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Wish to take a break from covidology … with this birdy !

Posted in Uncategorized on July 5, 2021|

“Third wave? what is that”

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Acute pulmonary edema: Come’on let us blame it on Right ventricle

Posted in Uncategorized on July 2, 2021|

Basic science lessons are promptly forgotten by the time we reach the final year of medical school. How about recalling them decades into clinical practice ? The mechanism of systemic edema revolves around the interplay between hydrostatic pressure, colloid pressure, interstitial pressure. However, In the pulmonary circuit, it gets a little more complex. Acute pulmonary edema begins to occur at around 18mmhg  PCWP. What is special about this number 18? Nothing great. The lung begins to ooze when the LVEDP/LA mean pressure exceeds the colloid osmotic pressure, (that keeps fluid in situ) within the pulmonary capillaries, which is about 18mmhg. Interstitial fluid begins to collect as the basal rales go onto develop frank alveolar edema at 25mmhg. Of course, chronic situations like mitral stenosis both lymphatic reserve and thickened interstitial fibrotic process keep threshold still higher) 

To simplify, whatever be the mechanism on the left heart, during acute pulmonary edema for the lungs to get flooded, we need a well-functioning right ventricle. If only the RV has enough wisdom*, it should take the cue and slow down and help the LV out by reducing its preload. (RV’s afterload is LV’s preload right )

We know, the lungs are protected from congestion in a number of chronic right ventricular diseases, pericardial disorders, severe PH. This happens in RV infarction. This lung-protective effect might explain the heterogeneous nature of outcome in RVMI (bad to excellent) 

Final message

We know, the commonest cause of pulmonary edema is due to acute LVF. Now add one more mechanism in the genesis/and or maintenance of pulmonary edema. Vigorously contracting, RV is equally culpable. 

Here is an Important paper that discusses the key role of RV in the precipitation of acute pulmonary edema.

Download

Some more questions relevant to this topic

1.What is the effect of RV dysfunction on paroxysmal nocturnal dyspnea & orthopnea? 

2.Explain class 3 Forrester’s hemodynamic grading of acute MI. (Why PCWP goes down in grade 3 compared to grade 2?)

 

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MDM of mitral stenosis is a “mid diastolic misnomer”

Posted in Auscultation, Cardiology - Clinical, Clinical cardiology, Mitral stenosis, Uncategorized, tagged , , , , , , , , , on June 23, 2021|

Nearly a century ago, Carl Wiggers helped us understand the dynamics of cardiac cycle with a historical diagram depicting systole and diastole. We know diastole has 4 phases. They are  IVRT(nil)  early rapid filling,(70%) diastasis,(0-5%) atrial contraction(25%) (Percentage filling within the brackets)

What is mid diastole?

The easiest way to define mid diastole is to divide diastole into three parts with reference to time and call the mid-third as mid-diastole. (.5 seconds/ divided by 3). But, Physiologically we can’t do that. Even hemodynamically there is no distinct mid diastole as diastole is divided into 4 phases as described earlier. When there are 4 parts how can we slice out mid diastole without an overlap? 

So, what shall we do? Technically which is the best period to be referred to as mid diastole?

Maybe diastasis. In this period either little or no flow occurs. HR heavily influence the duration of diastasis. Cardiologists especially during auscultation created the concept of calling anything happening after mitral valve opening as mid diastole. ie after IVRT which equals* A2-MV opening interval (In the true sense,  it must be the early diastole that can begin with mitral valve opening for physiologists, but for cardiologists, it begins with aortic valve closure because we can hear only closing sounds)

What happens in mitral stenosis? 

Any significant obstruction of the mitral valve, the gradient builds up immediately after the mitral valve opens. The murmur gains momentum in the early rapid filling phase of diastole, gradient spills over to fill the diastasis, and finally accelerates in pre-systole to end up in loud S 1.

 Is there really an early diastolic murmur in mitral stenosis?

  (I can’t agree. We were never taught that way)

Yes for sure. In fact, it can be the dominant murmur in many, since the early rapid filling phase of diastole contributes 70% of filling. In mitral stenosis, the early diastolic gradient will always be present. So. mitral stenosis murmur indeed begins in early diastole and extends further depending upon the severity.

If there is really an EDM in mitral stenosis, why do we still keep calling it MDM?  

Just by tradition and for convenience. Auscultatory mid-diastole is different from hemodynamic mid diastole. This irony occurs because murmur descriptions are based not on time but on phases. So, by convention, a murmur that does not occupy the IVRT phase is labeled as MDM. This also helps us to differentiate MDM of mitral stenosis from aortic regurgitation which has the exclusive rights to be called an early diastolic murmur.(Since it occupies the IVRT phase) 

Final message

This is probably a too-long post to unmask a trivial nomenclature issue in the diastolic murmur of mitral stenosis. Still, it’s worthwhile to understand this. The word “mid in MDM” is arbitrarily used and doesn’t really reflect either the time or the true hemodynamics. In fact, the same reasoning is applicable for any flow murmur across the mitral valve that is inappropriately referred to as MDM. 

Caution  

*Let me not confuse the youngsters especially undergraduates. MDM of mitral stenosis will remain as MDM in exam halls. It will never become EDM as that of AR where the murmur starts in the IVRT phase. 

 

For advanced readers

What is the earliest murmur to appear in mitral stenosis?

The first noise comes in the early part of diastole or late presystolic when atria contracts. Never in true mid diastole and gets filled up the in mid part as the disease progresses. So, we can have mitral stenosis without murmur in mid diastole. The morphology of murmur can best be understood when we correlate with Doppler echo profiles.

Is MDM of mitral stenosis crescendo or decresedo or both ?

Normally in diastole crescendo murmurs are uncommon as pressures are falling.( Ventricular contraction only can generate crescendo pressures.) Still, In mitral stenosis, there is minimal crescendo at the onset even when the  E velocity decelerates. However, there is a definite presystolic accentuation with atrial contraction which can also be referred to as late diastolic crescendo. 

*Is IVRT the same as the A2-OS interval? 

It is almost the same but not the same. Find out the difference.

 

Further reading

ongley1955

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Democrazy in science needs some attention

Posted in Uncategorized, tagged , , on June 19, 2021|

 

 

Further reading 

Here is a book from Dr. Ralf Sundberg, a former general and transplant surgeon, a prolific researcher from the prestigious Karolinska Institue, is trying hard to spill some not-so-sweet truths. A must-read, especially for the heavily biased optimistic scientists.

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An Illustration of Aorta-PA relation in Normal, D-TGV & L-TGV

Posted in congenital heart disease, Embryology : Heart valve development, embryology of heart, Uncategorized, tagged , , , , , , , , , , , , on June 12, 2021|

The relationship between Aorta & PA is the key to diagnose many complex congenital heart diseases. Here is a simplified illustration for gross understanding. Please refer to other sources for complete review.

 

Further reading

CONGENITAL HEART DISEASE| VOLUME 118, ISSUE 9, P1390-1398, What Determines Whether the Great Arteries Are Normally or Abnormally Related?   https://doi.org/10.1016/j.amjcard.2016.07.050

 

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Fighting the pandemic : Real war is not against Corona as such !

Posted in Uncategorized on June 8, 2021|

Caution: Some language 

News

It is heartening to note the apex body that is leading the fight against Covid in India, has responded well. It has either recalled or censured many of the Investigations & drugs, procedures that were used in this pandemic. (Not because they are futile, but they also resulted in a meaningless escalation of cost and possibly worsened the outcome)

So, what?

Beware, “non-scientific mutations” are common in medical research even in ordinary times. It is omnipresent now, and no surprise they end up as a premature evidence base. The consequences of this can be as adverse as the viral variants we fear. The global economic drain of this pandemic is definitely more than what it really deserves. The bulk of resources consumed by Remdesviers, Tociluzumabs, Ivermectins, etc. will easily cross few billions. Further, it is estimated 100s of millions were spent on Indiscriminate diagnostics like CT scans and, Interleukins, D dimers, and even RTPCRs that made a mountain out of a mole. Infinite doses of antibiotics are diligently prescribed for a viral disease knowing fully well it won’t work. One estimate In India says 800 crores worth of Zinc and vitamins were sold over the counter. (The same budget for 1000 bedded state of art hospital!) Heartless marketing. It was painful to watch hard-earned savings was siphoned from not so wealthy & poor for a simple hospital stay.

 It must be acknowledged the Government (both state and central) is doing an exemplary job taking care of both private and public health against all odds. However, on a global scale, It is unfortunate many Governments of low GDP countries were politically compelled to spend on flimsy interventions for a self-expiring pandemic. If only these funds are diverted properly, that would help us build permanent health Infrastructure in each of the underdeveloped districts. The only thing, that’s worthy to spend now, is towards the largescale manufacturing of a quality vaccine. Health economists from WHO shall genuinely audit the global expenditure of this pandemic that will help tackle future pandemics better.

(In)conclusion

The virus has decided to play its own game with humanity for whatever reason. The great news is that the vaccine is working. We hope the virus will show enough mercy and leave us shortly. Please follow the required covid hygiene and learn to live in a  personal lockdown mode so that countries need not shut down. Meanwhile, a strict embargo on excessive covid related information in the public domain seems as critical as the vaccine. (the demarcation between true knowledge and misinformation is as blurred as one could Imagine)

Postamble 

Wishing for a  smooth landing with abundant common sense (Image courtesy TIME magazine )

Happy days will be here again soon. But, never forget the harsh lessons taught by this tiny virus .“We must learn to cohabitate on this planet along with other lives peacefully. If we are adamant, God is likely to lose his patience and may not hesitate to discard us permanently “

 

 

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3-D printing of heart : Moving from the labs to bed side

Posted in Uncategorized, tagged , , , , , on June 3, 2021|

3D printing technology is growing at a rapid pace. Both cardiologists and cardiac surgeons are expected to benefit a lot.It helps us in understanding deformed anatomy in complex congenital heart disease as well as planning for synthetic cardiac implants. 

Currently, the technology is limited only by the chemical material used to print the heart and its components. The American chemical society is working at it to create more realistic heart models. Once we master this,  biological printing with synthetic tissue equivalents is the ultimate aim. 

Major Indications

  • Planning cardiac reconstructive surgeries in congenital heart disease. 
  • Aortic grafts in Marfan syndrome and other endovascular grafts.
  • Valve prototyping

What could be possible in the future?

A dream possibility is that, 3D printing of a patient’s own coronary artery that is diseased with an exact replica that may either act as a surgical graft or deliverable percutaneously.

It is 3D cloning of a coronary artery with a live blood flow experimental setting.(Image clipped from above video)

Final message

It is a merger of biology, chemistry, tissue engineering, and computing. Already it is used in specific conditions.(How about ordering a designer RVOT in severe TOF ?) We are approaching fascinating times in cardiology. Of course, everything would come at a price. We can reap the benefits of this path-breaking progress in science, if and only if, technology is regulated well, Indications are liberally coated with common sense.

Reference

A review article on 3D printing in cardiology Nature review 

Giannopoulos 2016

 

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Who is going to save medical science from “peer reviewed” madness ?

Posted in Uncategorized, tagged , , , , , , , , , , on May 30, 2021|

This 90-second video clip is a “perfect provocation”

Allan Savory  is a renowned ecologist from Africa. He is a global leader in environment and eco protection. He is making this famous comment, during one of his interviews from the deep forests of Zimbabwe, after years of ground-level work in the field of desertification and climate change. I can understand his feelings, as we also encounter similar situations at ground zero of the health care delivery system. (I wonder if there is anything called peer-reviewed bedside caring)

We realize wide gaps between academia, patient care, and research are the norm, not an exception. One reason for this is, even well-learned medical professionals find it difficult to comprehend, that the practice of medicine is essentially an art, administered with love, care, service-mindedness. A cost-effective infrastructure with an immense amount of teamwork is critical ( Of course, guided by a fair amount of knowledge, expertise based on good scientific principles)  

Final message 

As Savory says, let us hope, the future looks bright, that welcomes young researchers from the fringes of the scientific community. Let them be conferred with all courage and resources to course-correct medical science from its frequent aberrant and awkward turns.

 

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Coronary physiology update : Why did the “French FLOWER” failed to blossom ?

Posted in Uncategorized, tagged , , on May 20, 2021|

The concept of Fractional flow reserve ( FFR) has dominated the coronary interventional field for over a decade. It gave us a (false) sense of security and pride that we have been advocating physiology-based appropriate stenting.

The much-expected FlOWER-MI trial was presented in ACC & NEJM a week ago. (May 16th  Issue 2021)

FFR, though physiologically an attractive concept, has many well-known confounders right from the technical factors, lesion-related errors in physics, mirage of true hyperemia induction with Adenosine, finally & most importantly microvascular dynamism. The value of FFR in the ACS setting was always a suspect. So, no surprises with the FLOWER trial conclusion. It has concluded FFR guided interventions in the non-IRA vessels following STEMI had no use in terms of the hard endpoint. Lesson: We can’t really expect true coronary physiology rules to be alive when severe pathology has set in)

Wait, there can be quixotic ways to Interpret this study be as well.

FLOWER trial reveals the number of stents used with FFR guidance was 50% less (mean 1.01 vs 1.5 stents). Though there was no difference in deaths, the incidence of nonfatal myocardial infarction was more in FFR group 18 (3.1%)  than the non-FFR group (1.7% ). Similarly, unplanned hospitalization leading to urgent revascularization was more in FFR  (2.6%)  than non-FFR (1.9%). Though all were not stat significant, FFR has helped reduce the number of stents in non-culprit lesions. Still,  recurrent non-fatal MI and urgent revascularisation were high in the FFR group. So, is it possible FFR related procedural hazards are real? Who can (& how) quantify that? or Is it Inappropriate non-stenting due to FFR misguidance responsible for this trend?

There is one more risk with the potential demise of FFR as a concept. Extreme scientists, might ditch physiology to the backyard and go for free for all stenting again. (Back to shadow physiology & oculocardiac reflex) 

Final message

There is an extrapolated lesson to be learned from DEFER*/ FLOWER trial combo. FFR or no FFR, never touch the non-IRA lesions in stable STEMI* however tempting it may be. (*This rule applies even in some unstable STEMIs (Please recall Culprit shock trial ) 

*DEFER 15 year follow up EHJ 2015 ( Note : DEFER contain significant non ACS population)

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Cerebral hemodynamics in AF :”Irregularly irregular” brain perfusion and risk of “dementia cordis”

Posted in Uncategorized, tagged , , , , on May 4, 2021| 1 Comment »

No doubt, the heart is a biological wonder with its non-stop pump function. Still, it cannot function as a continuous rotary pump like the electrical motors do. It has no other option but to contract in a pulsatile manner. However, the mean pressure in circulation is fairly constant, flow is kept continuous, and fairly laminar. This is made possible by the built-in elastic pressure in the aorta and the poorly understood but vitally important parameter vascular tone. Aging widens the pulse pressure due to dissipation of vascular tone. Atrial fibrillation adds new bizarre dynamism to this pulsatility and challenges the aortic wall’s competence and compliance further. This is the basic mechanism behind the classical description of an irregularly irregular pulse in AF. The pulse can be  so unpredictable, it was originally referred to as acute confusional status of heart (Delirium cordis)

What is the effect of AF on systolic, diastolic, and mean blood pressure?

In AF systolic BP varies considerably from beat to beat. Diastolic BP does show some changes but less obvious. So far mean pressure fluctuations in AF have not been given much significance.  

Clinical significance of AF on the brain: Thinking beyond stroke 

From a stroke perspective rate and rhythm control did not show much difference. The prime reason for AFFIRM  trial not showing benefit with rhythm control was embolic stroke was much more common from sources other than left atrium proper and hence the usage of oral anticoagulants was more important than rhythm control in overall stroke control. 

Now, an important study trying to look at this hitherto ignored aspect( Andrea Saglietto,  EP Europace, 2021). It raises concern about the impact of AF on long-term cerebral function. Should we restart the debate in favor of rhythm control? No doubt, the pulmonary venous electrophysiologists will be too glad to welcome this concept.

Now, we have new evidence based on near-infrared spectroscopy AF does cause unpredictable beat-to-beat changes in cerebral microcirculation that leads to neurocognitive dysfunction. It is possible there can be a breach in cerebral autoregulation limits in a significant number of post-long RR  beats. We may soon look forward to a new entity of “dementia cordis“as a sequel to chronic AF.  

 

Reference

1.Andrea Saglietto, Stefania Scarsoglio, Daniela Canova, et al Increased beat-to-beat variability of cerebral microcirculatory perfusion during atrial fibrillation: a near-infrared spectroscopy study, EP Europace, 2021;, euab070, 

2.Atrial Fibrillation, Cognitive Decline and Dementia Alvaro Alonsocorresponding author Eur Cardiol. 2016 Aug; 11(1): 49–53. doi: 10.15420/ecr.2016:13:2

 

 

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