LV dysfunction is one of the most commonly used terminology by cardiac professionals.It can be systolic, diastolic or global, regional etc. But, before dysfunction sets in, the heart fights. The Left ventricle can behave in many different ways when confronted with stress. It increases the force of contraction, elevates it’s Intra cavitary filling pressure and still accomplishes its task of pumping adequately. Further, It can build fresh muscle (LVH). It can double up with more heartbeats. (All these factors are referred to as cardiac reserve mechanisms)
These reserve mechanisms can be activated in the short or long term. In the long term, autonomic activation with neuroendocrine factors joins the compensation process. These will work for some time till the circulatory system settles down to new homeostasis. However, they become counterproductive and becomes decompensated, ultimately heart failure sets in(Unless Intervened)
No one calls LV dilatation as a reserve or compensatory mechanism. (I wonder, why not ?) I think like RV , LV too has some potential to reversibly dilate . The quantum of which we are unable to estimate.This happens usually in response to chronic volume stress* like regurgitant valves or high output states. Though cardiomegaly and a huge heart convey a sinister outcome, many hearts shrink if the primary issue is corrected.(Typically in Anemia, Beri Berri. We also know LV may transiently dilate in response to some toxic /pregnancy-related cardiomyopathy.
* Mind you LV poorly tolerates acute volume stress as in Acute AR/MR
The critical gap in our understanding is about this question.
When does LV dilate physiologically and when pathological persistent LV dilation sets in (The absolute state of irreversibly lost cardiac elasticity.) We also know dilated LV will consume more oxygen due to enhanced wall stress (Laplace law) and hence its possible LV dilatation begets further dilatation. Optimal timing of mitral and aortic valve replacement in patients with AR and MR directly depend on this knowledge.
Final message
We need clarity in the following queries
Is LV dilatation (with normal EF ) a sign of LV dysfunction?
If so at what level of dilatation?
Since LV dilatation occurs in diastole can we fit this entity “Isolated LV dilatation” in the already confused spectrum of diastolic dysfunction?
Let us wait for the knowledge to evolve. Young cardiologists could take up this area for research.
One popular definition of Intelligence goes something like this “It’s a global capacity of a living organism to deal effectively with environment and live peacefully”
When myocytes are confronted with acute ischemia , they don’t always jitter . It expresses many behavioral pattern.The damage inflicted is variable as the molecular mechanism of ischemic tolerance appears to be a virtue ! This might make much revered time window of myocyte ischemia irrelevant .Each cell has got a unique capacity to survive or die . In chronic ischemia this myocyte intelligence and intention to survive is glaringly evident. How about this phenomenon in ACS ?
Art of survival
Why some cells die instantly , some fully recover and few go for hibernation and others are just stunned . While apoptosis is programmed cell death with intact cell membrane , hibernation can be termed as programmed cell survival .We don’t know how many intermediate forms of cell surviving mechanisms exists.
One of the famous questions is does the myocyte need blood or fuel for survival* ?
It is a fine balance of various cell surviving (Anti ) mechanism.How energy is utilised with available ATP molecules is a different science altogether .It’s possible like brain, heart too has myocardial intelligence , which does some independent thinking aided by fuzzy logic and problem solving algorithms built within.
Ignorance based ACS care
While we slog with metals inside the large coronary arteries , the response of the micro vascular territory is at the mercy of God . mRNA instructed DNA codes determine acute mitochondrial respiratory sensitization.Finally ,the successful reversal of ischemic injury depends upon the cell repair molecule’s crisis management skills !
How else one can explain , some broken hearts recover so well from a major ischemic injury others sink with first insult !
The concepts of pre and post ischemic conditioning are related phenomenon which can be pharmacologically mimicked .They are the major areas of research in myocyte revascularisation.
Final message
What is written above is pure non academic fantasy . Now, read the following article by Dr Kloner which describe the molecular mechanism of ischemia modification and its impact on clinical cardiology.
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.
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.
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
The right ventricle is considered as a docilecardiac 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 .
I stumbled upon this excellent work by Alexandru G.Fredriksson published in APS (American physiology society ) This MRI study have documented RV fucntion in a dramatic fashion.
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.
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.
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 hypertrophyin 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 !
After 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 ?
I used to tell my students ,the relationship between the heart and kidneyis 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 !
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 .
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 ?
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.
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.
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 ?
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 !
Carotid doppler
Holter monitoring and event monitors
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 )
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.
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 )
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)?
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Dr.S.Venkatesan MD 