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Pulse rate in ventricular bi-geminy : A missing link ?

February 17, 2015 by dr s venkatesan

ecg pulse deficit biventricular bigeminy

 

Answer : Most probably  B .

What we feel in peripheral pulse ,  is one weak and the one strong beat in sequence .The later is due to post VPD potentiation. Since there is a compensatory pause , ECG rate (Number of QRS complexes /mt)  and pulse rate are same .

Ironically , heart rate and ECG rate are not same as VPDs impact mitral valve more than aortic valve  and cause additional  S 1 than S 2 making heart rate considerably more than pulse rate and logically it must be  double the pulse rate . This may be difficult to  appreciate by auscultation, but can be documented by phono-cardiogram or by M mode echocardiogram.

 

 

 

Posted in Auscultation, Cardiology -unresolved questions | Tagged , , , , , , , , , | Leave a Comment »

Determinants of gradient across coarctation of Aorta

February 16, 2015 by dr s venkatesan

The gradient across coarctation  is not  simply (& solely ) determined by degree of obstruction , as one would believe.Understanding the hemodynamics and various factors that can influence the gradient is essential Relieving the  obstruction /gradient by stent or surgery  may not be synonymous with successful treatment as we understand now the entire aorta right from the root to abdomen can influence the gradient ,along with systemic factors.We also know , some of these patients harbor histological abnormalities in the entire stretch of  Aorta , what is  being  referred to as pan aortopathy  , that may influence the long-term outcome.

coarctation gradient collaterals002

Posted in Aortic diseases, coarctation of aorta, Infrequently asked questions in cardiology (iFAQs) | Tagged , , , , , , , | Leave a Comment »

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 »

Ignorance based Electro-physiology : Why chronic RBBB is a benign entity ?

February 12, 2015 by dr s venkatesan

In the last few decades  we have  understood a major concept in the genesis of cardiac arrhythmia.Slowing in the propagation of cardiac impulse is a key  trigger to precipitate a reentry circuit and initiate a tachy- arrhythmia.Still , many conditions like first degree AV block, chronic RBBB or even LBBB are  benign entities  as along as the heart is structurally normal .They seem never increase the incidence or life time risk of  cardiac arrhythmia . Longevity is unaffected.( Or do we assume many things ?)

How is this possible ? or is the theory of slow conduction triggering reentry is flawed ?

Think again . . . if these patients who later on develop a structural heart disease , with an episode of ACS , myocardial or valvular disease,  the original slow conduction substrates these people were harboring ,  will it become important ?

Surprisingly , we have no answers in literature.When Haissaguerre et al found preexisting ERS pattern could be a trigger for primary  VF in case they develop ACS  , he opened up a huge debate as it involved converting  a vast number of normal population electrically anxious.

Now ,is it possible the so called  benign  blocks of heart like first degree AV blocks , RBBB , LAHBa , would be important  at times of ACS  and possibly make them prone for for primary ischemic arrhythmia .

Is bundle branch re-entry possible in structurally normal heart ?

We need answers. Some one , (Any EP fellow) somewhere  could take up the issue and enlighten us !

Posted in Cardiology - Electrophysiology -Pacemaker, RBBB/LBBB | Tagged , , , , , , , | Leave a Comment »

Innovation in pacemaker battery technology : ICDs go slim and live longer !

February 10, 2015 by dr s venkatesan

ICDs are one of revolutionary devices , invented last century  that can defy “death & fate”  in high risk cardiac patients who are threatened with ventricular tachycardia or fibrillation .A decade long hard work by  Mirowski  and team from John Hopkins culminated in the dramatic  the first AICD implant in 198o. ( In my opinion, this medical invention can be compared to an event of such  significance as moon landing by Armstrong and team ! ) Ironically , in the last decade such a revolutionary device was sort of misused and thousands of devices were explanted for inappropriate indications.

Fortunately , better sense prevailed recently .The indications are getting  refined. I am sure ICD will go a long way in prevention of  both expected and unexpected sudden  electrical deaths .We are into  the 4th decade of its evolution.While the electrical circuitry has been mastered , power supply remains an issue as they require continuous power supply like a mobile phone. Current technology allows about 6-8 years of battery life.

EL-ICD boston scientific longest life icd smallest profiale dynagen inogen madit indication for icd

Now , Boston scientific  has come out with new technology which make its  battery life extend  by 100%  to 12 years.  It is a major break through , expected to evolve  further  until probably we have rechargeable  batteries or biological power sources .Stretching a wild thought , the days couldn’t be far off  when the smart phones which are omnipresent in every human-being  , could not only power the ICD  remotely and control it too !

 

Indications (ESC/AHA 2012)

CAD

  •  Post MI* /LV dysfunction  ≤ 35% /NYHA   class II or III  (*  > 40 days)
  •  Post MI* /LV dysfunction ≤ 30% /NYHA Class I (* > 40 days )
  •  With non-sustained VT due to prior MI, LVEF < 40%, and inducible VF or sustained VT at  EP study

Non ischemic structural disease ( Idiopathic DCM, ARVD etc)

  • With structural heart disease and spontaneous sustained VT, whether hemodynamically stable or unstable.

Primary electrical disease

  • With syncope of undetermined origin with clinically relevant, hemodynamically significant sustained VT or VF induced at electrophysiological study

 

Reference

Link to Product manual form Boston scientific.

Boston scientific

 

 

Posted in Cardiology - Electrophysiology -Pacemaker, ICD -Tips and Tricks, ICD and Pacemakers | 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 the mechanism of systolic murmur in Pulmonary hypertension ?

February 6, 2015 by dr s venkatesan

A short systolic murmur over pulmonary area (ie Left second inter coastal space ) is listed among 6 other auscultatory  feature  of pulmonary arterial hypertension.Though it is an accepted sign  many would question  the existence of such a murmur or its relevance in PHT.

Why does it occur  ?

Acoustics  principle  tells us whenever  velocity of blood  flow exceeds a critical point(Raynolds number*) in a specific anatomical territory , a  turbulent zone is created  and  a murmur could be generated .This is why many physiological situations like pregnancy, anemia, and some benign outflow murmurs occur.

 

In pulmonary hypertension , three things are thought to contribute for the murmur generation

  1. Dilated pulmonary artery  promotes Raynauld turbulence
  2. Increased flow velocity (This is correlated with pulmonary artery acceleration time in Doppler)
  3. RV contractility  (A normally functioning   RV is required to generate the murmur .Once RV dysfunction sets the  murmur of pulmonary hypertension usually disappear , of course a TR murmur may appear and confuse the picture )

Reference

* Reynolds number is a way to predict under ideal conditions when turbulence will occur. The equation for Reynolds number is:

Reynolds number(Where v = mean velocity, D = vessel diameter, ρ = blood density, and η = blood viscosity )

Posted in Uncategorized | Tagged , | 2 Comments »

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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