Dr.S.Venkatesan MD

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What happens to PR Interval in Sinus bradycardia?

Posted in Uncategorized, tagged first degree av block in sinus bradycardia, pr interval in sinus bradycardia, sinus bradycardia, vagal tone in sa vs av node on September 1, 2024|

This ECG can help you find an answer .HR is 50/mt. Find the PR interval .It is also printed right there.

What happens to PR Interval in sinus Bradycardia ?

A. Remains normal

B. Prolonged but within normal

C. Prolonged beyond normal

D. Depends on the cause of Sinus bradycardia

Answer

When cardiac cycle slows down, every interval must get prolonged. PR interval is no exception. If you apply that rule the answer would be simple (Its B ).But this question has much more issues hidden into it. In this ECG it touches on the doors of first degree AV blcok. Normally PR doesn,t stretch that far in isolated benign sinus bradycardia.

Sinus rate is determined by SA nodal, funny pacemaker current(if) .The rate of which is determined by the delicate balance between sympathetic and para-sympathetic signal flux. The dynamicity of the slope of phase 4 , ie spontaneous resting membrane is another key determinant apart from sift in the density of mean P cell firing focus .(see below)

The sinus rate depends upon the cranio- caudal shift that occur within specialized tissue .(10-15mm slender the basmati rice shaped SA node)

When do PR interval prolong in sinus bradycardia ?

The commonest cause of sinus bradycardia is due to increased vagal tone . It is no secret , vagal tone do Influence AV node as much as it does the SA node . So, what can we expect ? Logically .the AV node must also slow down . But does it happen really ?

No, most of the time the AV nodal delay doesn’t not occur in sinus bradycardia . Does that mean the vagal spill over do not reach the AV node ? It does, but the fact is, the reduced heart rate attenuates the normally prevalent decremental conduction property of AV node. So we do not expect a prolonged PR in sinus bradycardia.

However, if PR interval is prolonged in sinus bradycardia , we can except silent pathological states like , sinus node dysfunction where AV node can also be affected. Also, prolongation of PR is very common in ACS situations in Infero- posterior (RCA/LCX) territory where both SA and AV nodes are simultaneously targeted.

Prolonged PR in bradycardia some times is a hemodynamic necessity as ventricular filling time is prolonged.

Clinical Implication

It is a good habit to have rapid glance at PR interval in every patient with sinus bradycardia. This will ensure a rare miss of AV nodal dysfunction .

Final message

PR interval is normal or show little prolongation in most of sinus bradycardia. If it is prolonged, without any circumstantial evidence for enhanced vagotonia , then, it could indicate some thing wrong in the conduction system. Atropine test might help us out in differentiating true vagotonia from intrinsic delay.

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Why many Ischemic VTs are not abolished by revascularization ?

Posted in Uncategorized on August 19, 2024|

Who said this non-sensible statement? ( I guess ,this would be the first response from many cardiologists !) If you feel the same, then this post might not be for you.

Relationship between Ischemia and arrhythmia

While the relationship between Ischemia and VT is really complex, the term “Ischemic VT” itself adds more twists. Its all about timing, intensity of Ischemia , associated factors and finally the baseline arrhythmic risk that includes the mystery defects in myocyte gap junctions and ion channels.

Following are some of the observations.

Primary VT

This is the true Ischemic VT. Even here, it is the associated factors, like hypoxia or acidosis are the triggers which of course are resultant of Ischemia. There are further problems . Even critical Ischemia, as in high grade unstable angina, rarely Initiate a VT, while STEMI seems to have the exclusive rights to trigger it , by its ability to produce acute transmural ischemia . (Note: Whether primary VT occurs before or after myocardial necrosis is not clear) There is evidence to prove, susceptibility to VT at times of Ischemia is in the genetic make-up of ion channels, as pointed out by famous French electrophysiologist Haïssaguerre. (NEJM 2008)

Post Infarct VT : (24 hrs to 2 weeks ,an empirical criteria we use)

This can be called as Ischemic, still we ‘wouldn’t know whether the arrhythmia is originating from dead or live tissue. It can even be combined Ischemic-Scar VT

Late Ischemic VT

These are the typical scar – substrate -mediated ,micro/macro reentry VT .The strip of tissue on the border zones of conflict (between viability and non viability is always restless (Gaza strip of VT?) This is rarely amenable to revascularization, unless some one is able make that area 0% Ischemic , which is a highly improbable scenario. The alternate option is diagonally opposite .EP guys are empowered with a deadly solution, and authorized to shoot down focus (or isolate) instead of the futility of revascularisation. (Please note, this doesn’t work and should not be attempted in early ischemic VT, though few case reports of RF ablations during VT storm li- Juan Qu et al AMJS 2924 )

Final message

The relationship between Ischemia and VT is poorly understood, (rather than to say complex.) It is true ,acute Ischemic VTs has more closer relation with Ischemia, often settles down with prompt revascularization.

In chronic VT , shooting down the ischemic focus by ablation is more likely to extinguish the arrhythmia ,rather than revascularization. This is because partial revascularization irritates the viable myocardium and keep the ischemic focus active. ( Class C evidence) ICD though a revolutionary technology to prevent a SCD in these circumstance it makes a poor choice to reduce the arrhythmic burden .At best , it is just a back up device to tackle the escaped VTs in spite of RF ablation and drugs.

Reference

1.Haïssaguerre M, Hocini M, Cheniti G, Duchateau J, Structural Alterations Underlying a Subset of Unexplained Sudden Cardiac Death. Circ Arrhythm Electrophysiol. 2018 Jul;11(7):e006120. doi: 10.1161/CIRCEP.117.006120. PMID: 30002064; PMCID: PMC7661047.

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Its time WHO,may declare CVD as a “communicable disease” equivalent

Posted in Uncategorized, tagged bmj, cvd prevention, jama network, journal of medical ethics, lancet, medical education, medicalethics, nejm, prevention quotes, sdg, sustainable development goals, who on August 5, 2024|

*Lifestyle definition

 A set of attitudes, habits, or possessions associated with a particular person or group. and such attitudes, etc, are regarded as fashionable or desirable.

Final message

Communicable disease need not be an Infectious disease like covid. The word “Communicable” shall soon convey a new meaning, to the enlightened. Adverse life styles ,disseminated into the community that vigorously propagate CVD, has every reason to be referred to as a ‘Neo non-infectious pandemic”

Postamble

In the strict sense, CVD is not a communicable disease ,rather the risk factors are …but technically it is.

Reference

1.Rippe JM. Lifestyle Strategies for Risk Factor Reduction, Prevention, and Treatment of Cardiovascular Disease. Am J Lifestyle Med. 2018 Dec 2;13(2):204-212. doi: 10.1177/1559827618812395. PMID: 30800027; PMCID: PMC6378495.

3.A comprehensive narrative review

Click to access ijerph-20-04427.pdf

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Trying to answer two casual queries on RV dysfunction

Posted in Uncategorized, tagged lv function impact on rv function, rv dilatation vs hypertrophy, rv dysfunction, tapse limitations, transverse vs longitudinal rv function on August 3, 2024|

1.What is the response of RV to pressure overload ?

A. Dilatation

B. Hypertrophy

C Both occur together

D. Hypertrophy is the Initial response, followed by dilatation

Answer :

Since we believe RV’s behavior is generally opposite to that of LV , many would tick, dilatation as the first response. This may be correct when there is acute raise in RV after load, as in PE. However, It is surprising even in chronic pulmonary hypertension , the degree of RVH is not constant and homogenous .This is because , different parts of RV chamber has different wall thickness .Further, the pressure distribution from PA to RV is uneven. The co-existing TR confounds the loading conditions. It is not yet clear, how the RV would respond to raised PA pressure. In the bed side, we are seeing both flight(dilate) ot fight (RVH) reactions from RV (more often the former than the later) It is possible RV behavior is be pre-programed and built into the genes of the contractile proteins.

It is worthwhile to note, RVH is constant feature in non pulmonary hypertension related “after-load” conditions as in valvular or sub valvular PS. This is more to do failure of regression of RV mass early after birth, rather than the actual effect of high after load. Another point is purely technical. RVH is measured in RV free wall, in subcostal view in diastole and inspiratory phase.(upper limit is 4mm) Many of us could miss RVH in routine echocardiography unless specifically looked for.

2.Which is the first echocardiographic parameter to get impaired when RV fails ?

A. RV FAC (Fractional area change)

B.TAPSE

C. RV Ejection fraction

D.RV longitudinal strain

E. RV S‘

Answer : I am not very sure about the right answer , but TAPSE is last to get Impaired .(Still, we celebrate it like anything is a different story) Many believe transverse functional Indices like FAC is impaired early. and is less influenzed by the spurious spill over of Left ventricular contractile force in transannular plane (Which augments longitudinal functional Index like TAPSE),

The following illustration (From Ref 2 ) summarizes all RV functional parameter in a succinct fashion. Fellows must be familiar with at-least half of them.( RIMP is less practical and error prone can be ignored)

Reference

1.Gorter TM, van Veldhuisen DJ, Bauersachs et al Right heart dysfunction and failure in heart failure with preserved ejection fraction: mechanisms and management. Position statement on behalf of the Heart Failure Association of the European Society of Cardiology. Eur J Heart Fail. 2018 Jan;20(1):16-37. doi: 10.1002/ejhf.1029. Epub 2017 Oct 16. PMID: 29044932.

2.Harjola VP, Mebazaa A, Celutkiene J, Bettex D, ET AL  Contemporary management of acute right ventricular failure: a statement from the Heart Failure Association and the Working Group on Pulmonary Circulation and Right Ventricular Function of the European Society of Cardiology. Eur J Heart Fail 2016; 18: 226

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Aortic dissection reporting format: Not complicated, yet comprehensive.

Posted in Uncategorized on August 2, 2024|

Though foundational and prodigious, moving beyond De-bakey ,Stanford is a necessity in the management of Aortic dissections in current times. The first step is to understand the perfect 3 dimensional anatomy of entire Aorta from its origin to bifurcation and even beyond. (The 11 or12 segment demarcation of aorta is well established and gained acceptance.)

The society of vascular surgery and society for thoracic surgery has come out with land mark nomenclature in 2020.

This labeling tells us instantly about whether the dissection is A, B, or Indeterminate .It also reveal the origin of dissection, extent of dissection and the exit point, if available.

Naming & coding of Aortic dissection

Aortic dissection : Management cues

The above scheme is just a part of Initial work up with the help of MR angiogram or spiral CT. There are more critical factors like, clinical stability, time since dissection, false vs true lumen identification, its volume ,rate of propagation, branch involvement, mal-perfusion , etc need to be counted.

The curious Irony about this dreaded entity lies in the fact that in type A dissection, the surgical team need to be alerted well before they embark on this most complex cardiovascular emergency, usually in a state of the art CTVS unit. Meanwhile, most uncomplicated type B dissection demands total inactivity on the part of surgeon(as well as some cardiologists !) while the patients can be casually shifted to the intensive care ward, essentially for monitoring , bed rest and few drugs to reduce BP and shearing stress on aortic wall. The dissection can heal themselves.

The role of Interventional cardiology in Aortic dissection is evolving rapidly , still at best supportive or can buy time to bridge to surgery in some late presenting type A dissection. There has been lot of experience in some centers, where type B dissections are exclusively managed by scaffolding. But, the concern is, catheter based Interventions in low risk subsets of dissection is always a tricky decision.

Medical strategies should never be looked down upon as enemy of endovascular Interventions. So, one of the live and debatable issue is, how & where can we fit-in the hyper-talented endovascular Interventionists in the complex vascular arena of aortic dissection.

Reference

Lombardi J.V., Hughes G.C., Appoo J.J., et al. “Society for Vascular Surgery (SVS) and Society of Thoracic Surgeons (STS) reporting standards for type B aortic dissections”. Ann Thorac Surg. 2020;109:959-981

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Two troubling medical quotes in tandem …

Posted in Uncategorized, tagged doctor patient relationship, medical ethics, patient demands, patient democracy, patient empowerment, patient rights and duties on July 28, 2024|

One

Two

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I know, we can measure “cardiac-output” accurately in two minutes by Echo, but, I rarely do it !

Posted in Uncategorized on July 18, 2024|

One of the foundational lessons in echocardiography is, How to measure the cardiac output ?

Echo formula for estimating cardiac output is

(HR X LVOT area X LVOT-VTI*)

* VTI (Velocity time Integral -a Link ) is complex sounding, but a simple parameter. It is expressed in CMs .In simple terms, it tells how many cm, the blood will move per second ? with a single ventricular contraction.

Image courtesy : http://www.pocus101.com

Sample calculation

If the normal LVOT diameter is about 2cm. Area will be πr² . Since the radius is 1cm, area will be same as value of π ie 3.14

Normal LVOT VTI is about 20 cm & HR is 70

Stroke volume = 3.14 X 20 =63 ml . Cardiac out put = 63 X 70 = 4410 ml

It can be converted to cardiac Index with body surface area.

Stroke volume measurement is not a big deal .

All currently available echo machine has automated soft ware .It beams the cardiac index live. How reliable it is ? It is as bad or as good as our trust levels. We can Imagine, how the machine vision traces the borders of LVOT. But, carefully done manually measurement is always reliable . Even then, many of us are reluctant to use echo for stroke volume . Here is an Important paper that compared cardiac output calculated by Echo with that of the the gold standard of thermo-dilution technique. Zhang Y, Wang Y, Shi J, Hua Z, Xu J. Cardiac output measurements via echocardiography versus thermodilution: A systematic review and meta-analysis. PLoS One. 2019 Oct 3;14(10)

Such a simple calculation, why is it not popular among cardiologists. ? (Many ER physicians still use it effectively )

I guess being a humble and simple, works against it. It is surprising, the awareness about EF% is all to pervasive (which is a crude and load dependent parameter) while the info about stroke volume per beat finds difficult to enter bed side cardiology. Generally, we tend to trust complex things and ready to spend ( waste) lots of time with equations, such as in PISA, EROs , DVIs , PAPIs, , stroke work etc . Mind you the probability of error increase directly with number of factors you take in a calculation

The potential bed side usage of stroke volume data

1.Cardiac Index is one of defining criteria for cardiogenic shock. I rarely see my fellows documenting LV stroke volume in any major STEMI, that can detect an impending cardiogenic shock.

2. It will help assess the efficacy of inotropes .Find, objectively how much the Dobutamine really worked in LVF ? and correlate it with clinical assessment of S3, rales and BP. (Mind you BP is very poor surrogate marker. for stroke volume. )

3. More Importantly, Similar to LV stroke volume, we can measure RV stroke volume by RVOT area x VTI x HR. This can be of critical value in the management of RV infarct, where two ventricular stroke volumes often mis-match often. Once RV stroke volume equals the LV , we can presume recovery.

4.The enigma of high output cardiac failure can be studied with this simple formula.

5.In any mechanical assisted circulation LV, stroke volume is going to give important prognostic info.

6.Finally, assessing stroke volume will aid in fluid therapy in ER with any cause of systemic hypotension.

.Final message

Its time, we concentrate & fine tune the echo derived stroke volume as a definitive circulatory volume data in day to day practice.

A request to all ER physicians and cardiology fellows, try measuring the cardiac output whenever you see patient in shock and hypotension .Make it a habit to measure the stroke volume. You need just two minutes. It is cheap, you can repeat as many times as you want in follow up. It can totally change the way you understand hemodynamics of cardiac failure and shock.

Reference

Zhang Y, Wang Y, Shi J, Hua Z, Xu J. Cardiac output measurements via echocardiography versus thermodilution: A systematic review and meta-analysis. PLoS One. 2019 Oct 3;14(10):e0222105. doi: 10.1371/journal.pone.0222105. PMID: 31581196; PMCID: PMC6776392.

Further reading

There is one more methodology, called EIT electrical Impedance tomography, that can provide live online stroke volume , comes inbuilt in ECMO and other MCS systems

da Silva Ramos FJ, et al Estimation of Stroke Volume and Stroke Volume Changes by Electrical Impedance Tomography. Anesth Analg. 2018 Jan;126(1):102

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Why tackling fake, with facts is a daunting task? but,..there is an illegitimate solution!

Posted in Uncategorized on July 12, 2024|

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Blind faith in EBM, could be an early sign of Impaired clinical wisdom.

Posted in Uncategorized on July 3, 2024|

I don’t want to do this …but EBM compels me to do it

The word “Evidence” is the most powerful in the world of science and enjoys disproportionate bias towards positivity (of course in any walk of life). But, the fact of the matter is, it can result in either monumental breakthroughs or mindless havoc to mankind in equal quantities.

EBM is not a sacred movement. It came into the medical domain in the early 1970s and grew at an unprecedented pace, invading the medical practice and literally robbing the charm & goodness in clinical medicine.In fact, many point out ,EBM is in direct conflict with Individual-based holistic medicine. If you rely only on EBM without Individual patient data, it might take you to the doorsteps of department of clinical negligence.

But, unfortunately, EBM in an unpure form has grown to gargantuan proportions and penetrated deep into medical academics. Armed with a possible legal authenticity, ignoring it, could easily push us into clutches of criminal negligence. (In fact, the opposite may be true)

Final message

Does trusting EBM too much imply a reduced wisdom?

If you offer a free pass to EBM*, to enter into all your decision-making process, then wisdom will quietly leave through the back door. Taking evidence, at its face value is going to be the biggest intellectual insufficiency or inefficiency for the future world, especially in medical science.

Further reading

Wyer PC, Silva SA. Where is the wisdom? I–a conceptual history of evidence-based medicine. J Eval Clin Pract. 2009 Dec;15(6):891-8. doi: 10.1111/j.1365-2753.2009.01323.x. PMID: 20367679.

Postamble

*I know, It is unwise to blame EBM in such a disparaging manner, rather we need to cleanse and eliminate the limitations of the EBM .That would be a more correct approach, but is it possible ? , since both appear to be built into it.

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• 

• The contents of the this blog is being published as Kindle E book , as per the request of many of the readers. Every article will continue to be open source in this site. Again I shall reiterate the book format is not aimed at any commercial intent. It is only to facilitate learning in a single book format Here is the link to book
  https://amzn.in/d/euhL5vu

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