Feeds:
Posts
Comments

Archive for December, 2013

Auscultatory  findings of mitral stenosis is the most common question asked in clinical cardiology right from first clinical year to higher specialty examinations . It should be answered in a systematic way.
What happens to  the murmur and sounds in mitral stenosis after the onset of AF ? When I asked this question  in my class  , many struggled . Hence this post .
 Mitral stenosis auscultation
* Correction
The A2-OS interval in critical MS  is relatively short and only is minimal variation is expected in spite of AF .This is because, A2-OS interval is primarily determined by instantaneous  LA pressure  at the beginning of MV opening which is always high and does not vary much with RR interval .
Reference
Criely mitral stenosis pressytolic accentuation ausultation atrial fibrillation

Read Full Post »

Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

myths-truths-300x300

When false truths are synthesized to conceal a true myth . . . where will the poor myth complain ?Following are revered  facts  . . .  among the  “Guardians of   Cardiology” !

  • Primary PCI  is a greatest innovation  in modern day cardiology .Without this modality  most  STEMI patients will buy Instant  tickets to grave yard !
  • A cardiologist who intends to  thrombolyse  a STEMI is considered as a low quality cardiologist .
  • Streptokinase should have  no place in the crash carts of modern coronary care units.
  • There is nothing called “Time window” for rescue angioplasty.
  • VVI pacemaker  will convert an electrical problem of heart block into a mechanical one by depressing LV function .
  • Digoxin is an obsolete  drug even in well established cardiac failure with dilated heart.
  • Beta blockers not only fail to control  blood pressure smoothly , it often converts  a hypertensive individual into a unhealthy one  by it’s prohibitive side effects !

 

Read Full Post »

CokeMini_Happiness_03

  It costs just one Dollor !

Harvard school of Public health has  recently  published some  hard data about  the adverse effects of bad diet habits especially the impact of  soft drinks on long term cardio vascular health.

soft drinks and impact on healthAnother prestigious journal confirms it . . .

risk of soft drinks and coronary artery diseaseThe ultimate journal for the cardiologists Circulation reaffirms it .

soft drinks carbonated and coronary artery diseaseWe  have overwhelming evidence , prolonged use of soft drinks
increase CAD (Like tobacco ). Still , we haven’t added the customary caution on the bottles of these soft drinks ?

Why  ?

My guess would be, there are powerful forces in  modern society that would love to keep  the  threat of diseases high in the  human domain  so that all  stake holders  make a profit .

The poor , World health instigation(WHO)  and various public health forums  simply watch it .If they protest , they are at risk of sucked into the loop of deceit !

Failure to reverse public health hazards  may be a  lesser crime  in modern days  . . . But , here comes  a series of  advertisements in Indian media , that is a strong indicator that human  intellect and the sixth sense  is going nuts !

It suggests , Do you want  ever lasting happiness . . . Drink  it  . . . earnestly believe  in it  . . . and drink again  !

Coca-Cola-12

I was also told  a shocking fact that , The beverage war in India has  started and the soft drink giants have heavily Invested to take it into the rural markets .Their aim is to  provide  “health  for all Indians”  by 2020 !

Concluding question

Read Full Post »

electrical CONDUCTION OF HEART

Image source and courtesy http://www.heart-consult.com

Answer

I am afraid the 4th response is closer to truth .Readers may share their thoughts. If there are three distinct pathways   spreading widely connecting the two spacious chambers and   converging again with  precision at the compact  AV node , it  is a  marvel .

Further , If these pathways are real ,  we must  experience different types of  inter nodal re-entrant  tachycardias.Of-course ,we do come across few macro re-entrant tachycardia in the form of atypical atrial flutters  They need a close  watch .Tracking these arrhythmia may throw light on existence of these pathways.

However, the presence of nodal approaches  with preferential inputs to AV node from different parts of atria would indeed  suggest existence of such pathways !

Further study

What does  sophisticated carto and other electro anatomic mapping say about these inter nodal pathways ?

Reference
An excellent article from imperial college London
Atrial anatomy and inter nodal pathway thorel bachman wenkeback

Heterogeneous three-dimensional anatomical and electrophysiological model of human atria . Seemann G, Höper C, Sachse FB, et al. Institute of Biomedical Engineering, University Karlsruhe (TH), Kaiserstrasse 12, 76128 Karlsruhe, Germany. Transact A Math Phys Eng Sci 2006 Jun 15; 364(1843) :1465-81.

Read Full Post »

Recently , I came across a   young women  who underwent the following three tests for one episode of syncope after witnessing her pet dog bleeding with  an Injury !

  1. Carotid doppler
  2. Holter monitoring and event monitors
  3. Brain MRI /MR angiogram

This was followed up  by Head up tilt(HUT)  in a premier hospital

After 1 week of investigation ,a diagnosis of  Neurocardiogenic syncope was made and she was reassured and no drugs were prescribed.

(The collective yield of the above three investigation in fixing  a specific diagnosis is  less than 10 % of all known causes of syncope )

Syncope  approach  evaluation

To diagnose  common syncope . . . we need common sense !

Syncope is a dramatic  symptom.It is one of the commonest symptom in ER as well . Life time incidence of syncope is at least one episode in 50% all human life ! The definition  of syncope until recently , was liberal .Any transient loss of consciousness with spontaneous recovery  was termed syncope.

This includes

  1. Hypoglycemia
  2. Anemia
  3. Siezure disorders
  4. Structural  neurogenic (Including ,  brain tumors , Dural hematomas etc )
  5. Panic attacks (psychogenic)

Cardiologists wanted to fix syncope as an exclusive disorder of  circulatory insufficiency.By bringing in a modification in the definition  , ie  syncope is  now defined as a transient loss of consciousness due to   reduction in cerebral perfusion  .

This definition helped cardiologists  to exclude the above entities . Still many would include all in single basket as patient should be seen as a whole and we can’t expect them to  land according to our convenience and classification.

Here is an incomplete* list about causes of  syncope (* 99% complete ?)

Vascular

  • Vaso- vagal syncope in young ( Neuro-cardiogenic , Common , Benign)
  • Autonomic dysfunction of elderly ( Including postural hypotension )

Cardiac

Arrhythmic ( Sinus node dysfunction /CHB/Idiopathic VT/Long QT syndromes)

Structural heart disease

  • Valvular  heart disease  (LVOT/RVOT obstructions)
  • Myocardial disease
  • Rarely ischemic heart disease

Miscellaneous

  • Severe pulmonary hypertension (Including PPH ,  pulmonary Embolism )
  • Paradoxical embolism.
  • Aortic arch disease -Takayasu related arteritis .

Investigation

We have a sophisticated array  of investigation for syncope .It can be a never ending exercise , ranging from  spinal cord evoked potentials to diagnose Shy-drager syndrome ,   . . .  to implanting long-term loop recorders to decode  heart beat behavior.

However , evaluation of syncope is the ultimate wake-up call  to all current generation cardiologists  . . . Why clinical cardiology  should  never  be allowed to die (and  it  will not ! )

Common sense begins with answering  few simple questions . Is it really syncope ?

If  you ask this question three times and with  specific leads to the patient  and the witness ,  truth will come out  . 90% of times it may not be syncope at all (Near syncope, accidental  fall, dizziness ,extreme blurred vision, drowsiness  etc)

If it is syncope , Is there a non cardiac cause ?

It may related to the Hypoglycemia / Anemia /Panic attacks.Get a neurologist opinion , it would be terrible mistake if you miss a space occupying lesion  within the brain. (Missing chronic silent sub dural hematomas is  frequent   in the evaluation of syncope of elderly !)

Ruling out  cardiac syncope is relatively easy

In the remaining  patients  basic investigation like routine blood tests,ECG, ECHO   will help us  rule out most serious cardiac disorders.Similarly  bulk of the electrical cardiac syncope can be diagnosed.(Holter , carotid study in selected few )

Need for neurologist -cardiologist interaction.

Syncope due to VBI,  transient Ischemia attack , Senile vascular dementia  is a grey zone . Many have complex neuronal -vascular mechanisms . What is Consciousness ?  and  What is LOC ?  :Is it the lack of blood or severely depressed nerve signal in the reticular activating system? Lots of interaction between cardiologist and neurologist is required to clear our ignorance.(I  have one such  elderly patient who is intermittently awake ! I call this chronic syncope !)  .

Undiagnosed syncope is not  a crime

Realise the most important lesson in Medicine . If you  have ruled out all serious  causes of syncope you should have the courage to be satisfied with that !

Scientific pursuits has a limit. Searching for the mechanism of a psychogenic  fainting attacks with intra cerebral electrodes is a clear case of  physician acquiring a psychotic  behavior !

Final message

Syncope is not only a dramatic symptom for the patient , it also unfolds a drama of costly  investigations  . .  . many  with  dubious value.

Talk to the patient personally for  10 minutes in a quiet room, try to apply that elusive  clinical sense  . . .   it would rarely let you down !

After thought

What is the true clinical value of * Head up tilt Test (HUT)?

Will be posted soon

Read Full Post »

Last week  there was a heated debate in our CCU regarding thrombolysis for  a patient with severe rest angina  and ST elevation in AVR  and ST depression in V2-V5  as it implies  Left main disease  Few argued left main disease is an exception where one can thrombolyse even with unstable angina !

One of my fellows argued ACC guidelines vouched for lysis in UA involving left main .( I do not agree )

A logical attempt to differentiate Left main NSTEMI//UA and STEMI

(In the strict sense Left main NSTEMI is misnomer as AVR shows ST elevation  isn’t ? )

left main disease

Final message

Such  patients with suspected LMD   are to be rushed to cath lab .  . . agreed . If it is not feasible , manage it as high risk unstable angina and do not thrombolyse .Let it be left main disease . Indications for lysis are clear. ST  elevation in AVR alone can not be taken as an Indication for lysis.For thromolysis to be effective there should be high thrombus burden with total occlusion . ST elevation in single lead (AVR ) is not a good  marker for left-main thrombus !

Read Full Post »

Oral anticoagulant usage has been steadily increasing for variety of  indications.Dengue fever is also  appearing in different avatars with  low platelet counts  and bleeding being a primary risk.

I was recently contacted by a physician , regarding a therapeutic dilemma .A young lady with mitral prosthetic valve and a febrile illness diagnosed as dengue . She has a platelet  count of 100,000 .She is on regular warfarin and aspirin .The physician  wanted to know , should he stop the OAC and aspirin ?

What are the options ?

  • Confirm if it is really dengue.
  • Look for clinical bleeding.INR, platelet function tests are not helpful.
  • Continue OAC.You can do that in most situations.
  • Stop OAC only if there is clinical bleeding  episode.
  • Anti-platelet drug usage  is more tricky .One may stop it if the trend of falling platelet is steep by at least two serial measurement.(or 50% fall from baseline)
  • Fresh blood and platelet infusions should be ready .
  • Finally and most importantly , Inform the patient and family about the difficult decision we are making.

*Is  OAC  safer than aspirin and clopidogrel in dengue ?

It is believed OAC has no major  Impact on platelet function .It may not  pose a threat of excess bleeding in the setting of  falling platelet levels .(*Evidence base -nil )

Another potential situation : DES and dengue

The number of DES in developing countries are increasing  where Dengue is endemic . It is not a surprising  to expect  both to  occur together.

Anti-platelet agents  can be problematic .It is better to withhold it during the active phase of dengue.(If the  stent has recently  been deployed you have no option !)

Final message

1.  Prosthetic valve , Warfarin Dengue .

2. DES, Dual antiplatelet agents ,Dengue.

They  extraordinary events  throw a complex therapeutic task .There are only two options .Continue or discontinue ! Whichever way you do , you explain to your clients (patients!)  the (un)reality games we play.

My personal option would be , with hold all hematological drugs during the active phase of dengue .

It is better to believe in the  natural thrombus fighting force . Leave the job of anti-platelet action  to the dengue virus for a week or two and give oral anticoagulants and dual anti-platelet agents a holiday

It may be foolish to rely on the dengue virus to guard against  prosthetic  valve  and DES thrombus , In reality we have to do that !

Reference

No reference exists.It is a statistical mind game.Individual assessment  should prevail. Either way, if something adverse happens court of law should protect us !

Read Full Post »