Archive for June, 2016

medical ethics stastistics www.drsvenkatesan.com

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One casual question in my class led to this search for an anatomical mystery. When we were discussing why left atrial oxygen saturation never reaches 100 % ? , it was attributed to desaturated bronchial venous blood draining into pulmonary vein.

How does this bronchial vein enter pulmonary venous circulation ? How many bronchial veins are there ? What anatomical plane it runs ?

Surprisingly, even in this hi-tech era of academic excess, literature is sparse for this basic anatomical question. It is reported (In Greys anatomy ? ) Bronchial veins are two in number and both drain to Azygos and Hemiazygos veins (systemic) rather than pulmonary veins.

So is our assumption wrong ?

May not be.We realise these are only two visible and named bronchial veins .It is learnt they probably carry only about 13 % of bronchial venous blood to systemic venous circuit.

bronchial venous drainage bronchial circulation

Image showing right and left bronchial veins draining to Azygos and hemiazygos veins.

It is assumed , remaining 87 % of bronchial venous blood drains to pulmonary venous circuit in an invisible fashion (By unnamed twigs ?) desaturating the LA blood by about one percent from 100 to 99 %. This is our current understanding. I haven’t come across any specific human research that quantifies the bronchial venous channels and it saturation . It’s gratifying to find one study specifically looked answer this question in sheep study .(Charan H.B et all Reference 1 )

where does bronchial vein drain drainage circulation pulmonary vein saturation

True physiological bronchial venous drainage seems to be different from anatomical bronchial venous circuits .

Clinical implication of bronchial venous circulation.

In physiology it may not be important . However bronchial circulation (both arterial and venous) can take many anatomical tracts when pulmonary micro vascular bed is structurally and functionally altered as in COPD, , pulmonary atresia with aorto-pulmonary collaterals , congenital left to right shunts,post Fontan circulation pulmonary AV malformations,lung tumors etc .

Hemoptysis in acute pulmonary venous hypertension is thought to be due to rupture of these bronchial veins as elevated pulmonary venous pressure reflect into bronchial veins (As in mitral stenois and other conditions. ) This again would vouch for bronchial veins draining to pulmonary veins.

Final message

As on today , it can be concluded bronchial vein drainage goes both systemic and pulmonary venous circuit.Bulk of them appear to end in pulmonary veins though clear anatomical evidence is lacking.


Exploring human anatomy appear a grossly unfinished agenda even today, especially the micro and histo-anatomy. Teachers of basic sciences should impress upon youngsters entering the medical school to pursue translational research relevant to specific clinical problems.

Students may contact <drsvenkatesans@yahoo.co.in> for specific areas of clinical cardiac anatomy topics that still requires answers.


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We know, atrial fibrillation is the commonest clinical cardiac arrhythmia , that is extensively studied , subjected to exotic investigations and state of the art treatment strategies.Interestingly , this arrhythmia also drags the economics of cardiology practice of a community in a big way with heavy influence on drug , device and usage.We know, RF ablation of pulmonary vein is one of the modern ways to manage this arrhythmia.

Iam sharing this article from medscape by an EP specialist Dr. Jhon Mandrola , surprisingly exposes our fundemental ignorance about this arrhythmia and the near futility of certain procedures.


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Scientific cardiology has forced us to believe ACS management must be catheter based and all others are inferior  and  those who pursue the later , carry a risk of  being labelled as unethical in near future. However ,experienced cardiologists will know  where the truth lies.

Now,in the interventional cardiology board rooms  there is a big  debate going on regarding the value of early total revascualrisation in STEMI with multivessel CAD.Suddenly , every lesion looks suspect ( Ex,current or future culprit ! ) and all stentable lesion are stented  either in an emergency or semi emergency fashion (The new age post PCI dialogue goes something like this “I have tackled one culprit , other one seems to hide in LAD ,  we will arrest it  next 48 hours or so* ? ( This is the concept of  deferred or staged  non-IRA stenting )

*Ironically it brings   one more dubious therapeutic time window in ACS !

ptca ira non ira multivesssel pci

The recent  studies like  PRAMI, PRIMULTY ,CvLPRIT are trying to find out an answer to this issue  and suggest acute multivessel PCI may be  good strategy. Some of them advocate a FFR guided non IRA intervention , knowing fully well micro-circulatory bed is completely altered by the index acute thrombotic event.( Mind you , for FFR,  we need to induce maximum hyperemia with Adenosine in a highly varying local autonomic milleu within the thrombus clogged capillary network)

Final message ( Intentionally biased !)

Till we learn or unlearn  it is vital to go with conventional wisdom.Don’t pursue a random hunt for coronary culprits in acute phase of  STEMI.Many of them are innocents and likely to suffer in cross fire.Tender coronary arteries need some rest,peace and time to heal thyself  . Just keep away , they will definitely say big  thanks with folded hands !


1.Gershlick AH, Khan J, Kelly DJ, et al. Randomized Trial of Complete Versus Lesion-Only Revascularization in Patients Undergoing Primary Percutaneous Coronary Intervention for STEMI and Multivessel Disease: The CvLPRIT Trial. J Am Coll Cardiol. 2015;65(10):963-972.

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