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Archive for the ‘cardaic physiology’ Category

We know pleural effusion (hydrothorax) is disproportionately more common on right side in cardiac failure.Though its a well observed phenomenon, the mechanism of which  has not been clear to us. It could be due to multiple  anatomical , physiological factors.

 

*The are  right and left lymphatic (Thoracic) ducts that drain the corresponding lungs and pleural space . There can be overlap and contribute to the differential occurrence of pleural effusion

 

Reference 

A meticulous paper written some 75 years ago (1946) from Harvard medical school teach us some important points in this phenomenon.

There is still lot, to be understood about pleural effusion in cardiac failure. We need to know why some pleural effusions tend to occur independent of hydrostatic forces.  It is also noted long-standing transudative effusions can become true exudates. Role of local pleural capillary hypoxia resulting increasing permeability is underestimated.Hepatic congestion and trans-abdominal seepage of fluid is a distinct possibility.

One more area we are not clear is  the relationship  between the  genesis of  pericardial effusion in cardiac failure and concomitant pleural effusion. Post operatively , after univentricular repair (as in Fontan ), pleural effusions can be much problematic with high venous pressure interfering with  pleural drainage.

Impact on symptoms

Finally, even mild pleural effusion can increase the work of breathing and result in dyspnea which is out of proportion to cardiac dysfunction.While we expect the diurteics to clear the effusion of cardiac failure, it doesn’t happen always arguing for a non transudative mechanism in at least some of them.

Further reading

Discerned readers are advised to study the pleural space dynamics in detail.

Link to the original Article of Edgar Mcpeak and Levine 1946

 

 

 

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Cardiologist are always worried about the supply side of coronary blood flow. It’s fair enough, we can condone our brain for this one way thinking , afterall arterial supply remain the life-line for the heart. Some of us could (should) realise the importance of these  humble coronary veins which are anatomically and physiologically tied together.Its existence is as unique as their arterial counterpart.Coronary blood flow of about 250 ml traverses both the arms every minute.Imagine the scenario if the veins refuse to clear the blood from previous cardiac cycle . . . total hemodynamic chaos right ? Luckily such situations are rare !

See how the the two coronary arteries and its branches interwine with the 4 major coronary veins.

J. M. Bourgery from Atlas of Human Anatomy and Surgery / Atlas d’antomie Humaine et de Chirurgie by Jean Marc Bourgery (1797-1849) Los Angeles: Taschen, 2005. Atlas Case QM 25 .B67 2005

Is the LAD flow coupled with Great cardiac venous flow ?

It is curious to see the LAD  hugging its spouse great cardiac vein within the anterior Inter-ventricular groove , but directing the flow exactly in the opposite direction . One should  wonder is it the same stream of blood from LAD ?(Near 100% So2) goes out into myocardial tissue comes back with 30 % *saturation in GCV ? If this is true , one can measure the “LAD micro-circulatory bed” integrity by computing the arrival time of levo phase blood in GCV.

J. M. Bourgery from Atlas of Human Anatomy and Surgery / Atlas d’antomie Humaine et de Chirurgie by Jean Marc Bourgery (1797-1849) Los Angeles: Taschen, 2005. Atlas Case QM 25 .B67 2005

* Its an important physiological fact the most desaturated blood(30%) in the body is from coronary veins as the aerobic organ extracts maximum oxygen .(For comparison IVS/SVC saturation is around 75% )

What happens to GCV flow in LAD  STEMI ? or CTO ?

In  ATOs of LAD there is temporary collapse of GCV. If it prolongs it may end up in complete thrombotic occlusion of GCV which has implication in slow flow , no reflow and poor myocardial salvage.

What happens when there is  acute  coronary venous occlusion ?

Nothing alarming happens. God’s masterly protection  ? Yes it is .Still its a mystery , sudden death is not the rule if we clip the coronary sinus as  thebesian venous system take over which drain direct to chambers.The fact that obstruction of  these veins may not result in acute coronary syndrome brings  less attention to this circulation , in spite of vital hemo dynamic role . Acute venous infarct due to coronary sinus infarction is still  possible.

Is there chronic coronary veno occlusive disorder ?

We know ,venous system is Intrinsically prone for thrombosis  in susceptible individual as the flow velocity is sluggish . Almost every venous system right from portal, hepatic pulmonary , renal cortical venous , experience this pathology. It’s surprising to note coronary venous system is largely devoid of this.(or at least it’s not recognised as often !)

Some of the patients with chronic CAD with syndrome X /Y show extreme slow flow with normal epicardial coronary arteries.We need to study them for sluggish coronary venous flow syndromes.

Assessment of coronary venous hemodynamics 

Coronary venous circulation integrity is critical component of  coronary micro -circulation.We have done original studies in the timing of filling of coronary sinus that reflects integrity  coronary micro circulation.( Sangareddi V, Alagesan R. Coronary sinus filling and emptying time: A new parameter to assess coronary microcirculation by a simple angiographic frame count. 59th Annual Conference of the Cardiological Society of India December 7–10, 2008. (Abstract).)

Microscopic analysis of coronary venous debris following PCI is our future area of study to assess the mechanisms of no reflow.

Clinical utility of  coronary venous circulation 

  • Coronary veins are popular with  electrophysiologist.The typical CS catheter is used to record intracardiac ECG around the AV groove .
  • They also provide an alternate site for ventricular pacing and cardiac resynchronisation therapy. However the efficacy of CRT is related directly to the coronary venous finger print .Unless it matches with the scar free areas of ischemic cardiomyopathies the response is likely to be less. So essentially EPs are at the mercy of these veins and scars.
  • Coronary veins can be used for retrograde perfusion of myocardium in diffuse obstructive  coronary arterial CAD where CABG is not possible with some success.
  • There is one trial (COSIRA) which suggested increased microvascular perfusion if we narrow the CS diameter with a device .This is hemodynamically Ironical though as coronary  perfusion gradient is increased still because of stagnation suggest some improvement in perfusion( Verheye S ,NEJM 2015)

Reference

Coronary venous circulation has an Integral link with micro circulatory bed .It will be of huge importance to understand the highly unpredictable response of PCI with reference to myocardial salvage in STEMI and revascularisation in chronic CAD.Youngsters are encouraged to dwell deeper into the mystery of coronary microcircualtion .

This one from Dr. Muller ,Florida  is a perfect review to start with.


A good review about the venous anatomy with reference to electrophysiology

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The right ventricle  is considered as a docile cardiac chamber with passive filling and  emptying  properties .

This belief  was reinforced when Fontan  in early 1970s suggested a principle in the management of  cyanotic heart disease  when  the right side of the heart is underdeveloped. He  proved  RV can be by-passed safely , with  great veins  (IVC/SVC)  by  themselves  take care of filling the pulmonary circulation  without the need of RV pumping function.

While it is true for few complex cyanotic heart disease, largely this a misleading  concept. In clinical cardiology practice  ,sudden or non sudden  RV deaths happen every day in the form of . . .

  • RV Infarction
  • Acute RV dysfunction in massive pulmonary embolism
  • COPD with RV dysfunction
  • Most cases dilated cardiomypathy  the terminal event is due to RV  failure.

So , RV function can never be dispensable in day to day cardiac hemodynamics.

RV has some unique properties in terms of shape , size and  hemodynamics . We are getting more insights from  modern blood pool imaging by MRI , about  how the RV handles the blood volume .

We know RV has a unique shape  triangular ( partially  pyramidal ) . It can be inferred the RV cavity is formed by fusion of  many  eccentric spacial planes. We have always believed  RV handles the blood it receives from right atrium in a unique way .Now we are beginning to understand it .It is now documented the RV segregates the blood it receives into 4 components.

 

right ventricle physiology anatomy hemodynamics

It is curious  to know  RV inflow is connected to the outflow by an invisible   physiologic Bridge . About 44% of  blood traverse the RV in this fashion.

 

RVOT blood flow right ventricle

Note : RV blood flow preferentially enters the RVOT with out transiting RV body and apex.Image courtesy http://ajpheart.physiology.org/

 

Which is the most important part in RV ? (Among Inflow, Body, Apex, Out flow)

After reading this article it seems to me , the mechanical  function of RVOT could be most  vital. If it fails to handle the first increment  which  comes directly from  RV inflow, stasis  is likely in RV body and apex , elevating RVEDP and later promoting stasis leading to clinical events.

Clinical implication of this study

  • Differential dilatation RV chambers to pressure or volume  overload is observed .
  • We need to analyse why RV dilates in some   but   goes for hypertrophy in others when confronted with pressure overload (VPS vs PAH)
  • RV apical clot in restrictive cardiomyopathy  is a direct consequence of stasis  of blood  in RV apical zone .
  • RVOT pacing  may have a hemodynamic advantage  over RV apical pacing  . However , for anatomical reasons RV apical pacing  is  far safer than RVOT pacing where the lead  is subjected to constant life long strain due to this busy RV inflow to outflow express  high way !

Final message

Traditionally we have labeled  RV  as a  passive venous chamber .It is clearly a misnomer.It  has to handle both the venous and pumping function beat to beat with precision  without  back log .Obviously ,  RV has to think and work  more than it’s  big brother !

Reference

I wonder , if  there is  any other site other than APS . . . to  find crucial  answers in cardiac physiology  !

 

Right ventricle physiology blood flow  3d 4d analysisAfter thought

  • There is huge gap between physiologists  who work in research labs and the physicians at bed side .
  • I appeal all young cardiologists  to visit  APS  once in a while ,between your busy cath lab schedule and help narrow this gap.
  • Without understanding the physiology properly how are we going to intervene the pathology ?

 

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I used to tell my students ,the relationship between the heart and kidney  is so close , it is never justified for  the  two departments of Nephrology and Cardiology  are  physically away by two blocks in our institute .

Kidneys are vital to maintain the volume and pressure of body fluids and heart is responsible for keeping this fluid circulating.

In clinical setting  it is a well known secret ,most deaths in patients who are on dialysis is cardiac while  most  deaths in patients  with CHF are renal.

It remains a mystery  why kidneys were   ever considered as a circulatory organ  , when  our medical pundits de-compartmentalised  human organ systems !

CKD is pre-cardiac failure and CHF is pre-renal failure

The Heart /Kidney affair is so intimate in many  pathological situations both either succeed or fail  simultaneous or sequentially.

While CKD  results in and pressure and volume overload of heart , cardiac failure cause pressure and volume under load (pre-renal  factor) which worsen the renal function and aggravate cardiac function alter.

In essence,  it is vicious cycle of two  serial organs  performing  the vital circulatory function with body fluids playing a  role of diligent mediator.Whenever the kidney  fails heart  is stretched and stressed  to its Frank starling limits by the volume  as well as the accompanying HT load.

While text books link these two organ as simple cardio-renal syndrome it is not happening at the level of patient’s bed side.

Cardiologists and  Nephrologists must realise they need do work in tandem like  their  respective  departmental  organs  which accomplish this task easily !

To tackle this much  maligned  cardio-renal conundrum

Consider CKD as CHF equivalent  and CHF as CKD’s

I would recommend this concept to be infused  right in the third year medical school and  try de- compartmentelise  clinical  medicine.

Need of the hour : How to Moderate ACEI dosing in CKD

ACEI has been a major pharmacological   revolution in controlling and reversing the adverse events of cardiac failure . Some where along ,  a significant fear complex arose regarding the damage it could cause to kidneys.

Recently , we know the role of  ACEI in CKD made U turn(Like what  Beta  blockers did to CHF) .Now, it is presumed ACEI are indeed  safe in most CKD and may  even regress  CKD. Still this concept  has not been fully disseminated  into general physician domain.

Let cardiologist and Nephrologist sit together and sort out this issue.

I guess ,  ACEI controversy is  a sort of  ongoing ego clash  between Nephrologist and Cardiologist . Both like it , both make fuss about it ! In my observation , if  a cardiologist titrate it upwards  Nephrologist would  lower it  and reverse happens if cardiologist express caution about it ! Do you agree ?

Final message

Mankind has  accrued  great benefits  from stunning break throughs in modern medical science . . . but it has come  only at a huge  cost ! Medical knowledge has completely fragmented the physician mind-set .Every good therapeutic concept is  hanging aloof .It requires periodic de-fragmentation (As we do it to our PCs by anti-viral soft ware !)

To begin with , let us  consider   CKD and CHF as single sequential circulatory  entity !

Let us vouch to  create new generation medical professional  devoid of skewed  medical vision !

Reference

Guidelines for ACEI in CKD

NKF national kidnye foundation

https://www.kidney.org/professionals/kdoqi/guidelines_bp/guide_11.htm

acc aha  accf guidelines chf 2013

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Note :This is a copy of  my earlier blog on coronary micro-circulation  published few years ago.Recently this got numerous hits .Hence I have just reposted it with slight modification.

Human coronary circulation stands unique among  others as it is a  life-sustaining circulation.It is indeed a great medical achievement  to visualise  the right and left coronary artery  system by coronary angiogram.  Actually,  what we see is  only a fraction  of  the surface area of coronary circulation .The surface area of  epicardial coronary arteries   constitutes  less than 5 % of entire coronary vascular tree .

And  . . .

An in vitro heart with special catheters showing the true extent of coronary circulation: Courtesy http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

This  is the reason  normal coronary angiogram can never mean normal  coronary circulation !

This huge gap in our perception is the single important factor  that  explains the vagaries  of modern coronary care .

This also make any clinical coronary  scenario  a  reality .

“A patient with normal coronary angiogram getting a myocardial infarction , the next day and a severe triple vessel disease living comfortably  for  decades with medical management”

So , it is essentially a  false  sense of  scientific accomplishment  by the cardiac scientists  at  least in the  of coronary circulatory physiology.

What determines the extent of these invisible coronary micro circulation ?

There are innumerable channels of micro vessels traversing across the heart, sharing , bridging , branching, penetrating  and  perfusing the muscle mass.They can be anatomically patent , physiologically non patent .They can be recruited by hemodynamic stress .These are never visualized by current imaging modalities..It is also influenzed by  favorable growth milieu and hormonal and neural stimuli.

Ignorance based cardiology

What is the mechanism  of primary VF following acute STEMI ?

The quantum of  coronary micro circulation is like the vast  cerebral neuronal net work .We have every reasons to believe they are have unique genetic imprint.How else you can explain a man with full blown STEMI come 24 hours later comfortably to the OPD while another loses his life with a stormy primary VF before even boarding the ambulance !

Why many cardiologists   do not give due credit  the   coronary collateral  circulation  ?

Right from the days  of  Levine in 1970s( Who made a seminal contribution  about coronary collateral)  the  utility value of  coronary  collateral  circulation  was never able to convince the cardiology professionals .

It has been our traditional  teaching ( without much evidence of course  !) coronary collateral circulation  is not effective to support blood flow during exercise . This fact has been  disproved  many times . Coronary collateral circulation was indeed useful in limiting damage in ACS and  relieve symptoms in stable angina.It helps  in reverse remodeling and provided electrical stabilty as well in post MI population.

Still , the concept  was  alienated  and   made   totally irrelevant  in the interventional  era  . Many   cardiologists  found well-developed collateral’s as an interference to their expertise and ego since it has a potential to alter the indication of PCI.They  continue to have  strong  scientific conviction (Pseudo ?)   that man made collaterals must always been superior to God made collaterals !

Whenever  some credible  reports emerge about  collateral circulation   being   equivalent to  revascularisation procedure , these concepts were  prematurely buried for some reason.

In the last decade there was a concern  about  performing  PCI in patients with well-developed collaterals  .The argument was , they tend to develop early stent occlusion and restenosis . It  was a genuine  query  raised by few thought leaders in the field as  collateralised vessels  suffer from  low flow   after PCI ,   if the pre -existing collateral continue to function.

But  then , few  studies countered this , and PCI was shown to be safe and  in fact may  fare well   in  patients  with  extensive collaterals .

In these  studies  interventionist’s  argument looked  amusing !  as they  seem to  define a  successful  PCI  as  not only to open the occluded vessel  but also  make sure to close  all functioning  collaterals  .(What a  a pity for our natural biological  angiogenic forces which had  worked  and  grown meticulously for months!)

Cardiac science in the current format,  makes   the future look  bleak for coronary a collateral circulation .With  early PCI  becoming a norm we will never ever allow the natural collaterals to  grow  ,  and even the  established collaterals  will have to face a stiff   fight  for survival  with  sophisticated coronary interventions .

Competing interest in the filed of  coronary collateral   research

While the basic scientists want  to  grow collaterals with angiogenesis ,  stem cells etc  interventionists   continue to  indulge in rampant angioplasties which  will suppress  collateral growth.

This implies we will struggle to  establish  the true  importance of  coronary collateral circulation .

Final message

Can it be an  effective form of revascularisation  ? 

My personal  inference  is   coronary collateral  circulation  “would and should”  have  a definite role  in at- least  some of the subsets  with chronic coronary  syndromes. If we think otherwise . . .    it’s against the principle of  natural biological science .

A good  collateral   system with optimal medical management  can save not only our  patient’s  lives but also  their hard earned currencies !

Reference

Here is a rare article in European heart   journal that discuses coronary collateral circulation  . Let us welcome such wonderful  reviews which keep the interest alive on the filed.

http://eurheartj.oxfordjournals.org/content/28/3/278.full.pdf+html

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All left to right shunts are  acyanotic heart disease to begin with. Cyanosis appears if there is progressive PHT and reversal of shunt .We know this happens late in ASD.(third decade)

It is important to remember some of the  patients  with large ASD  can show significant desaturation without severe pulmonary HT.  This should not be mistaken for Eisenmenger reaction.

How ?

In  any large ASD ,

  • IVC blood can stream into LA by hitting preferentially the lower part of IAS.( It is the old fetal route that heart does not forget  and indulges whenever the  local hemo-dynamics permits !)
  • During straining , (Valsalva and equivalents)  right atrial pressure can exceed LA and small amount of shunts occur across RA.
  • ASD is often (15%) associated with systemic venous anomaly. The common one is persistent LSVC.  LSVC  is usually connected to coronary sinus . If it has a communication with LA (Un-roofed CS) , there can be significant cyanosis .
  • Further , a large ASD can act as a single atrium and considerable mixing happens and cyanosis results.

Finally ,two conditions should always be considered

  • ASD if associated with VPS auguments R-L shunt .
  • TAPVC can be mistaken for Eisenmengerisation of  ASD in bedside which presents as clinical signs of ASD + Cyanosis

* It is useful to recall ,even PFOs can shunt right to left at times of extreme RA pressures like during PEEP ventilation and orthostatic  deoxia in sick ICU patients are reported (If PFO can shunt R-L , why not huge ASD ?)

Final message

Cyanosis  in ASD is not always  an ominous sign .There are few important causes other than Eisenmenger. Though it  occurs intermittently , persistent mild desaturation is also possible.

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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.

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