this article from NEJM 2009