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electrical CONDUCTION OF HEART

Image source and courtesy http://www.heart-consult.com

Answer

I am afraid the 4th response is closer to truth .Readers may share their thoughts. If there are three distinct pathways   spreading widely connecting the two spacious chambers and   converging again with  precision at the compact  AV node , it  is a  marvel .

Further , If these pathways are real ,  we must  experience different types of  inter nodal re-entrant  tachycardias.Of-course ,we do come across few macro re-entrant tachycardia in the form of atypical atrial flutters  They need a close  watch .Tracking these arrhythmia may throw light on existence of these pathways.

However, the presence of nodal approaches  with preferential inputs to AV node from different parts of atria would indeed  suggest existence of such pathways !

Further study

What does  sophisticated carto and other electro anatomic mapping say about these inter nodal pathways ?

Reference
An excellent article from imperial college London
Atrial anatomy and inter nodal pathway thorel bachman wenkeback

Heterogeneous three-dimensional anatomical and electrophysiological model of human atria . Seemann G, Höper C, Sachse FB, et al. Institute of Biomedical Engineering, University Karlsruhe (TH), Kaiserstrasse 12, 76128 Karlsruhe, Germany. Transact A Math Phys Eng Sci 2006 Jun 15; 364(1843) :1465-81.

Recently , I came across a   young women  who underwent the following three tests for one episode of syncope after witnessing her pet dog bleeding with  an Injury !

  1. Carotid doppler
  2. Holter monitoring and event monitors
  3. Brain MRI /MR angiogram

This was followed up  by Head up tilt(HUT)  in a premier hospital

After 1 week of investigation ,a diagnosis of  Neurocardiogenic syncope was made and she was reassured and no drugs were prescribed.

(The collective yield of the above three investigation in fixing  a specific diagnosis is  less than 10 % of all known causes of syncope )

Syncope  approach  evaluation

To diagnose  common syncope . . . we need common sense !

Syncope is a dramatic  symptom.It is one of the commonest symptom in ER as well . Life time incidence of syncope is at least one episode in 50% all human life ! The definition  of syncope until recently , was liberal .Any transient loss of consciousness with spontaneous recovery  was termed syncope.

This includes

  1. Hypoglycemia
  2. Anemia
  3. Siezure disorders
  4. Structural  neurogenic (Including ,  brain tumors , Dural hematomas etc )
  5. Panic attacks (psychogenic)

Cardiologists wanted to fix syncope as an exclusive disorder of  circulatory insufficiency.By bringing in a modification in the definition  , ie  syncope is  now defined as a transient loss of consciousness due to   reduction in cerebral perfusion  .

This definition helped cardiologists  to exclude the above entities . Still many would include all in single basket as patient should be seen as a whole and we can’t expect them to  land according to our convenience and classification.

Here is an incomplete* list about causes of  syncope (* 99% complete ?)

Vascular

  • Vaso- vagal syncope in young ( Neuro-cardiogenic , Common , Benign)
  • Autonomic dysfunction of elderly ( Including postural hypotension )

Cardiac

Arrhythmic ( Sinus node dysfunction /CHB/Idiopathic VT/Long QT syndromes)

Structural heart disease

  • Valvular  heart disease  (LVOT/RVOT obstructions)
  • Myocardial disease
  • Rarely ischemic heart disease

Miscellaneous

  • Severe pulmonary hypertension (Including PPH ,  pulmonary Embolism )
  • Paradoxical embolism.
  • Aortic arch disease -Takayasu related arteritis .

Investigation

We have a sophisticated array  of investigation for syncope .It can be a never ending exercise , ranging from  spinal cord evoked potentials to diagnose Shy-drager syndrome ,   . . .  to implanting long-term loop recorders to decode  heart beat behavior.

However , evaluation of syncope is the ultimate wake-up call  to all current generation cardiologists  . . . Why clinical cardiology  should  never  be allowed to die (and  it  will not ! )

Common sense begins with answering  few simple questions . Is it really syncope ?

If  you ask this question three times and with  specific leads to the patient  and the witness ,  truth will come out  . 90% of times it may not be syncope at all (Near syncope, accidental  fall, dizziness ,extreme blurred vision, drowsiness  etc)

If it is syncope , Is there a non cardiac cause ?

It may related to the Hypoglycemia / Anemia /Panic attacks.Get a neurologist opinion , it would be terrible mistake if you miss a space occupying lesion  within the brain. (Missing chronic silent sub dural hematomas is  frequent   in the evaluation of syncope of elderly !)

Ruling out  cardiac syncope is relatively easy

In the remaining  patients  basic investigation like routine blood tests,ECG, ECHO   will help us  rule out most serious cardiac disorders.Similarly  bulk of the electrical cardiac syncope can be diagnosed.(Holter , carotid study in selected few )

Need for neurologist -cardiologist interaction.

Syncope due to VBI,  transient Ischemia attack , Senile vascular dementia  is a grey zone . Many have complex neuronal -vascular mechanisms . What is Consciousness ?  and  What is LOC ?  :Is it the lack of blood or severely depressed nerve signal in the reticular activating system? Lots of interaction between cardiologist and neurologist is required to clear our ignorance.(I  have one such  elderly patient who is intermittently awake ! I call this chronic syncope !)  .

Undiagnosed syncope is not  a crime

Realise the most important lesson in Medicine . If you  have ruled out all serious  causes of syncope you should have the courage to be satisfied with that !

Scientific pursuits has a limit. Searching for the mechanism of a psychogenic  fainting attacks with intra cerebral electrodes is a clear case of  physician acquiring a psychotic  behavior !

Final message

Syncope is not only a dramatic symptom for the patient , it also unfolds a drama of costly  investigations  . .  . many  with  dubious value.

Talk to the patient personally for  10 minutes in a quiet room, try to apply that elusive  clinical sense  . . .   it would rarely let you down !

After thought

What is the true clinical value of * Head up tilt Test (HUT)?

Will be posted soon

Last week  there was a heated debate in our CCU regarding thrombolysis for  a patient with severe rest angina  and ST elevation in AVR  and ST depression in V2-V5  as it implies  Left main disease  Few argued left main disease is an exception where one can thrombolyse even with unstable angina !

One of my fellows argued ACC guidelines vouched for lysis in UA involving left main .( I do not agree )

A logical attempt to differentiate Left main NSTEMI//UA and STEMI

(In the strict sense Left main NSTEMI is misnomer as AVR shows ST elevation  isn’t ? )

left main disease

Final message

Such  patients with suspected LMD   are to be rushed to cath lab .  . . agreed . If it is not feasible , manage it as high risk unstable angina and do not thrombolyse .Let it be left main disease . Indications for lysis are clear. ST  elevation in AVR alone can not be taken as an Indication for lysis.For thromolysis to be effective there should be high thrombus burden with total occlusion . ST elevation in single lead (AVR ) is not a good  marker for left-main thrombus !

Oral anticoagulant usage has been steadily increasing for variety of  indications.Dengue fever is also  appearing in different avatars with  low platelet counts  and bleeding being a primary risk.

I was recently contacted by a physician , regarding a therapeutic dilemma .A young lady with mitral prosthetic valve and a febrile illness diagnosed as dengue . She has a platelet  count of 100,000 .She is on regular warfarin and aspirin .The physician  wanted to know , should he stop the OAC and aspirin ?

What are the options ?

  • Confirm if it is really dengue.
  • Look for clinical bleeding.INR, platelet function tests are not helpful.
  • Continue OAC.You can do that in most situations.
  • Stop OAC only if there is clinical bleeding  episode.
  • Anti-platelet drug usage  is more tricky .One may stop it if the trend of falling platelet is steep by at least two serial measurement.(or 50% fall from baseline)
  • Fresh blood and platelet infusions should be ready .
  • Finally and most importantly , Inform the patient and family about the difficult decision we are making.

*Is  OAC  safer than aspirin and clopidogrel in dengue ?

It is believed OAC has no major  Impact on platelet function .It may not  pose a threat of excess bleeding in the setting of  falling platelet levels .(*Evidence base -nil )

Another potential situation : DES and dengue

The number of DES in developing countries are increasing  where Dengue is endemic . It is not a surprising  to expect  both to  occur together.

Anti-platelet agents  can be problematic .It is better to withhold it during the active phase of dengue.(If the  stent has recently  been deployed you have no option !)

Final message

1.  Prosthetic valve , Warfarin Dengue .

2. DES, Dual antiplatelet agents ,Dengue.

They  extraordinary events  throw a complex therapeutic task .There are only two options .Continue or discontinue ! Whichever way you do , you explain to your clients (patients!)  the (un)reality games we play.

My personal option would be , with hold all hematological drugs during the active phase of dengue .

It is better to believe in the  natural thrombus fighting force . Leave the job of anti-platelet action  to the dengue virus for a week or two and give oral anticoagulants and dual anti-platelet agents a holiday

It may be foolish to rely on the dengue virus to guard against  prosthetic  valve  and DES thrombus , In reality we have to do that !

Reference

No reference exists.It is a statistical mind game.Individual assessment  should prevail. Either way, if something adverse happens court of law should protect us !

cardiac output  during labor and postpartumcardiac output  during labor and postpartum 002

Cardiac output in pregnancy is increased by 30 %  physiologically . Hence  loss  of blood at the time of labor is  pregnancy is  sort of physiological correction .Cardiac patients do get a relief  with loss of about 500 ml of blood .

Stress of Labor

Each uterine contraction is a stress to the heart  and is akin to infusing 500 ml of saline into maternal circulation .This is further amplified in patients with severe mitral stenosis.

However , the maximum hemodynamic stress for the mother  occurs just after delivery  when about a 1 to 1.5 litre is auto transfused.One has to watch for deterioration at this point of time.

Why caeserian section is being preferred by many obstetricians  in cardiac disease complicating pregnancy ?

Traditional and modern text books clearly mention , natural delivery is best for both fetus and mother in cardiovascular disease .However it is  still  a debatable issue  in real world labor rooms, especially in obstetrical emergencies.These concepts are probably old when surgical risk were considered too high for LSCS .

My  current understanding of the issue ( Subjected to correction )

  • Normal  labor hemodynamics is unpredictable , even so in a women with critical valve obstruction
  • It is  a  “4 cornered obstetrical stress”  situation ,  almost equally distributed between  mother , fetus ,spouce  and the obstetrician !
  • A brief period of controlled stress is better than prolonged uncertainty of labor.
  • Since LSCS  is done  in the presence of an anesthetist in a monitored  and controlled setting, even a brief  high risk period is acceptable  till the baby is taken out.
  • Though technically LSCS may add a little risk to fetal life , It has been observed mothers are getting more rapid relief  from  post partum dyspnea who undergo LSCS.

*There is another reason for the heart  to feel comfortable with LSCS  in critical mitral stenosis,  which threatens  to precipitate  acute pulmonary edema .The post partum spike in cardiac output could theoretically be less if  blood loss in LSCS is accounted .(sort of venesection !)

http://www.ncbi.nlm.nih.gov/pubmed/4025461

hemodynamics of labor in  mitral stenosis

In one of my  meetings , I told a small gathering  , that regular exercise can shrink atherosclerotic plaques and regress CAD. I also quoted , a recent  large  study which  has proven this fact convincingly !

I concluded, simple  exercise  and other life style changes,risk factor correction  may convert a 90% lesion to 70 or even 50 % . I stressed the importance of this study and asked my colleagues to avoid misuse of  Angioplasties .

When many  seemed to agree with me , one  angry  Interventional cardiologist questioned me, and  asked  the name of the  study, and in which journal  it came , What was quality of the paper ?

evidence based medicine ebm experince

I told him , It is an Imaginary study done  in my back yard . It never got published in print. You may call it as E-journal* , not exactly though.It is not available in any websites , but located in the  biological servers, and  neuronal circuits as digital imprints in learned brains !

*Journal of experience

You may call it , a scientific  forgery , to quote a non-existent study,

But this study  benefits whole lot of my  patients”.

He was amused , and became agitated !

He told over the mike , “You are making  foolish statement. . . don’t corrupt young minds” !

May be , he is true !

I asked him to be calm and  requested  to listen to another study which I was about  to quote  . . .

He couldn’t sit any more  and rushed  out of the hall !

Final message

We  are ready to believe all those  rubbish stories about a fourth  generation   self disappearing BVS that is  able to scaffold a coronary artery and maintain a MLD by 2.5mm  and TVR by 20 % and prevent near MAZE  at 30 days  by 9 % and improve long term survival  by 6 months at  the cost of 100, 000 Rs  per month  .Only to realise, it may be a farce  . . .  5 years down the lane !

How to cleanse the darkened face of science ?

When falsehoods come with evidence and harm people , Good deeds can  be preached without evidence to save our fellow human beings !

modern medicine ethics hippocrates

Every pacemaker has  a metallic “Reed switch” . Putting this switch on and  off is possible with an external magnet .The circuitry is such that , switching on  makes sensing function null and void.It functions as asynchronous mode.In other words  pacemaker converts to a mandatory  pacing mode .All  sensing  related issues are immediately removed.

magnet rate reed switchNote : This switch can be activated by any strong magnetic filed applied externally .And removing the magnet disconnects the circuit.

When a magnet is applied the pacemakers changes the mode in the following way.

  1. VVI  to VOO (Paces only ventricle  without sensing)
  2. AAI  to AOO (Paces only Atria)
  3. DDD to DOO  (Paces both ventricle and atrial with a fixed AV interval )

magnet application permanent pacemaker ecg 002

Purpose of magnet application .

Essentially it may be called as a safety mechanism to prevent external sensing in strong electrical fields in case the need arises.

Indirectly , it may aid us in detecting end of life  of  battery as well

During elctrocautery and related procedures  application of magnet will help.

What is magnet  rate* ?

  • The moment you apply the magnet the pacing rate  changes
  • This is variable with each make and preset.
  • End of life magnet rate will be different . It can be 65 to 85  fixed depend upon the make.
  • Some pace makers  fire initial magnet rates with 3-6 beat fast run and later revert  to steady baseline rate.(One should not be confused )

* Always check with the pacemaker manual for the exact response.

When I put a magnet over nothing happened .What is the inference ?

  • Magnet is not placed properly
  • Pacemaker battery  is totally dead.
  • Very rarely some pacemakers  have magnet function  turned off

What happens  during magnet application in ICD ?

  • There is no change in ICD mode.
  • All anti tachycardia functions are immediately suspended. (A major use in an unusual runaway inappropriate  ICD shock situation )

Is there any risk of applying magnet ?

Since magnet removes the sensing function , interfering a cardiac rhythm which  is dependent on sensing can be  problematic.Similar situation arises in MRI scans and other magnetic fields.

Hence , application of magnet in a patient  as a part of pacemaker trouble shooting who has no pacing spikes is rarely a problem While one should not do it without supervision of  a learned cardiologist.

What is smart magnet ?

Each pacemaker  and ICD  is interrogated with the respective programmer.As such , there is no cross brand  programmer  available.This makes it difficult for patient( as well as physicians)  to call for help in case of malfunction.

The solution is to make standard universal analyser and programmer .This requires  cooperation between various stake holders.Meanwhile as temporary relief a magnet which can community two way with  basic functional switches can be developed .

There is a need for universal smart magnet with constant interaction between device and magnet ..

Since , the generation next generation human  heart  is going to be wired and deviced in a complex manner,  we need to know the basics about these  issues.

Final message

Magnet application is akin to novice’s  pacemaker analyzer. Every cardiac care unit must have one in their shelf. It aids us to diagnose over-sensing as a cause for pacemaker  malfunction.(* please note , it has little  role in all other pacemaker issues !) .In an emergency it can help stop inappropriate ICD shocks.(More importatnly  It gives  time to call an expert ! )

Reference

role of magnet application on pacemkakers icd  oversensing magnet rate

Distribution of Left main disease.

  1. Ostial
  2. Ostio-proximal (Within 1 cm of  origin )
  3. Shaft -Discrete  mid left main
  4. Shaft -Diffuse
  5. Isolated distal shaft( 1.0.0)
  6. Bifurcation ( Medina 1.1.0 -LAD)*
  7. Bifurcation (Median 1.1.0-LCX)
  8. Bifurcation ( Median 1.1.1)*
  9. Trifurcation ( With ramus )

* These three locations account for nearly 75% of all left main lesions.

left main disease coronary angiogram

We know atherosclerosis is  a branch point disease .Normal left main measures 1 mm to 20mm.The shorter the left main lesser is the the incidence of LMD. Short left main can not engage the atherosclerosis much (No left main = No left main disease ) However ,very short left mains  may increase ostial lesions .

  1. The commonest left main lesion is distal left main with one of the branch involvement (1.1.0.LAD is more common )
  2. Least common entity is discrete mid shaft lesion.

Simple strategy.

First dictum : All complex looking LMDs should be referred to a good  surgeon.

Final dictum : Remember medical management for left main disease is still an accepted strategy in stable , non flow limiting situations .

Interventional  Cardiologists  feel they have the exclusive rights   to indulge between these two  spectrum of LMD .May be true! But extreme caution is required as we are playing  our game in the most critical  coronary high way .

Some suggestions and thoughts.

  • 50 % diameter stenosis is significant. But significance does not mean we should tackle the lesion by aggression.
  • Symptomatic flow limiting lesion only to be intervened . (Flow limiting means both angiographic and a stress test .FFR <.8 is also an index for flow limiting .Symptom means Angina on exertion )
  • IVUS, OCT, FFR,NIR ,SYNTAX  are not path breaking tools .They essentially  add  more glamor  to left main disease than anything .
  • Most bifurcation LMDs are  managed by single stent with stent jailing the major side branch (Yes side branch can be LCX !)
  • However ,two stent strategies is not banished .It can be vastly  superior in some selected cases .(Especially with huge plaque load at carina )But needs expertise .
  • In very small vessels two stent strategies are risky .

Reference (2012 update)

left main disease  coroanry angiogram management  Fajadet

PRECOMBAT left main disease south korea everolimus
Link to related articles in this site

We know Nitroglycerine(NTG) as a most powerful epicardial coronary dilator  . We use it for instant relief during episodes of coronary arterial spasm in cath lab.

What will happen if we administer NTG over a stented segment ?

Does it dilate it with same vigor ? What will be the consequence  ?

A perfect setting for stent migration isn’t ?

Let us bust the myth around  NTG . NTG  rarely  show  visible coronary dilating effect except in the setting of coronary spasm .

NTG and coronary vasodilatation

Does a LAD with 3 mm diameter become 3.1 or 3.2  and so on with NTG ?

No .It won’t .It is my belief. It is well known , NTG’s action varies significantly in normal and diseased endothelium . Again , there is an irony .It seems , it can act only in normal endothelium , but  we need require it’s therapeutic action only in pathological segments.Further any stented segment would contain   clusters of  both normal and abnormal endothelium .

One more inference is that, stented segment exerts constant pressure on intima making any  pharmacological vasodilatation irrelevant .

Importance of  radial strength of a stent

This issue of vaso-dilator induced  stent migration may not arise in self expanding wall stent with high radial force.But we do not know how long these metals will carry this metallic property .Balloon delivered  stents ( currently used 99% of times ) do not have permanent radial strength .

Final message

I am yet to comprehend what nitrates are expected to do (and what it really does ?)  in a patient post PCI ? (By the way  . . . why we need to prescribe Nitrates it in the first place ? but  In real world most continue to take this for many reasons .)

We need to analyse the micro-vasomotion at the stent -coronary intimal interface.The dynamism in this  narrow space  can be critical  , and may make the difference between life and death !

After thought .

In the hind sight,  this post appears quixotic  for myself . But some one , some where , may generate a great idea  out of it , that will help our patients.