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It looks like adult cardiologist should avoid doing pediatric echocardiograms !

February 14, 2015 by dr s venkatesan

A cardiologist  is  a physician who has  trained himself  in a special  way  to deal with any problem of heart.Ironically , it exists only on paper.The field has developed so vast  no one can master everything .There is no such  “Pan or global cardiology expert” .In fact it would be shortly become unethical to try to become one !

Pediatric cardiology  has developed into such a big field , doing a echo in newborn or  infant has become a comprehensive job and  requires  special talent .This unique  and excellent study from Narayana Institute , Bangalore published in the  prestigious Annals of pediatric cardiology   throws up interesting realities about the quality of echo report done by adult cardiologists in children .The error rate  appears  huge and stands at  prohibitive 38%. While many errors were minor , major  were also not insignificant (23%)

pediatric echocardiography by adults cardiologist

With bulk of the pediatric echo  involves  in the critical decision making  process of device closures and interventions the  data required  becomes vital .The commonest cause for  error is probably not due lack of  knowledge and but to due to lack of commitment and  continuous  exposure in doing echocardiograms in  those age group.

While this paper  decently skirts the issue of quality of pediatric echo done in medium sized hospitals without pediatric cardiology service ,I can say the error rates or inadequate reportage could be significant  in such hospitals  with apparently good ranking .

Final.message

Of course ,we have many  adult cardiologist who do  excellent  pediatric work , It looks like , as a general rule  performing pediatric echocardiograms  by non -institutionalized  adult cardiologist  may not be appropriate ! It may be wise for them to avoid doing echocardiogram in small infants with  truly complex disorders (even perceived  complex) till they gain the required expertise and confidence.

I recall an  adverse  issue happened years ago ,  when I had  missed an associated    PAPVC  in ASD that made my surgeon anxious on table .In a country like ours there is no one to audit our work , “our conscience remains the only option” to deliver the best for our patients  especially so, when they are tiny lives in distress.

After thought

Who am I to suggest  who should do echocardiogram ? , after all every cardiologist is licensed  to do that . One simple  suggestion  would be , if  not confident  they can at least mention in their report it is only  preliminary evaluation and need to be followed up with  an expert . I do that whenever its required  and gives me peace of mind as well !

More controversies* to come

Can adult cardiologist do pediatric intervention ?

* Controversy : One of the meaning for this word  is  “It is a thought  process  set into motion , that aids digging up hidden truths ”

Reference

 

Posted in bio ethics, Cardiology -Therapeutic dilemma, cardiology-ethics | Tagged , , , , , , , , | Leave a Comment »

Where is the run off in Aortic regurgitation ? Is it central or peripheral ?

February 13, 2015 by dr s venkatesan

We know aortic regurgitation causes  a deluge of   hugely popular peripheral signs of aortic run off  , which are taught  right from 2nd year medical school.

aortic runoof

When the aorta  leaks it reflects in the entire vascular tree .How is that a  leak in the remote aortic valve cause a quincke’s to and fro pulsations in the finger pulp ?

aortic-insufficiency

Is the blood in the finger  trying to follow  the regurgitant  jet  that  go back into left ventricle ? Does the to and fro murmur of  Duroziez over the  femoral artery imply  there is reversal of  blood flow in femoral artery ?

Things are  little complex than it appears

It is true the initiating event of collapsing pulse is the regurgitant jet , however the mechanism that amplifies and sustains it , lies in the altered peripheral hemodynamics.

The systemic arteriolar resistance is  dramatically low in chronic  severe AR  by a reflex phenomenon ,  as cardiac out put is increased and vascular tree adopt to it. So, with each  beat when blood is ejected two things happen in diastole .While a small fraction runs back into LV , the rest of  blood runs off , as if it goes in a free way  making all peripheral pulses dynamic , bounding and collapsible.

Hence as the name suggest all the peripheral signs of AR  are due to the peripheral mechanisms rather than primary event of aortic run off  into left ventricle.

Why carotid pulse does not show the collapsible nature of  pulse in AR  ?

If aortic leak into LV  is the dominant mechanism ,  carotid  artery should obviously manifest a collapse ,but it doesn’t  ,as carotid has no direct continuity with the  peripheral low resistance circuit

What is the hemo-dynamic  correlates of    descending  aortic flow reversal  in  severe AR ?

The central vascular tree  manifest  some  reversal till the regurgitant  velocity fades off . This can occur in severe AR, extending into certain length of aorta. This can be picked up by Doppler probe. Please realise  it is only  the wave form that get reversed  not the actual blood stream.( The momentum gained in systole  continues to push forward in-spite of the pulling back forces of regurgitation)

Why peripheral signs are  absent in acute AR ?

Acute AR even if it’s  significant does not cause a collapsing  pulse because it takes time for the peripheral vascular tree to go for vasodilatory mode.Further ,LV is also less compliant keeping the LVEDP high and regurgitant fraction low.

Summary

Answering  the title question ,the mechanism of  Aortic run off  in AR is both central and peripheral.  However  clinical  signs are largely due to high cardiac out put and the resultant   adaptive  response  of the  vascular tree due to low  systemic   vascular  resistance  triggered by  reflex  dilatation of small arterioles of the  peripheral vascular bed.

 

Posted in Aortic diseases, Aortic regurgitation, Cardiology - Clinical | Tagged , , , , | Leave a Comment »

How did rate control in atrial fibrillation easily tamed rhythm control ?

February 8, 2015 by dr s venkatesan

We have two options to manage AF.Rate or rhythm control .(Of course , in the strict sense , rhythm control also confers  rate control that is built in-situ with SR ) .There was an initial confusion which strategy would fare better .For a decade or so rhythm control was thought to be supreme. That’s logical to expect as we restore physiology in the later .” We know, medical science  often disrespects logic , and  scientists reinvent this harsh fact in regular fashion” Now , we have clear, consistent data that proved  rate control is a better strategy in most situations of AF .(AFFIRM, RACE 1 and 2 studies). The aim of treatment of AF are the following .

  1. Improve symptoms of palpitation
  2. Improve hemodynamics
  3. Reduce MVO2 and hence avoid ischemia
  4. Prevent tachycardic cardiomyopathy in the long-term
  5. Avoid stroke .

Unfortunately or fortunately rate control strategy was able to fulfill all these aims with fair degree of success. There are at-leaset  3 reasons why rhythm control fared poorly .

  1. Rhythm control is actually a myth. Only about 35 % patients  remained in SR at any time in rhythm control .Runs of transient AF can occur at  any given day* and make a mockery of the much hyped rhythm control !(*Due to heightened adrenergic tone or adverse biochemistry/ hypoxia)
  2. The drugs used to maintain SR are far more toxic . The complex EP procedures to convert to SR has not helped either.
  3. Most importantly , rate control with anticoagulants were able to achieve better  stroke reduction than rhythm control group.The reason being stroke risk was unabated even if rhythm is back to sinus,  as risk of ischemic stroke continue to emanate  from as many  sites like aorta, aortic arch and carotid. Hence, in a stroke prone population with AF  , it is the meticulous anticoagulant that’s is going to prevent strokes  rather than rhythm control .Since the rhythm  control patients would  need  to  continue anticoagulants , they lose  a  presumed logical therapeutic advantage.

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What is current status of self expanding coronary stents?

February 5, 2015 by dr s venkatesan

Originally used in early 1990s,  self expanding coronary stents (Wall stent from Boston scientific )  subsequently lost interest because of delivery related issues. Many feel , it makes cardiologist judgment tentative and delivery system prevail over our hand skills. It is possible stents can longitudinally jump with high radial force making a geographical miss more likely.While it could be true with any technique till we master it, one should recall ,most endo-vascular work other than coronary still involve self expandable techniques.

Balloon expandable  stent is ruling the PCI field  for more than 2 decades. There has been recent surge of interest in the self expanding  technique and it could make a great difference in the PCI arena provided we take the proper cues.

Self expanding stents have some unique advantage

  • It has  high radial force.
  • Approximation with lesion is best
  • It tends to take the shape of the vessel than any other stent
  • Since the mal-opposition and gap between stent and vessel wall is minimal stent thrombosis is theoretically is  lower.

Where is self expanding stent useful ?

  • Ectatic and very irregular lesions
  • Bifurcation lesions where multi dimensional vessels with different shaped ostia converge.
  • Eccentric lesions (Non calcified) may be benefited by self expanding stents
  • Self expanding covered self (Is it available >)  may be the best bet for perforations and for thrombus  to be plastied against the wall.
  • In some small vessels PCI
  • Finally it may have a  role in primary PCI (APPOSITION 1 to 5 )

What are the self expanding stents available ?

  1.  Devax system   ( 2003)
  2.  Stentys
  3.  Radius (Boston scientific)
  4. Capella Sideguard.
  5. Cardiomind Sparrow
  6. vProtect luminal shield.

Final message

For some reason , self expanding stents were not tested widely  and  large scale data is not available. However ,  they are unique modalities in metal delivery and must be mastered and many patient subsets will be benefited by it. They are not obsolete yet, APPOSITION 5 study will answer some of the issues.

Reference

1. Agostoni P, Verheye S. Novel self-expanding stent system for enhanced provisional bifurcation stenting: examination by StentBoost and intravascular ultrasound. Catheter Cardiovasc Interv 2009;73:481
2.Jsselmuiden A, Verheye S. First report on the use of a novel self-expandable stent for treatment of ST elevation myocardial infarction. Catheter Cardiovasc Interv 2009;74:850
3.Verheye S1, Grube E, Ramcharitar S, Schofer JJ,.First-in-man (FIM) study of the Stentys bifurcation stent–30 days results.

EuroIntervention. 2009 Mar;4(5):566-71
4. van Geuns  R.-J., Tamburino  C., Fajadet  J.,  Self-expanding versus balloon-expandable stents in acute myocardial infarction: results from the APPOSITION II study: Self-expanding stents in ST-segment elevatation myocardial infarctiion. J Am Coll Cardiol Intv. 2012;5:1209-1219.
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Posted in Cardiology -Interventional -PCI, Infrequently asked questions in cardiology (iFAQs) | Tagged , | Leave a Comment »

Oculo cardiac reflex : An unique neural link between the eyes and heart

February 3, 2015 by dr s venkatesan

Heart by development  originates from near  the same spot , where the brain develop (Neuralcrest) .Hence there is no surprise  to note,  heart being a primary  vascular organ still retain many neural connections with brain .Eyeballs with it’s  extensive neural inputs  can be considered as adirect extension of brain.

Oculo cardiac reflex .

When the eyeballs or the ocular muscles are manipulated or massaged slowing of heart rate can occur .This is due to  a reflex called  Oculo cardiac reflex mediated by  vagal stimulation .This phenomenon is also referred to as  Aschner phenomenon

The circuit

  • Afferent _Trigeminal branch of opthalmic nerve
  • Center- Medulla : Trigeminal  neural signal  spill over signals  to Vagal nucleus
  • Efferent- Vagus -SA node

Biochemical mediator -Acetyl choline

Prevention

  • Adequate local anesthesia
  • Retro bulbar block of ciliary ganglion
  • Prompt Atropine injection
oculo cardiac reflex

Courtesy :Indian journal of Ophthalmology

 

Clinical scenarios

  1. Opthalmic surgery : Serious bradycardia  even  asystole can occur as a rare complication especially in elderly and very young (Cataract /Squint surgery) .
  2. Cardiac events and  strokes  are clustered around opthalmic surgery in many elderly  for some unknown reason ( OCR triggered ?)
  3. OCR can unmask hidden sinus node dysfunction in elderly.Routine cardiac evaluation before eye surgery may be recommended .
  4. Orbital fracture especially Medial orbit can elicit dangerous bradycardia (BMJ Case Rep. 2014 Apr 15;2014.)
  5. Rarely sudden death has been reported (Smith R (1994). “Death and the occulocardiac reflex.”. Can J Anaesth 41 (8): 760. )
  6. OCR for termination of SVT/AVNRT : , One can use the eyeballs  to stimulate the brain stem nucleus of vagus to terminate a rapid supraventricular tachycardia (Like carotid sinus message) .Cold water immersion of eye is effective way to stimulate the vagus.(Diving  reflex -Mathews 1981)

Neural control of heart how Important it is ?

Many sudden cardiac deaths are now believed to be neurogenic in origin . Though,  somatic nerve  supply of heart is least important except over pericardium , extensive sympathetic and parasympathetic nerve supply is present . They can  now be visualized by  adrenergic receptor imaging  . Neuro cardiology is distinct developing field. A hyperbole:  Of course  one could argue , these connection has less overall significance as a person can live with an entirely new donor heart with zero neural connection with brain.

Reference

1.Lang S, Lanigan D, van der Wal M (1991). “Trigeminocardiac reflexes: maxillary and mandibular variants of the occulocardiac reflex.”. Can J Anaesth 38 (6): 757–60

2.Mathew PK (January 1981). “Diving reflex. Another method of treating paroxysmal supraventricular tachycardia”. Arch. Intern. Med. 141 (1): 22–3.

3.Borumandi F1, Rippel C, Gaggl A.BMJ Case Rep. 2014 Apr 15;2014.Orbital trauma and its impact on the heart.

 

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Discovery of Circulatory system : Sharing credits with unknown pioneers !

February 1, 2015 by dr s venkatesan

William  I am Harvey first discovered human circulatory system in the year 1628 .Published his work in  “De Motu Cordis” (otherwise known as “On the Motion of the Heart and Blood”) as a 72 page booklet in Frankfurt book fair. The world of medicine changed  forever , and new system of human circulation was born.

Read this now

Who first invented human circulation william harveyExcerpts  from   Chinese classic of Internal medicine , written  2000 years before William Harvey,

All the blood is under the jurisdiction of the heart .Twelve blood vessels are deeply hidden between the muscles and cannot be seen.Only on the outer ankles are visible because there is nothing to cover. All other blood vessels that are on the surface are  veins. The harmful effects of wind and rain enter the system first through the skin , being conveyed to the capillaries. When these are full , the blood goes in and turn empty into the big vessels .The blood current flows continuously in a circle and never stops

Post-amble

Of course , this in no way takes credit away from any body .William Harvey collected  every data on circulation available at that time , and  came with that classic De Moutu Cordis ,  the importance of which is undisputed. But ,history time and again tell us there are silent restless brains pondering over important  concepts all over the globe .Whoever has the access to scientific  facility , proves the same  point ,  publishes first and gets attention . After all thoughts are never rewarded in human domain ! (God , does it I guess  !)

Reference

1.Hume E.H Medicine in china ,old and new,American medical history 1930; 2;272-280

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Say “nay” to ICUs, we need more Intensive “human care” units !

January 26, 2015 by dr s venkatesan

As I was mulling about  the misplaced  priorities  in modern health delivery  , today’s (25-01-2015) edition  of  “The Hindu” , India’s National newspaper carries an exact article by Dr B.M.Hegde .

No doubt  ,his articles are constantly criticized  by the scientific community for  the simple reason, he is forcibly  trying to add wisdom to science !

 

 

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What to do with this curious 90% LAD obstruction ?

January 24, 2015 by dr s venkatesan

A patient with near 90% LAD disease who had a significant TMT/EST positivity with no clinical angina  was  subjected to FFR by a scientific  cardiac physician. Since FFR was recorded as  .9 , he was adviced against a stent and sent home with drugs.

Now , in the  physiological assessment of a coronary lesion ,  which one you are going to trust , TMT positivity or FFR ?

FFR  measures trans-lesional pressure drop  by creating a artificial exercise physiology  in a particular coronary bed by injecting just one of coronary vasodilators  namely Adenosine. FFR assessment can never be considered truely  physiological .There has been huge discrepancy in the amount , rate and route of administration and the hyperemic response to Adenosine.

Final message

In a single vessel disease population , if TMT is positive the lesion is to be taken as significant, irrespective of FFR.(Provided Anemia and other systemic factors are excluded )

*Read this and get ready to get  confused further , single vessel disease with TMT positivity  doesn’t mean medical management is never an option .OMT ,(optimal medical therapy ) even though a battered concept is not yet dead for SVD !

 

 

Posted in Cardiology -Interventional -PCI, Cardiology -unresolved questions, cath lab tips and tricks | Tagged , , , , | Leave a Comment »

Can you diagnose infective endocarditis without vegetations?

January 22, 2015 by dr s venkatesan

Traditionally , vegetations are sine qua- non for diagnosing Infective endocarditis.

The following  are major criteria to diagnose IE

  1. Evidence for endocardial involvement in the form of  visible vegetation or New onset regurgitant murmur.
  2. Positive blood culture

There are six minor criteria .

To diagnose IE we need

  • Two major or
  • One major and 3 minor or
  •  5 minor criteria alone

Duke criteria for infective endocarditis

 

duke_ie1

Now ,we realise  IE do  occur in the absence of visible vegetation.This happens because, vegetation can appear late, it is too  small and missed , burroughs inside tissue plane instead of entering cavity , may form  micro abscess or vegetation growth is prevented by prompt empirical antibiotics.

Final message

Vegetation is still a prime sign  to diagnosis of IE. However , please do not insist  on it .There can be significant endocardial infection  without formation of vegetation.The current criteria allows us to make a diagnosis of IE without documenting a clear cut visible vegetation.

 

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Cervical Angina : An under-diagnosed entity !

January 11, 2015 by dr s venkatesan

We know cardiac pain is often  referred to Jaw and neck .

What prevents the neck pain of cervical spinal disease to be referred over the  heart ? Can pure spinal lesions mimic angina ?

The answer seems to be “Yes” . The neuronal  circuit is  there .Only , the traffic has to be reversed. Medical logic is always puzzling. There is indeed an entity called cervical angina.

The cardiac pain  can be  referred any where between  dermatomes  C3 to T 10 It is generally  believed cervical radicular pain  can go only one way . . . ie towards the nape of neck and  arms .Dermatomal overlap ,neural cross talks  thalamic inputs and cortical  reflection and perception always make the subject of referred pain too  complex.

Now,It seems possible ,the neck  pain can  spill over into the anterior chest wall ,mimicking  angina .Imagine the  confusion  if the patient  has both  cardiac and cervical entities ! Does the pain signals from the two sites  collide in the local spinal network ? Does one extinguish or amplify the other ?

 

refered pain

This article which was published  in the Spinal Cord .

cervical angina reverse referral pain

Read also linked angina

http://www.nature.com/sc/journal/v44/n8/pdf/3101888a.pdf

 1.Guler Net al.Acute ECG changes and chest pain induced by neck motion in patients with cervical hernia: a case report. Angiology 2000; 51:861–865.
2.Wells P. Cervical angina.Am Fam Physician1997;55 2262–2264.
3.Jacobs B. Cervical angina. NY State J Med 1990;90: 8–11.
 4.Baba H et al. Late radiographic findings after anterior cervical fusion for spondylotic myeloradiculopathy. spine 1993;18: 2167–2173.

Posted in Chest pain, Clinical cardiology | Tagged , , , , | 2 Comments »

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