Archive for January, 2016

medical education critics cardiology evdnce based medicine growth ethics

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Dizzines , giddiness , light headedness , fear of fall or true fall (Syncope) are the  most common symptoms beyond middle  age .They usually end up with consulting physicians , neurologists and cardiologists .Cervical disc is commonly blamed for this.While all these symptoms can be a manifestation of cervical disc , true syncope seems to be rare with cervical spinal disorder.

how common is suncope in cervical spondylosis Why true is  syncope rare with  cervical spinal narrowing ?

There is a fundamental ignorance here. We are not yet clear  whether giddiness /dizziness is neural or vascular .(Or combinations of both ) in cervical spinal disease.

Many of the patients experience momentary unsteadiness and feel like falling but very rarely end up in a fall or syncope.By definition syncope requires global transient hypoperfusion of brain to trigger a fall .

Cervical canal carries only the vertebral artery .Both internal carotids are no where near the spine. So, however severe the vascular compromise within the cervical canal , syncope is unlikely as anterior cerebral circulation compensates at the level of circle of Willis. Is that the correct way of reasoning ? Unilateral vertebral compromise rarely matters as other side takes care.It is very unlikely both vertebral artery get compromised by cervical spinal spurs simultaneously.

How many seconds of vascular compromise is  required to produce syncope ?

Brain seems to be a funny and sensitive organ .In erect posture it is very sensitive. It reacts  in a  fraction of time for any transient reduction of blood flow.The same cardiac events which can cause symptoms of impending syncope in erect posture is quiet comfortably tackled in recumbent posture .

In erect posture , blood pressure need to much higher to get it pumped above the heart against the gravity. Though , it seems absolute blood pressure and cerebral perfusion that matters, there is something more we are missing.  The brain-stem -vestibular system perceives differently when a recumbent person develop cerebral ischemia than when he is erect . The reflex circuit that activates on/off switch  for abrubt loss  generalised muscular tone is not yet been identified .

It is a biologically  heartening irony that syncope is a natural counter mechanism by which  the organism assumes instant recumbent position to maintain perfusion of brain .A fall promptly does this.(Ofcourse with a risk of Injury )

We think more than 3 second pause will initiate a  syncope circuit .But it is not a fixed number. Some can tolerate up to 5sec or even more especially in lying posture.

Final message

Syncope , as such in isolated cervical spondylosis is rare even though it can potentially interfere with  the vertebro basilar system .Why the vascular compromise almost always fall short of syncope and end up with just momentry unsteadiness is not clear.

Further queries to be addressed

Is dizziness, giddiness , presyncope  are vascular or neural  event?

Can vertigo occur with cervival spine disease ?

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Every time , patients ask me  what diet he or she  should follow , Iam sort of  amused , as my understanding of diet and cardio vascular disease is at best primitive.I used  go with a standard single phrase  advice “Anything in moderate should be okay  “
What about going for a saturday night party doctor? One of  my shrewd looking  patient who was recently double stented with DES , asked.
Human body is a biological marvel.While medical professional divide it  into various systems  for our convenience. God doesn’t  think that way .He has no systems in mind when the body was designed . There is no wonder , the alimentary system and hematological system has to interact on a daily basis  with the help of circulatory system  to keep the  body alive. Platelets are unique blood cells that exist primarily to plug physiological bleeding if any  or for self-healing at sites of tissue injury.
 platelet lipid ldl tgl triglyceride ineraction 002
With human vascular system increasingly invaded by various metals and wires , platelet are a confused lot since their original biological functions are altered. They simply don’t know whether  fight these foreign body , aggregate over it , flush or simply pass over these .Adding to this  the powerful anti-platelet drugs targeting critical functional pathways .No wonder every other cardiovascular  patient  consumes at least one anti-platelet drug.
It seems diet  can have direct influence of platelet function
With human beings desire to add style to food consumption and eating habits  competing with  top slot of purpose of living , we often forget it is same prevent us from living a good life.
There has been numerous anecdotal and study population and experience  acute coronary events are more common after a heavy meal especially a fatty one .The immediate suspect has been high triglyceride and chilomicrons in blood stream shunted  intestines .
It is logical to expect , these high TGLs some how act a s trigger for pro-coagulant trigger .With the core thrombus  rich platelets it is assumed platelet stickiness is augmented and  maintained  by transient raise in triglyceride formation(Reference 1,4,5)
Glycerol component of  TGL is know for  its sickness and  making the companions wet.
The million dolor question is , at what level of TGL and which forms of TGL make the platelet cry and attract each other ?
Diet, anti platelet drug efficacy  ?
 Now , patients with coronary stents has to live at the mercy of these anti-platelet drugs. The drug resistance(Clopidgrel) is  threatening to be major issue.Like warfarin do we have real issue of dietary binge and acute neutralisation  of anti-platelet drug efficacy that can trigger acute stent thrombosis . This is potentially  important  area of study .
Final message
So does a fatty meal  a new trigger for ACS ? It may sound an alarmist statement .but as of now , its difficult to ignore this.So my advice for that  the that smart young man with soluble stent  was to avoid binge dinners that carries a definite risk of interfering with  stent maintenance .

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What are the mechanisms of cyanosis in  cyanotic heart disease ?

Most of my fellows have difficulty in answering this question. (It is not the lack of knowledge though !)  In my view ,cyanosis can occur , by six  different  modes

  1. Reduced pulmonary blood flow  with some form of anatomical obstruction in RVOT with a communication between ventricles  (TOF physiology  ) , atria or both
  2. Reduced pulmonary flow with obstructive pulmonary vasculature (Eisenmenger physiology )
  3. Wrong way origin ( RV to Aorta/LV to Pulmonary artery ) : Transposition physiology
  4. Simple mixing of arterial  and venous  blood channels within the atria  ,ventricle or great vessel  without RVOT obstruction .This, in fact can causes increased  pulmonary blood flow (Technically left to right shunt ) and still there is cyanosis (These are called as Admixture lesions ) It is  also to be noted some of the admixture lesions  (Truncus, DORV,etc ) the mixing takes place only during systole  , while TAPVC,Common atrium, Tricuspid atresia*  admixture is more complete as it happens during  entire cardiac cycle.
  5. Isolated Right to left  shunt are  very rare ( Pulmonary AV fistula , SVC to LA )
  6. Complex combination of first 4 (Like bi-directional shunting , TGA combines ,  AV canal defect , with varying degree of pulmonary obstructive disease) Note : TOF and Eisenmenger are physiologically mimic each other , the  only difference is site of resistance to pulmonary flow. RVOT vs Lung vasculature )

* Essentially Atrial admixture is more complete than when it happens at ventricular or great vessel level

For advanced readers only

Now, is it possible for “Net” left to right shunt to  result in cyanosis ?

Yes*.Very much possible. The bulk of this group is referred to as admixture lesions with certain caveats.There should be an obligatory mixing without contribution from RVOT obstruction or raised PVR( *Please note theoretically  admixture can either be right to left  or  left to right shunt )

All pure admixture lesions are in fact net left to right shunts. (TAPVC, Single ventricle , Common atrium , Common AV canal ,Truncus, ) This is the group we have been traditionally calling cyanosis with increased pulmonary flow.

Its may also to be noted with  surprise some admixture lesions often  has less intense cyanosis than other forms as long as pulmonary blood flow is normal and the lung does its job perfectly .

*Please note Isolated classical left to right shunts , ASD, VSD, PDA can never cause significant cyanosis unless there is reversal of flow .However ,many Eisenmenger physiology  show net Left to right shunting only ( 1.2-1.5 : 1 or so ) but with a definite right to left component .What we call as typically bi-directional shunt .

How can cyanosis be minimal even in some cases of single ventricle ?

  • Even though there is single ventricle , there can be preferential (favorable)  streaming of right heart blood flow without gross mixing .
  • As discussed before good uninterrupted pulmonary blood flow will make the cyanosis less intense .

Is single ventricle with PS  admixture lesion or TOF physiology ?

Though single ventricle in isolation is an admixture lesion, when it has associated RVOT obstruction it ceases  to be admixture by definition  as mixing is augmented by the obstruction rather than by simple mixing.The complexity could be understood in certain situations  where admixture lesions  like common AV canal  go for raised PVR .Here the various quantum of contribution to cyanosis is mind boggling. (Original admixture, augmented by RVOT resistance, differential mixing at atrial and ventricular level  , hypoxia  at lung level due micro pulmonary AV fistulas in grade 4 heath Edwards etc )

Can TOF behave  like an admixture lesions ?

Technically Yes.If the RVOT obstruction is minimal , (What was called then as pink Fallot ) We haven’t  understood this entity properly for so long.Atleast  I was baffled to read when J.K Perloff mentioned in his book  during my DM fellowship days,  that  TOF can manifest  with predominant left to right shunt with little or absent cyanosis.

The  aortic override in TOF facilitated by large malaligned VSD make it a sort of admixture  situation as  RVOT resistance is too little to offer any resistance, (rather it welcomes more blood from left side ! ) So , should we call it simple VSD physiology , admixture physiology or  just acyanotic forms of TOF ?)

Key points

Though admixure lesions are discussed separately , bulk of them  actually represent cyanosis with increased pulmonary blood flow situations.

The  net pulmonary blood flow is much more important than the quantum  of admixture in determining the degree cyanosis

Finally , one should appreciate  there can be combination admixture lesions with obstructive RVOT components . (Tricupid atresia+Pulmonary stenois )

Further reading

An excellent review article on this rare topic of  admixture physiology

  1. Jaganmohan A Tharakan Admixture lesions in congenital cyanotic heart disease Ann Pediatr Cardiol. 2011 Jan-Jun; 4(1): 53–59.


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On this special day , wishing all the readers and followers of this blog  an energetic, creative , insightful and  of-course a happy new year 2016 !

Just wanted to share the 2015 annual report of this site with the readers.

wordpress annual report dr venkatesan

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