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Archive for 2008

     The greatest discovery in medicine is  “ common sense” and

    “democracy”.           

                       The greatest medical discovery  is the realization that medicine is an constantly evolving science. It needs lot of knowledge to know our ignorance . Common sense has probably saved more lives and reduced suffering in this world than any other single discovery. Note this glaring irony ! It has required a large multi national long term follow  up study (INTERHERT) to prove exercise and physical activity is good for health. Whatever science is teaching us it is we, with our sixth sense have to act appropriately .It is the only defense against the potential exploitation against man kind by various forces.

Another great development is the freedom of expression and democracy in medicine,  for which journals like BMJ, Internet are striving hard . . .

Dr .S.Venkatesan ,Assistant professor of cardiology . Madras medical college Chennai , India

     

 Click on the title to view the article and all nominations . 

 

 

 

 

                         

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Answer: Do  coronary angiogram  for all patients  who had suffered from an acute myocardial infarction* ( Forget about all those mulitpage ACC/AHA  guidelines !).

For an  interventional cardiologist ,  it is often  considered a crime to  follow a conservative  approach !

*Caution This one line guideline is not based on scientific fact  but reality based . Ideally one should identify  high risk subsets among the patients who had an AMI .Patients who had complications during the MI get immediate CAG. Others need  a focused LV function asessment ,  pre discharge  sub maximal excercise stress test or perfusion studies .But this concept has been  virtually replaced by pre discharge coronary angiogram for all ,  in many  of the centres in the world.

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Please click  below to enter my web site

 

 

 

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One of the greatest physicians of all time,  I have come across , is my professor Dr.T.K.Ganesan from Coimbatore medical college.

dr tkg professor t k ganesan coimbatore medical college

A man who taught  medicine to generations of doctors.During those years  (1980-1990) learning medicine was simple and also not contaminated  with  commerce . Dr TKG made it so lively .He infused passion in the subject.

dr k a sambasivam dr s venkatesan  dr tkg dr t k ganesan coimbatore medical college

Myself and Dr K.A.Sambasivam (Son in law of DrTKG at his residence in Coimbatore )

* Dr K.A .Sambasivam  was my class mate during both my under and post graduation . He is now a senior Interventional cardiologist in GKNM Hospital Coimbatore .

This post will be updated.

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During acute  ischemia the most immediate requirement for the heart is

A.Blood

B.Oxygen

C.Glucose

D.High energy ATPs

E.Free fatty acid

Answer : A  will be considered  by most , as  correct answer .  A can provide B to E . But it is also a fact heart can survive without  A.  

Myocardium requires energy first  ! it does not in fact bother about from where it is coming at the time of crises.It may be right if you restore the coronary blood flow all other components (B-E) are made available to the heart .

The heart can survive off  the coronary circulation with only chemical support during cardiac surgery and also a during  heart transplantation  explanted  donor heart survives on a ice box during transit and till it is transplanted into the recipient heart

But ironically we spend much of our energy and efforts in restoring blood flow.One need to spare a thought about the quality of blood also . This is especially important  in the setting of ischmia  where a  metabolic centric approach will add further benefit.

Energy based approach to ischemia : Is it relevent ?

Heart is a fascinating  mechano biological organ  pumping   millions of  gallons of blood  .Fuel for this is self generated  on a continuous basis  from the circulation blood .So  the key to human survival is the coronary blood flow that supplies the fuel and nutrients to the heart. When this key supply line is under threat  during  acute coronary syndrome cardiologist have  the only option of restoring the compromised blood supply by any means . But during chronic ischemia there is  no  urgency. There has always been an option of enriching the  blood with energisers like ATPs,  glucose,  hemoglobin etc .Providing energy support to the failing heart has never captured the imagination of cardiac physicians until recently.Still most are skeptical about  the concept of biochemical ischemia.

Click to download full PPT presentation

Metabolic manipulation of  CAD( Will be available shortly)

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Humans have roughly 5 to 6 liters of blood at any given time in their  body  . Out of  this*

50% (2500ml)  is located in the systemic venous compartment.
18% is within the pulmonary circulation participating in the vital oxygenation
12% (500-600ml) is within the cardiac chambers.
8%  is in the arterial tree of  the body.
5%  is  within the  capillaries.
2%  is in the aorta.
* Source : Best & Taylor Physiological basis of  medical practice 1966, 8th edition

What is the implication of this predominantly venous distribution of blood  at rest ?

  • A competent venous tone is essential  for the human beings to maintain the erect posture.
  • Bulk of the cause of syncope in humans is due to peripheral  mechanism like loss of vascular tone and resultant venous pooling.
  • The  concept of venous reservoir is so important in emergency situations like  hypotension  as  simple elevation of legs  is equivalent to  infusing 500 -800 ml of intravenous saline .
  • Similarly during acute left ventricular failure trunk elevation and legs dangling down can reduce the pulmonary congestion very significantly and reduce pulmonary capillary wedge pressure (LVEDP)

 Autonomic dysfunction and venous insufficiency

 Autonomic dysfunction and resultant  orthostatic hypotension is directly related  to venous reservoir dysfunction.Increasing effective circulatory volume by elastic stockings or administration of mineralocorticosteroids like fludrocortisone (.5mg/day ) can be useful in this condition

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                             Glucose is the molecule of life   ,burnt every second inside the body at the energy store house called mitochondria. Heart , the most active organ in the body  gets  bulk  of it’s energy supply  from fatty acids,  glucose and a little from keto acids. Under anerobic conditions this energy substrates shifts towards glucose .

                             We are  rarely inclined to think  that heart  can ever suffer from hypoglycemia ! But hypoglycemia can have distinct direct and indirect effects on heart.  In fact indirect effects due to activation of adrenergic activation is more obvious.An episode of hypoglycemia can precipitate an arrhythmia . Glucose potassium insulin infusion

 

 

 

Final message

Hypoglycemia , can be a trigger of ACS .This aspect is poorly recognised and studied.

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Ventricular fibrillation is invariably fatal if not treated . When can atrial fibrillation be fatal ? 

                                     Atrial fibrillation is relatively a benign arrhythmia especially when it occurs in isolation with  structurally normal heart.This is sometimes referred to lone atrial fibrillation . Even otherwise, atrial fibrillation is rarely fatal except in few situations.But AF commonly destabilises the patient  who have baseline valvular or myocardial disease.(Post MI, dilated cardiomyopathy etc)

There are few situations where AF can be life threatening

  • In patients  with WPW syndrome*where , AF  enters into a electrical short  circuit , downhill to enter the ventricle and make it fire at the same rate as that of atria . ( ie 400-600) and result in ventricular  fibrillation.Note , even here it is the VF that kills  not , AF per se.
  • AF in acute MI  often precipitates LVF , but rarely fatal.
  • In patients with critical aortic stenosis, or hypertrophic cardiomyopathy, sudden onset of AF can result in acute cardiac failure.
  • AF is often a terminal event in primary pulmonary hypertension

While atrial fibrillation is  less likely to cause  death , it is  a highly morbid arrhythmia .It is one of important cause of stroke in elderly as well as young !

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               Usually in the the vascular  system both artery and  vein  go together .It is an  irony in pulmonary circualtion  these two never go together .Another paradox is that pulmonary artery carries the most deoxygenated  blood and pulmonary vien carries the purest  form of blood in the entrie body , probably God has kept them widely seperated as  communication between them  seriously affect the physiology.

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Ventricular tachycardia is considered as one of the most  dangerous  cardiac arrhythmia .Rather , it is the label  VT  that spreads more  fear than the arrhythmia itself. It is a fact many patients with VT walk into hospital , still  VT will always be a sinister arrhythmia as long as it carries a risk of degenerating into ventricular fibrillation.

What determines hemodynamic stability in VT ?

  • Origin and location of VT
  • The ventricular rate
  • Presence or absence of AV dissociation
  • Impact on mitral inflow pattern
  • Associated left ventricular dysfunction or valvular heart disease.
  • VT in the setting of acute coronary syndrome.(Ischemic VT)
  • Inappropriate drug selection

Origin and location

VTs originating high up in the ventricle( High septal VT,Proximal VTs) have more organised ventricular contraction  and they are more stable.Distal VT  originating  in the myocardium away from the conducting system has chaotic myocyte to myocyte conduction.These are very unstable.

The term fascicular VT is nothing but VTs originating  in the His bundle and it’s branches( Can also be termed Septal VT ).These VTs are also stable and some of them respond well to calcium blockers indicating that they are very close to the AV junction and carry the properties of junctional tachycardia. QRS width gives  a rough estimate about the location of VT. Narrower the VT higher it’s origin.( But remember even in VT ,  qrs can further widen on it’s way downhill !)

LV dysfunction.

This is probably the most important determinant of the outcome in VT. Patients with severe LV dysfunction (EF <30%) fare badly .Hence the land mark concepts from MADIT 1& 2 demanded ICDs in these patients.The most common clinical setting is  dilated cardiomyopathy.SomE of them have bundle branch re entry(BBR).This particular  VT can be stable for many  hours.

Ventricular rate.

Usually VT has a rate between 120-200.Higher the rate of VT more the chances of instability .This rule is also not always true as fascicular VT can be well tolerated at high rates.So location of VT focus  and LV dysfunction usually over rides the impact  of ventricular rate.

Mitral inflow pattern

Proper left ventricular filling is the key to hemodynamic stability in VT. In proximal, septal,fascicular, LVOT VTs doppler studies  suggest (ACC /AHA Type C evidence : Personal observations in CCU during VT) near normal preservation of  bi modal filling of mitral valve inflow.In ischemic myocardial VT  the mitral inflow profile is critically affected . There is no distinctive forward filling was observed .In fact  at rapid rates a short pulsatile MR jets are noted instead.

Associated valvular diseases

It is obvious,  aortic  and mitral valve disorders can aggravate the hemodyanmic instability.

Final message

The clinical behavior of  ventricular tachycardia is widely variable and dependent on multiple factors.

Associated LV dysfunction and  structural heart disease ultimately determine the outcome.

 

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