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We can consider Jugular veins of the neck as a naturally present right heart catheter. It faithfully reflects the live pressure and waveform data  from right atrium and ventricle .

Can JVP tell us anything about left heart pressures? Is there any relationship between JVP and PCWP or LVEDP ?

If you tell JVP reflects LV filling pressure in any graduate medical exams, you will be admonished. However in DM or post-doctoral exam, if you say there is no link between the two, you are likely to be chided.(It is unfortunate the answers vary depending upon the level of training , which I feel is not academically correct )

Though the JVP-PCWP link, apparently appears Illogical, it does  have a scientific basis. It is true, there is a huge (& multiple) anatomical barriers between the left heart and Jugular vein in the form of pulmonary arterial & venous circuits, the right ventricle and right atrium.Still ,the hemodynamic principles demand, whenever left heart filling pressure increases, the right heart pressure should increase correspondingly to drive the blood from RV across the pulmonary circuit.This raise should be in the mean pressure. (or diastolic pressure,) it’s rarely related to systolic pressures as RV systole normally generate more than twice or thrice the LVEDP.

 

This driving pressure across the lungs  is called the transpulmonary gradient. (PA mean minus LA mean) The normal being < 7mmHg. So if there is a sudden increase in LV filling pressure to 20mmhg, there has to be elevated right heart pressures.(20 +7) This will be reflected in JVP as well. So patients with acute diastolic heart failure as in HFpEF must show elevated JVP. This can be documented elegantly In patients with positive responses during diastolic stress testing.  (JACC: Cardiovascular Imaging 

There are important caveats in JVP-PCWP link

  • If the PH is long-standing and precapillary (Reactive PAH) has set in the right heart pressure will no longer reflect the PCWP.
  • If there is any organic Tricuspid valve disease (Both TR/TS) JVP can reflect PCWP.
  • Finally, any cause of RV dysfunction will immediately elevate the JVP so biventricular dysfunction makes correlation of JVP with PCWP meaningless.(Acute pulmonary embolism, and RV infarction)
  • Further confounding can occur if we contemplate RV diastolic dysfunction as seperate entity. (At what level of RV systolic dysfunction, does the RVEDP begin to raise ? I think we don’t have an answer for this . Researchers please note.)

Some more mechanisms of elevated JVP with left heart disease

  • Bernheim’s effect and ventricular interdependence can make JVP elevated spuriously without elevating PCWP.
  • Acute mitral regurgitation left atrial V waves can “tide-back” all the way to PA and the right heart to elevate the JVP
  • In ASD and Lutembachers syndrome  the RA pressure waveforms may reflect the LV filling pressure, though inconsistently.
  • Finally, and importantly in Fontan circuit JVP may exactly reflect the left heart pressure for the obvious reason, as SVC is connected to the pulmonary artery directly.

Final message

JVP will always tell what is happening to the right heart chambers only . It can, no way be taken as a direct marker of PCWP/LVEDP. However, there can be a correlation between JVP and PCWP/LVEDP in a certain subset of cardiac failure. (As in exclusive isolated left heart failure (typically HFpEF) the elevated JVP might just reflect the elevated LEDP provided there is normal RV function )

Reference

1.This study elegantly shows a correlation (or lack of it) in different subsets of heart failure. It tells us very clearly If JVP(RAP) is not correlating or disproportionate to PCWP, it implies RV dysfunction.

2. This paper suggests a really useful scheme to classify heart failure as concordant and discordant with reference to right and left heart.

It throws some interesting facts. I guess it will help us guide diuretic management and prognosticate chronic heart failure.

Covid has struck hard and this time it has consumed one of the Doyens of Neurology, from Coimbatore, India –Dr.M.B.Pranesh. Privileged to have him as my professor in Coimbatore medical college, my alma mater, watched him in close quarters during my undergraduate and MD days in the late 1980s.

Still recall, how he empathizes with the patient and their family in distress, practiced medicine in the best scientific manner at the same time with a humane and philosophical touch. I can’t forget, how the little genius standing beside the comatose patients In IMCU and tells so precisely the difference between metabolic vs structural coma without even asking for a CT or MRI scan.(We learned with awe, for the first time, how hyponatremia can cause havoc to the brain)  I have seen him so tired in many days and sleeping in the ward chair for a few minutes and comes back fresh for the rounds. He used to say sleep is a luxury in our profession. What a statement to make for our generation next.

His favorite quotes are from William Osler and ask us to read the life history Harvey Cushings. He encouraged us, to learn the history of medicine. He was so emphatic to say “Unless we know how our past physicians toiled with their astuteness and hard work, we will not understand the value of clinical medicine”

 

One of the pure souls who showed us what is the true meaning of teaching, learning, and caring. Got this small clip, wherein he continues to wish us good.

Let his legacy live forever. 

 

 

 

His bundle pacing is the new kid in EP lab. It involves exploration of few 3-dimensional cubic areas of His bundle (4-6mm³ ? ) in the crest of the IVS looking for optimal His pacing site. It aims to provide better recruitment of His Purkinje and hence more synchronous pacing. Still, the modality is in the early stages and has few key limitations. They are, requirement of very specialised leads,(Select Secure™ 3830 , Medtronic) lead instability (Susceptible to RV ejectile forces*), high threshold, and lower battery life and finally uncertainty of distal bundle disease. A need for temporary RV back up the leads in some centers will tell us how confident we are, about the concept of his bundle pacing.

The success rate of HPB pacing has not reached the desired levels.Meanwhile, the area His bundle lead explores is so thin and delicate that requires working around membranous septum. No surprise, a new adverse event is reported.  Yes, the first case of acquired VSD reported following his bundle pacing. (Ref 1)

Now, experts are moving down in the septum to capture LBBB to avoid the above-said limitations of HBP. I will not be surprised we ultimately reach the RV apex , the good old destination again, for absolute safety and stability.

*RV leads are naturally isolated and not much affected by RV contractile hemodynamics

Final message

Wish the concerns about His pacing are exaggerated , best of luck for this new mode of pacing. Medtronic is a pioneer and has a long passionate history. After all, cardiac pacing is one of their top Innovation in cardiology in the last century that made a huge impact in the management of electrical ailments of the heart.

Reference

 

 


 

Got it? One clue, you are part of these numbers! It crossed  5 million reads recently across 160 countries. Thanks. I know,It amounts to self-promotion. Such boosters are required when energy level sags. Sorry.

*The post is not meant for those who understood GLS (Global longitudinal  strain) in a proper perspective. I am writing this, after a surprising answer from many students of Echocardiography, when I asked them what is GLS?  Most answered, GLS currently is the best global LV functional index available. What a misunderstanding? The fact is, EF % will always be the best global parameter*, while GLS remains a regional function index.(*The limitation of EF% is in the methods of measuring it and not in EF itself.)

                                   We are trying hard to ditch LV EF%  by Teichholz’s / even 2D Simpson method, as they are considered a crude way to measure global LV function. Unfortunately, we are doing this without a credible alternative. GLS is being promoted as the next best. The normal GLS is around(-20 ± 2) . Nothing is perfect. Best global LV function probably can be achieved by 3D Voxel Echo/MRI)

Normal GLS with various machines

Please note, the bullseye 17 segment model though brings an illusion of a radial perspective of cardiac contraction, its purely longitudinal stain represented in short axis format.

The much popular GLS (Global longitudinal stain ) is a poor surrogate for global function. The word global is apparently misguiding and conveys a false message. When we refer to GLS, it is an adjective for longitudinal function and nothing to do with overall global LV function. (Though we have many studies to show it has good correlation with global LV function).

The longitudinal function is presumed to contribute 60 % of LV function.  This means GLS is at best 60 % accurate in determining global LV function. Mind you, the heart doesn’t work in a longitudinal plane alone. The muscle fibers of heart are arranged in three distinct fashion (LOC) subendocardial- longitudinal,  Mid-oblique, & Sub epicardial -concentric (Remember LOC ) Each fiber either lengthens or shortens.

The left ventricle not only shortens longitudinally, It also contracts radially, shrinks circumferentially, rotates clockwise at the base (5-10º) , counter rotates at apex (Up to 60º) twist,  & un-twists.  It’s worth reminding ourselves, we are ignoring all these components and happy to fall for GLS.

What can be done to improve the accuracy of true global strain?

The simplest way is, to look LV in  short-axis by 2D and confirm everything is okay with radial contractile forces and deformation. Mind you, the most accurate tool to measure stain is the good old M mode with undisputed temporal (time) resolution ad frame rate the M mode thickening best deformation parameter to measure radial stain ( at a particular plane though).

Is the measurement of true global strain possible?  (GLS+ GRS)

Probably yes. What about GLS plus GRS (Global radial strain)  GLS measured by speckle + RS (Radial thickening by 2D/aided by M Mode)  We are working on a project where the radial strain component is added to GLS. Roughly, it should pull the negative GLS  beyond + 20  (If we assume GRS is + 30 to 60 ) This should be correlated with 3D voxel Echo  /MRI .

Final message

Beware,The “G in GLS” is a perfect miscommunicator. * GLS  can never reflect global LV function. If EF% by M-mode was criticized, for measuring only one aspect of cardiac function ie radial, the same would apply for GLS, in that it measures only longitudinal function. Never discard M mode/2D. It still, pours unadulterated ultrasonic data from myocardial contractile units in the highest resolution. We should continue to use it. In the name of modernity, we make it look outdated.

Reference

M S Amzulescu, M De Craene, H Langet, A Pasquet, D Vancraeynest, A C Pouleur, J L Vanoverschelde, B L Gerber, Myocardial strain imaging: review of general principles, validation, and sources of discrepancies, European Heart Journal – Cardiovascular Imaging, Volume 20, Issue 6, June 2019, Pages 605–619, https://doi.org/10.1093/ehjci/jez041

*

 

Truely a great demonstration of life saving Mitra clip procedure.

Found this from

Can a bedside echocardiogram help rule out STEMI in patients with suspicious ECG?

No, it can’t  (Though, it may be tempting to use a rapid echo to look for wall motion defect to rule out ACS ) 

If your answer is No, probably you don’t need to read any further in this post.

Diagnosis of STEMI* is based on

  1. Clinical
  2. ECG
  3. Bio-Markers

*Please note, two of the most popular investigations namely Echo and Coronary angiogram are missing in the list.

A middle-aged man with  chest pain.  Can an echocardiogram help you confirm  STEMI here? Most likely not. It may still be an evolving STEMI. But, observation, serial ECGs, and Troponin is the answer. (ECG -Source http://www.emdocs.net/hyperacute-t-waves/ )

Though, echocardiography, a great noninvasive imaging tool at the point of care, it stands almost helpless in the diagnosis of the commonest cardiac emergency ie ACS. It can be called as mother of all paradox even visualizing the myocardium directly with high-quality imaging will not tell you, whether there is ongoing ACS or not. 

Relying on wall motion defects without diagnostic ECG changes to diagnose STEMI  can be misleading for the simple reason, both unstable angina and old MI can be a 100 % confounding effect. Similarly, absence of WMA doesn’t rule out an evolving STEM(Apart from the bizarre behavior of   Ischemic cascade,  In the early hours only subendocardial wall stress is noted, that is not good enough to cause visible WMA)

Role of CAG in the diagnosis of STEMI

Urgent CAG is an easy way out in confusing coronary conundrums. But, unless you know the background info even a CTO can be mistaken for ATO/ STEMI . So it is essentially new ST/T  shifts (corroborated with CAG) will be the guiding force. 

Final message 

The humble Clinical examination and ECG will prevail over all other modalities in the diagnosis of ACS. Mind you, ECG findings are built within the diagnosis of myocardial infarction ie STEMI (ST-segment) so can’t diagnose it with  Echo. Further, an indication of thrombolysis or PCI goes with ECG finding only.

Counterpoint

*Having said that, there is a key role for echocardiography in the ER to diagnose alternate cardiac emergencies like Aortic dissection, Acute pulmonary embolism or ACS mimickers like HOCM, etc. Further, echocardiography is used in a big way,  in the risk stratification or identifying complication during the ACS management.

Exceptions

In patients with atypical presentations, pacemaker rhythms, LBBB, especially elderly, comorbid, ECG can be quiet normal or non-diagnostic. Here, echo and angiogram may have some adjunct diagnostic roles.

What about newer echo Imaging modalities?

** There has been a suggestion, that regression of Global longitudinal strain(GLS) or new-onset regional loss of myocardial strain, detected by speckle tracked echo is a powerful and the earliest sign of myocardial ischemia.

A potential tool to rule out ACS by Echo -Global /Regional longitudinal strain (GLS) still trailing behind ECG.

 

GLS is proposed to be used in coronary units to rule out ACS. In spite of its Initial promise, we understand it has not been accurate enough to be included as criteria to diagnose ACS . So, as of now, it appears unlikely for echo criteria to be included in the  diagnose of STEMI.

Who is a doctor?  Where are they made?

I haven’t clearly understood the true meaning of customary Dr tag, my name carries for more than 3 decades, till I saw this. Wish, this video is played to all young medical students on their graduation day.

             I am realizing with guilt, it requires a Holywood movie buff to remind us the true meaning of the famous WHO – definition of Health, done in the most holistic fashion in the year 1948. 

Health is a state of complete physical, mental, and social well-being and not merely the absence of disease or infirmity.

So, technically, whoever serves to improve these three components and alleviate human suffering becomes a doctor. 

Happy to share this on July 1st, the official Doctor’s day in India in memory of the Bharat Ratna Dr.B.C.Roy of Bengal. 

Reference

The clip is from the movie Patch Adams, Directed by Tom Shadyac.  A Hollywood celebrity movie maker, Virginian professor of communication turned philanthropist, now retired to a minimalist life. He is also known for his famous documentary I am that talks about the problems faced by the world. Though his works are much appreciated, I  must say, they are underrated. Deserves more than an Oscar for communicating his thoughts on the medical profession perfectly and for social equality.

 

 

 

 

 

 

 

It’s halfway way through 2020 , still miles to go.

Welcome to a non academic break.This 3 minutes video definitley helped, amidst the paronia.

 

Wish, we can retire peacefully and join this family.

That’s how the title sounded to me, when I happened to read this paper from the reputed Circulation journal.

Even in the serene non-covid days, primary PCI rate in most countries is at best 10 % and thrombolysis* is the only savior in STEMI.(*with or without Pharmaco Invasvive )

It’s Covid times you know, can’t take science for a ride. Let us all take a pledge, in this deadly pandemic to increase pPCI rate to atleast 50% and ditch that dedicated, trustworthy , uncomplicated all weather friend !

Reference

https://www.ahajournals.org/doi/10.1161/CIRCOUTCOMES.120.006885