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Archive for the ‘cardiology -Therapeutics’ Category

It is a well known fact  ,   CABG and PCI  provides immediate relief  for patients with angina ,  which is refractory to medical therapy. Of course , this happens only if a critical occlusion of  at least one epicardial coronary artery is  opened . It need to be realised ,  angina  due to  microvascular  disease can not be cured by maintaining  epicardial  patency .

While angina  relief is prompt ,  dyspnea is not ! . If we  believe,  opening  up a  coronary artery  in a patient with LV dysfunction will  restore the LV function  ,  it  is grossly mistaken !

Why is it so ?

Angina  relief requires  simple  restoration  of  oxygen supply and correction of local ischemia .  This happens without any issue as the blood  seeps in to the ischemic cells and soothes the ischemic nerve fibres that trigger the pain signals   . While  ,  for LV function to improve , the blood flow has to be converted to mechanical activity in the form of myocyte actin/myosin interaction. For this,   there need to be an intact  cellular contractile mechanism . The myocyte architecture should be appropriate .In post MI ventricles we know there is  zig zag  orientation of myofibrils due to myocyte slippage that interfere with mechanical recruitment . Further , integrity of  extracellular matrix  namely the collagen frame work is also vital . Note ,  angina relief  is not concerned with any of the above .

And now ,  we also realise  dyspnea  in failing ventricles  is vitally  dependent on diastolic function ,  which is also very much  impaired in ischemic DCM .There is little proof for  PCI/CABG  to correct the  molecular   mysteries in  diastolic dysfunction !

Dysfunctional LV means what ? (read the link )

It is a collection of  variety of myocardial tissues . Viz : Fully  necrosed , partially necrosed ,  ischemic viable, non ischemic viable, ischemic non viable, non ischemic non viable , Apart from this patchy necrosis, patchy ischemic, areas are common. Finally , necrosed segments   may  also be perfused normally by  spontaneous reopening of an IRA.

One can imagine the complexity  of events in these segments  once we do the  PCI /CABG . The response  is highly variable and unpredictable. The major concept we  , the physicians  believe or ( to be precise made to believe !) is  the  sanctity  devoted to  the viable myocardium .For  many us ,  it is considered a  holy  exercise  to identify viable myocardium in patients following MI and then revascularise them if  found to have significant viable myocardium (Atleast 20% of infarcted area )

A full 2 decades were lost or (shall  we   say wasted on this futile exercise !) as   we have since  realised most of the cardiologists do not follow this rule .

Now , even a scarred myocardium is revascularised in the hope of recovery .As such , we have reached a stage where  there is no contradiction for not doing a PCI /CABG   with reference to LV dysfunction.

Now every  patient  with post MI  LV dysfunction  is considered to  have  some amount of viable myocardium that is  fit   enough  for revascularization

Are we justified in doing  this ?

Many clinical  trials  have revealed  , the  recovery of LV function  in these segments  has not been consistent at all .

The most surprising discovery is  a viable myocardium need not  be ischemic   .It might get adequate blood supply either  from invisible collaterals or trickle of antegrade flow .  Hence an adequately  perfused myocardial segment can  still be   non contractile . This shatters the myth  that  revascularisation must have a dramatic effect on the recovery of contractility in all viable segments.

The other major finding is  ,  even ischemic   viable   myocardium ( documented by metabolic activities PET etc)  need not regain it’s original contractility  after the ischemia is fully corrected .

*reference for  both the above statements are available from variety of sources including real life experiences .(Type C evidence )

Final message

  • Do a PCI/CABG promptly for patients with refractory angina.
  • Never  advocate PCI/CABG  for  a primary relief of dyspnea .  (Never is a harsh word,  let it be  “use it  with caution ” ! and  the  patient  should be  revealed  the whole facts  about  what we know and what we do not know regarding the complex  hemodyanmic events  in  revascularisation   )

Counter point

If  the above statements are really true ,   How does PCI/CABG   help  relieving  dyspnea  and functional class  what is your answer for thousands of patients  with CAD and ischemic DCM who have greatly benefited from CABG ?

The answer could  be  simple , The revascularization  piggybacks  over the   medical management (which , these patients pursue vigorously)     like  ACEI,  statins, salt restriction, betablockers  , optimal diuretics and tend to hijack the credits from the poor  drugs !

Read a related blog

Revascularisation for ischemic DCM

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Can  modern technology  bring back  the life from a   dead person ?

Yes it is possible  ,  not in the near future !  but  in the present era  . . .

This revolutionary new portable heart lung machine may just do that .

Imagine  this scenerio : A cardiac arrest  victim  – failed resuscitation  with  ACLS  ,   the patient  needs  to be taken for an emergency cardiac surgery or intervention .You need time at least ,  few hours .Till that time  this simple device   takes  over the  role  of GOD    i e  sustaining life   by   pumping  and oxygenating  6 liters of blood !

Learn more about this award winning wonder machine from lifebridge .Germany

LIFEBRIDGE Medizintechnik AG / Product / LIFEBRIDGE B2T®

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Pessimism, from the Latin pessimus (worst), is a state of mind which negatively colors the perception of life, especially with regard to future events.

Understanding pessimism is not that simple  . Some people argue  optimism   represents a strong mind while  a pessimism  is the domain of the weak . But it is not necessarily true.  Both pessimist and optimist are unreal , and playing the dangerous game of predicting the future. So realism is the answer .

In this era of information highways , commercial exploitation of science ,  our thought process is grossly determined by our perception of events.We hardly have an intention or time to analyse our thought process.

  • An optimist  ( Rather , unregulated optimist ! ) is a person who welcomes  any growth good or bad.*
  • A pessimist  is  a  person who welcomes only good growth.*

So how to identify good growth ? That is the million dollar question!

  • Many of the  optimists may not  bother about the final outcome of a treatment *
  • A pessimist bothers only about that .
  • An optimist  rarely asks questions, blindly accepts every thing !
  • A pessimist never believes any thing !

Actually the fundamental principle of scientific medicine lies in proving the null hypothesis null and void.Any treatment is useless until proved other wise .  So pessimist can be argued to follow true science , while  many of  the hardcore  optimists are blind believers ..

*It may be  a harsh   way of  interpreting an optimist  but  uncontrolled optimism  has played havoc in our  patients like many of the failed treatments (Some of them released prematurely into patient domain   has  killed many lives  . Power of positive thinking should be within the  realms of scientific feasibility !

So in  our  journey   to  conquer human health ,   we   may  proceed with  an optimistic mind and  a pessimistic eyes !

This understanding is all the more important in this era of contaminated science .It is a well known fact ,  now last 50 years of  planet earth has inflicted the maximum damage  to ourselves  than our ancestors did in 5000 years. That’s why we are compelled to meet at Copenhagen .(We never learn from our mistakes, that’s a different story !) .

There is definite and urgent  need for world summit  on  cleansing the medical science from  the clutches  of commerce  and ignorance . A medical green house effect, with dangerous holes in health care  is imposing on us (Another pessimistic thought . . . of course in the interest of human kind !)

World health organization ,  a sleeping giant has to be awakened on this issue


Final message:

Mankind has evolved over many millenniums ,  probably with a sole  purpose of living ,  that is reproduction and propagation of our genre without harming the environment and other species.

Unrestricted  and unregulated growth of any kind is dangerous we call it as malignancy in pathology .In science , we tend to call it a” great future ”

Our  sixth sense*  has  outgrown  miserably  out of  reality  , as have we decided to take on the nature and GOD .Now , many developing country men do not believe in death .They are fighting a losing battle against the God. And they suffer with escalating health costs of keeping the elderly ,  alive who are  knocking at the doors of heaven or hell . The same countries,  which deny funds for curable illnesses of the poor is a different story altogether !

The principle of modern medicine  would ideally  be

  • Reduce human suffering irrespective of economic status
  • Curing a illness if there is a cure
  • Prolonging life if there is useful purpose
  • Allow a good quality death if there is no cure.
  • Most importantly  , prey to god give us strength and capacity to identify which is good and which is bad for our patients  .

Read and learn for a  complete guide on optimism and pessimism

* It  is  important to recognise , the same sixth sense  has   made it possible to share our views through a great tool of  Internet  . So we should not be against the growth of science but against the misuses and wrong interpretations of it .

Pessimism

Optimism

The traditional characters  of  a pessimist

//

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Modern era of cardiology aims to treat ACS  as and when it develops .That is , as soon as the vulnerable plaque ruptures or a thrombus  blocks the victim’s coronary artery.

But this can be achieved only if the patient reacts to this event.We know 20% of ACS can be totally silent. Some produce very vague symptoms especially in elderly and diabetics. ECG and enzyme changes may help us in patients who do not have clear symptoms.There are variety of markers available for STEMI & UNSTEMI.(CPK-MB, Troponin T , myoglobin etc) Now we are working at finding a marker for ischemia without necrosis. Ischemia modified albumin is one such molecule that is showing promise.

The ER department world over have vigorous screening protocols to diagnose ACS  for  the patients with chest pain. There are thousands of triaging protocol in the  emergency management of chest pain.In spite of  the highest awareness and availability of  scientific expertise , knowledge base the error rate of diagnosing  ACS  stands at an astonishing 58%.  This may seem odd , but this is what  this land mark article in NEJM tell us  (Data from Boston , Milwaukee etc).

Out of 10500 patients with suspected ACS. Only 17 % had real ACS.  55% were admitted initially as ACS  later turned out to be non cardiac .This may seem  acceptable for many  even if it is  an act of unnecessary admission and investigation. It gives us , a sense of satisfaction for not missing a diagnosis of ACS. But it has it’s own risk of complication arising out of unnecessary investigations.It is a chain reaction of  suspicion that  may end up in a coronary angiogram in many ! .It is also a well recognised fact these patients    spend  atleast an average of  2 days  to get rid of the ACS tag over their  necks .

Experience has taught us  simple presence of a human being as a patient within an  ICU ( however short the stay  may be ) can be a health hazard and risk .  This  55 % error ,  which does exactly  this to  our  patients with chest pain  who reach the ER  never bothers us  This is because  we feel credited both academically as well as financially .

In the same study 2.3 %  (About 25 patients) with true ACS  were sent home  after a missed  diagnosis . Paradoxically  this 2.3%  has worried the medical professionals too much . . . This happens  ,  even as we  do not have proper data on  how many of them had a real adverse event after a missed  ACS.

So the message here is even in best centres both missed and wrong diagnosis are  rampant. while wrong diagnosis (25 fold more here  )  is easily accepted by the medical community .We can justify  this as a screening camp for ACS  ,  akin to arresting  a group of suspected  criminals in a  preventive raid ,  later releasing for want of evidence.

In the morals of  criminal judiciary  , it is often said one can afford to  lose  a real offender from the clutches of law  , but a  innocent should  never be punished in any circumstance .

In medical parlance this  goes something like this  . . . Thousand patients shall die because of his or her illness but not even a single healthy person should die due to unnecessary treatment.

The above thoughts  were in response to  the excellent original article on missed diagnosis  of ACS from NEJM.  http://content.nejm.org/cgi/content/full/342/16/1163?ijkey=652d8337709a8bf84c813f4c9d685863ee053162

Final message : (Sorry for the  lengthy message !)

Can we afford to miss an  ACS in emergency room ?

“Definitely not” . . .but do we succeed in that ?  The answer is same “definitely not “

When we are able to accept with pride every time  we make  a  wrong diagnosis of  ACS  in perfectly normal people , It may to provocative to say  we can  also  afford  to do  the same  when we occasionally   miss a  diagnosis of ACS  as well .  Law of statistics dictates for every correct diagnosis made there is many fold number of wrong or missed diagnosis takes place. May be , reducing that is the only aim of medicine.

We need to realise  with even with a 55% of false positive initial  diagnosis  2%  real ACS  escape net !The only  fool proof method  for  not missing  ,  even a single case of ACS   is to label every patient with chest pain as ACS .

In this vexing  issue , we should realise  , in field of  medical decision  making ,  errors  due to acts of commission  ( Making an  inappropriate drug/procedure /surgery  is easily accepted by medical professionals as well as   the court of law !) . But acts of omission ,   like missing a diagnosis or failure to prescribe  a  drug or perform a procedure  is rarely accepted   and  is  considered   a great negligence and  bring intense guilty feeling among the physicians .

This  perception is definitely  not warranted in this  greatest profession  of glorious uncertainties ! Both acts of commission and omission  cause significant damage to  patients . In this modern era  ,  we have clear  statistics  that   reveal ,  acts of commission  leads far ahead over it’ s counterpart in injuring our people .

Hippocrates got it right over 2000 years  ago .  First let us do no harm  . . .

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The   failing heart  enlarges progressively and  attain a globular shape . What  looks  for the  naked eye  as a simple global hypokinesia of LV  , when  analysed  ,  reveal multiple  forms regional desynchronisation .This is especially true if the QRS complex is wide.

It is generally divided into three groups

  • Intraventricular desynchrony (IV)
  • Ventriculo-Ventriculo desynchrony(VV)
  • Atrio ventriculo  desynchrony(AV)

In our search for improving CHF mortality and morbidity  ,  we have  stumbled upon this concept of restoring the lost synchrony of the heart. Cardiac resynchronisation therapy  has become ( Rather projected to become !)  a  great modality for patients  with cardiac failure.It was   initially advocated only   for severe forms of cardiac failure  , now  advised even for class 1 CHF. (CRT-MADIT 2009)

Restoring  the lost  synchrony  by rewiring the cardiac conducting system with multiple leads and optimally timed pacing increases the effectiveness of cardiac contractility.It can improve EF, and also regress mitral regurgitation.

The above concept was perfect on paper , but was very difficult to replicate on real patients. CRT was ineffective in 30% of patients.   Many had partial  effect. Few had adverse effect .

The reason for the poor efficacy  is  technical in many .  Identifying the optimal  sites for  positioning  the leads  and the futility of such an  exercise as the LV epicardial  lead is pre- selected by the patients coronary venous anatomy are the major issues.An electrically ideal site for pacing  can  contain a  mechanically dysfunctional scar.   While these  technical issues may  be addressed  in due course  what worries us is the conceptual flaws.

Emerging  facts indicate timing of asynchrony could be vitally important.

  • Systolic   synchrony
  • Diastolic synchrony

What is the incidence desynchrony with reference to the cardiac cycle ?

CRT resynchronisation

One major reason that was overlooked totally was the presumption cardiac dysynchrony occur only during systole. It is a less recognised fact is the ventricular relaxation is not uniform and synchronous.A  failing ventricle can not be expected to relax  systematically and coherently  for the simple reason the myocytic calcium reuptake into the sarcoplasmic reticulum  is grossly impaired. This  is directly responsible for the diastolic dysfunction observed in dilated cardiomyopathy . If this impairment occur uniformly throughout the  left ventricle it can be termed global diastolic dysfunction which is little easier to correct .But what really happens is  the  defect in calcium reuptake occurs in a random fashion with lot of regional variation. This is called regional diastolic wall motion defect or regional diastolic dysfunction.The above mechanisms result in the typical restrictive filling pattern of many of the advanced  patients with DCM . CRT as a concept should need to address this issue.

How to diagnose Diastolic WMD?

The  fact  is  ,we have not  mastered the quantification of systolic WMD as yet. It may take years before decoding the  nuances  of diastolic wall motion defects. At least we need to know such a thing exists.Tissue  doppler strain rates ,  velocity vector imaging could be useful tools. As such they are not clinical tools.

Final message

crt cardiac resynchronisation asynchrony echocardiography

Cardiac resynchronisation as a concept is good on paper . Heart need to be synchronous both during systole and diastole .This becomes especially important in an advanced stages of  heart failure. Without proper follow up  and potential adverse effects of CRT on diastolic WMD ,   CRT concept    has  miles to travel !  . Some  pessimistic thinking   cardiologists ( Me . . . !)   would even argue  it as a case of prematurely released device into the  patient domain. Of course there is  lot of  scientifc data that  will vouch for its beneficial effects .(The latest being from the prestigious NEJM ,  CRT-MADIT) but it has to prove it’s worth in individual patients. Physicians must exercise caution  before embarking on heroic  attempts to provide resynchrony of failing hearts .

Reference

This study from France published in JACC 2005  by Iris Schuster,

http://www.journals.elsevierhealth.com/periodicals/jac/article/PIIS0735109705021005/fulltext

Coming soon

ICDs are better bet than CRT

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The term cardiomyopathy generally denotes a  progressive disease  in clinical cardiology.There was a time   diagnosis  of dilated cardiomyopathy (DCM )  was synonymous with a  delayed death sentence !  Of course , the situation has vastly improved over the years  with the availability of  new medical , interventional and surgical management. Still ,  there is no denying the  fact  ,  DCM continues to  have a grave outcome  especially when it occurs without any identifiable cause .

While we have  variety of aggressive DCMs , we also  have  patients with relatively benign forms of   dilated and dysfunctional hearts  which recover totally .

This reversible forms of DCM is observed in  the following  situations.

Hypertensive dilated cardiomyopathy . The left ventricle  in  some of the  patients with severe SHT  respond to the stress (Increased  after load) by dilatation rather than hypertrophy. This is especially common after an episode of LVF.  If we do an acute echocardiogram the LV function is severely impaired and the LV may  also be dilated. With good control of BP and fluid management the ventricle promptly return  to it’s baseline dimension. The recovery is complete in many . (The mechansim of LV dysfunction acute severe Hypertension is referred to as Pre-load /After load mismatch) Link to concept of Pre load mismatch .

* Note in the past these entities were not called as  cardiomyopathy .

Peri partum cardiomyopathy.

This is a serious disorder of cardiac muscles that occur during pregnancy  few months before  or few months after delivery  . There is correlation between PIH and this entity. Prognosis varies between very bad to excellent. Very few cardiac entities  have a  natural history like this one disease of women.Most of the pregnant women regain their original cardiac status within  year or so. It should be recalled there is high chances of recurrence in next pregnancy.

Alcoholic cardiomyopathy.

The toxic response to alcohol or the additive cobalt can result in DCM .There is overlap  between holiday heart syndrome and alcoholic DCM , where atrial fibrillation is the major problem. Wet Beri beri is the advamced form of clinical DCM that respond to vitamin B therapy.

Tachycardic cardiomyopathy.

This is also a common entity that occur during persistent sinus tachycardia or AF , thyrotoxicosis.Beta blockers are  of great use here.  Recovery is usual if the primary cause is correctable.

Toxic and drug related  reversible LV dysfunction

Adriamycin cardiomyopathy

Tako -Subot  Cardiomyopathy canbe termed as classic form of reversible  stress cardiomyopathy

Miscellaneous conditions

Diabetes and chronic kidney disorders are known to have a reversible form of cardiomyopathy

Some rare toxins  , scorpion envenomation , selenium deficiency can result in reversible DCM

**Ischemic DCM are partially  correctable in many , still  we don’t include it as cause for reversible DCM

*** Many episodes of acute myocarditis can have transient or short term LV dialtation and  dysfunction.they are classified as myocarditis .But there is little  difference (Except acadmeic . . .)  between chronic myocarditis with LV dysfucntion  and cardiomyopathy.

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Cardiopulmonary resuscitation (CPR)  is  the major discovery of last century  that has saved many lives over the years. In spite of  this , there has been lot of debate over the exact methodology adopted  .The much published techniques  of Basic cardaic  life support (BCLS)  which is in vogue for over 2 decades has failed to deliver the  results  as  one would have expected.

The main reason identified was ,  the protocol seemed too complex and people hesitated to do the  mouth to mouth breathing in a stranger. Many were not confident about doing  proper chest compression and  inter spaced with breathing support.( The ratios  of chest compression : ventilation 30:2 /15: 2 tend to be too cumbersome in an emergency !)

Many of the  potential  resuscitators  preferred to  become silent spectators !

The world bodies ACC/AHA/ILCOR has been watching this evolving pattern and behaviour . Mean while when we looked into the data of survivors of cardiac  resuscitation  , we  realised even an  improper  and inadequate CPR had some positive  effect on survival . How was this possible ?

There have been  innumerable instances of  individual and institutional reports   about  many lives that  have been saved  simply  by compressing the chest  after cardiac arrest or  at least  kept the person alive  and breathing to  be taken  for advanced cardiac life support.

cpr hands only ilcor lancet

This simple experience has since become strong evidence when Lancet got it published in 2007 . Subsequently the ILCOR/ACC have also adopted a new advice namely compression only CPR

Read complete ILCOR  recommendations http://circ.ahajournals.org/content/vol112/24_suppl/

Excerpts from the above article reproduced

cpr chest only

Compression-Only CPR

The outcome of chest compressions without ventilations is significantly better than the outcome of no CPR for adult cardiac arrest.In surveys healthcare providers well as lay rescuers  were reluctant to perform mouth-to-mouth ventilation for unknown victims of cardiac arrest.

In observational studies of adults with cardiac arrest treated by lay rescuers, survival rates were better with chest compressions only than with no CPR but were best with compressions and ventilation . Some animal studies  and extrapolation from clinical evidence suggest that rescue breathing is not essential during the first 5 minutes of adult CPR .

If the airway is open, occasional gasps and passive chest recoil may provide some air exchange. In addition, a low minute ventilation may be all that is necessary to maintain a normal ventilation-perfusion ratio during CPR

Laypersons should be encouraged to do compression-only CPR if they are unable or unwilling to provide rescue breaths .

Final message

In this world of hi tech life support devices like LV  assist systems, implantable defibrillators robotic surgery  ,  it is  heartening  to note a pair of human hands can save a human life  or  at least sustain a life till the advanced emergency service reach the patient.

The fact that hands can act as a artificial heart lung machine at least  for few minutes  could be the greatest invention for the mankind by the mankind.

cpr hands only cpr lancet ilcor

* Note of caution

Under ideal conditions both chest compression  ,  proper airway , and assisted breathing is always better than simple chest compression .This blog wants to convey the point chest compression  alone could  also be  a effective CPR measure .

References

http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(07)60451-6/abstract

Newyork times  reports chest compression  only  CPR

cpr hans only newyork times

Click below to read the article .

http://www.nytimes.com/2007/03/17/health/17cpr.html


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10.14prescriptionRXStatins are projected to be  the saviours of human race against the  killer atherosclerosis .Now we have reached a stage  soon ,  where every healthy individual may be administered this drug. There are consistent evidence for statins to reduce , retard , prevent progression of existing atheroscelorosis  and possibly prevent future atherosclerosis.

This  wonder drug acts by blocking the HMG COA enzyme a vital  enzyme that regulates the lipid metabolism within the cells. It is made to appear  as if ,  the  God has  created this enzyme  with the only purpose for human suffering , by blocking this   we  expect  all errors in lipid  metabolism is corrected.

This enzyme is  part of the house keeping  system  that is meant to service the human cellular lipid layers 24hrs a day. If it  is impaired intentionally one can imagine the consequences. That’s what modern science is all about. Luckily God is kind enough the side effects of  blocking this enzyme is seen only in minority. The myopathies that are classically described with statins are due to possible mitochondrial dysfunction .

As the debate still  continues to find the   optimal bottom levels  of LDL  , we have more worries ,  real world experiences have brought us a new issue  namely  the  reduction of HDL with statins. While literature search on statins and HDL  tell  us there is marginal increase in HDL up to 10% the fact is there is marginal fall or significant  fall in many of the patients .

How can this happen ? A  huge difference between real world and trial world ?

statins hdl ldl

* Brands shown  not intentional

Readers are welcome to add their input on this question .

Reference

Visit HDL forum

http://www.hdlforum.org/

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atropine leafsAtropine ,  the extract from the  Belladona  plant  is an important cardiovascular  drug. It’s  presence is vital  in every crash carts .  This  unassuming molecule  probably has   saved more cardiac lifes than any other drug . It provides immediate  remedy for many of the bradycardias .It  works like a magic.  The physician buys  time with this molecule  and  proceed  on to resuscitate or  plan other interventional  procedures. It is most powerful antiarrhytmic agent known .It is an irony , many of  the standard cardiac texts do not even mention this while discussing anti arrhythmic agents .

In  this  era of  hyped  cardiac  care   , the  sartans ,  2b3a inhitors   , the fondaparinux’s  making merry !  we  have no spare time  to realise  ,   more  cardiac  deaths  have been prevented by atropine  than  all these   drugs    put together.  It is still working like a bull  across the coronary care units and cath lab world over. While  many mediocre  drugs  enjoy a  big  bash  time for  possibly  saving   few occasional  lives   , the atropine  like drugs never get the due recognition among cardiac literature for the simple reason ,  it being a  cheap  generic drug.This drug is available  for few  rupees , no marketing no advertisements, no celebrations.

Mechanism of action

The  biochemical  mediator :  Acetyl choline

Site of action :     It blocks the M2 (Muscaranic receptors) .

We will confine to the cardiovascular  actions.

  • SA nodal acceleration
  • AV nodal accelerated conduction

Effect on ECG

Sinus tachycardia

Short PR interval

Life saving situations in cath labs  in CCU.

Vagus  nerve richly innervate the heart and blood vessels . Acute coronary syndromes   especially involving the infero posterior territory  raises the vagal tone  , and can  in severe bradycardia and hypotension.  In cath labs , as we  manipulate  cardiac  structures with wires and  catheters  there is always  a potential to elicit the vascular reflex .It can occur  any where between the  access point , femoral or radial  artery to coronary arteries .

Further ,  whenever the  pain  intensity is more , the  central pain integrating  centre in  brain stem  and thalamus has a spill over effect into the vagal nucleus .

What happens if a vaso vagal reaction is left untreated ?

We have often  made  the term “vaso vagal  reaction” appear as an  innocuous  entity. The main reason for this perception is   due to the common occurrence of  “vaso vagal  syncopewhich  is largely a benign entity in the general population .This fact  has sensitised our brains . One should distinctly realise the vaso vagal syncope that occurs in  healthy people standing  in erect posture ,  from  vagal reactions that  occurs in  lying patient with a diseased heart  in a  cath  lab  or CCU.In the classical vaso vagal syncope , assuming the recumbent posture is the treatment and it  counters the hemodyanmic imbalance .No drug is required here. So the common vagal syncope can never be compared with potentially dangerous  vagal reflex that occur in CCUs and cath labs. If not recognised earlier and  immediately countered  it can lead on to asystole and death .Many of  the delayed deaths post PCI during sheath removal or an episode of vomiting are directly related to this.

atropine

Atropine is the Savior here . Can you imagine a  world without atropine .

The other reason we had always considered vaso vagal   reactions lightly is that the poor atropine is always available  in the side selfs and it acts   rapidly  and promptly with almost  100 % success  reversing the vagal action  in less than  60 seconds .

How often we here  this  “Oh it’s a brady . . . push  2cc atropine . . .  given sir, the rate has picked up . . .”

If only atropine has a failure rate of say  50%    we  would have  realised the full impact of   vaso vagal shocks (See … how we struggle with No reflow   with no effective drug available !)

Is there any other alternative  treatment  for vaso vagal shock other  than atropine ?

No.   (I guess so . . .Readers may correct me )

Other uses of atropine in cardiac practice

  • During stress testing along with dobutamine  to  increase the heart rate.
  • It can be used to differentiate AV blocks the two types of 2nd degree AV block. The mobitz type 2 worsens while type one accelerates.

Non cardiac uses.

Ophthalmology, pre anesthetic medication, bronchial asthma, various poisoning.

What is the future for this molecule ?

Remain bright .  But only very  few companies make this molecule.  It is a drug that can not  fill the cash boxes but  it is a drug to keep the human heart running at times of crises  . The only  threat to this drug  is  the  possibility of it being replaced with a  modified patented  version of this great  molecule  !

Final message

The evolution of medicine is based on strong foundations  put upon by clinical acumen   by great medical men of  past generation. Atropine was developed by such people   and it has withstood the test of time. This drug  probably  has saved ( and  continue to  save)  many  lives  than any  other drug  in cardiology . It should be recalled ,  another great cardiac drug   called digoxin  has almost succumbed to modern medical  forces  .Let us  keep developing   new molecules  ,  we shall also pay  tributes  to some of   the  unassuming drugs in cardiology .

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micro circulation shockHuman circulatory system consists  of  the heart , the arterial  and the venous  systems . Together they constitute the  three important limbs of circulatory system namely , the  pumping, delivering and retrieval systems .In physiological conditions approximately 6 liters of  blood  has to traverse  the entire   circuit every minute . The  purpose of the  circulatory system is not simply circulating the blood within the body,  but  it has to perfuse different vital organs like brain, kidney, liver . Of course ,   the heart has to self perfuse the coronaries  by it’s own contraction.The organ perfusion is determined by local and systemic  regulatory mechanism. A gamut of intrinsic and extrinsic neuro humoral modulators take up this job. A functionally intact autonomic nervous system is an absolute necessity to maintain tissue perfusion.  The perfusion pressure is highly variable in different organs and different cells. Similarly the ability to with stand ischemia and hypoxia also varies. Shock  is a general term used to imply ,  circulation is seriously compromised.Here we will confine our self  to the intricacies of peripheral circulatory shock

Traditionally shock is  classified as

  1. Cardiogenic shock
  2. Hypovolemic shock
  3. Vasodilatory /Redistributive/Septic /Warm shock (Can be called  as  arterial shock )

The hemodynamics of the first two are straight forward and easily understood. In  cardiogenic shock , the pumping action of heart is primarily affected .In hypovolemic shock  there is no  structural defect in any of the   circulatory limbs but there is  a loading defect due to low blood  volume as in hemorhagic shock .

The term vasodilatory shock or redistributive shock is most poorly understood and most difficult to treat.

The  concept is further confounded as  combinations of   above three mechanism in a same a pateint can occur . ( More commoner than we believe !) . An example could be a septic patient  with an  internal bleed and myocardial  depression either due to preexisting LV dysfunction or circulating toxins.

Since  we have always perceived heart as  the  sole  vital  component of circulatory   system , our understanding of the role of the vascular tree which is primarily responsible for delivering the blood is largely undermined and neglected. We are always happy if the EF %  is normal.

Classical features of  circulatory failure ?

The cardiac contraction is good.This is documented by normally contracting LV by echocardiography. The pulmonary capillary wedge pressure is normal (<12mmhg).Still the patient is in  hypotension with  evidence for vital organ under perfusion like oliguria and reduced mentation.

What is vascular tone ? What sustains  the flow of blood into the tissues  ?

The entire  vascular tree could form a   few 100 kilometer length.(Capillary /arterioles /venules included). While , it is easy to  percieve heart as  a dynamic pumping organ ,  it is a less recognised fact the entire vascular tree is also  pulsating  to every beat. That is the rhythm of life. What makes the vascular tree to pulsate ? Apart from  contraction of the heart  , there is an  intrinsic tone for the large , small arteries and the arterioles and veins  .This tone is vital for pushing the bllood into various organs and return into venous circulation and subsequently back into the heart.

microcirculation shock cardiogenic septic

The  millions of perivascular cuffings and the artreriolar smooth muscles  can be considered as  small micro pumping stations situated along side every cell.

It is very important to emphasize here,   if  tone in these microcirculation is less than optimal , the patient’s circulatory  system can never complete the desired circuit  even if the heart has 75% EF . This exactly is happening in circulatory shock . The vascular tree fails to accept and return the pumped blood  in timely fashion.

What controls this tone ?

It is chiefly under the control of autonomic nervous system.The endogenous vasoconstrictors , the adrenergic nervous system, the endothelins , the angoitensins constrict the vascular smmoth muscles while endothelial relaxing factors ,( EDRF -nitric oxide relaxes it ). There is a delicate balance between these forces.

A cardiovascular health of a person is not simply having a healthy heart , he has to have a healthy vascular system with intact biological activity.The fact that , not every one with sepsis react with poor vascular tone indicate inherent capacity to neutralise toxic vasodilatory neuro transmitters.

Is there a invisible parameter called vascular ejection fraction  in circulatory  system?

Yes. It must be . We rarely discuss it . The vascular tree has an important role for pumping the blood into the tissues.  It needs micro manometers to assess the systolic and diastolic dimensions of small arteries and arterioles . But  what  we know is ,  it is grossly impaired in circulatory failure.The vessels especially the arteriolar smooth muscles which determine the perfusion pressure of cells go into state of permanent relaxation. The vascular smooth muscles lose control from autonomic innervation and become flabby. It is the   DCM equivalent for blood vessels. The arterioles no longer regulate blood flow and fluids get sequestrated in various viscera,( often called thrid spaces) and organ dysfucntion sets in. The resultant hypoxia aggarvates the tissue stagnation by producing still unnamed vasodialtory mediators.

What are the pharmocological approches to increase the vascular tone of a failing vascular tree ?

It is a very difficult problem even in this modern era of vascular medcine. Once set in ,  these patients invariably go downhill .The primary underlying problem  ,  often sepsis  need to be corrected. Usually these  patients need multi organ support.Vasoconstrictors like epinephrine,nor epinephrine , dopamine  can sustain vasoconstriction temporarily . As we know the vascualr smooth msucles can not be kept on this assited contrection mode for long.It is bound to fail .Patients native autonomic function has to recover fast to wean of this support.

What is normal circualtorty time .How is it altered in circualtory failure  ?

The normal circualtory time is 15-20 seconds.It is many times prolonged in circualtory failure inspite of the cardiac contraction being normal

What is effective circulatory volume ?

The body fluid compartment is divided into ICF,ECF & interstitial  spaces.At a given time , the fluid in the extracellular space  can only  take  part  in circulation. A good blood pressure does not always mean a good tissue perusion why ? This is very important to realise as blood pool has to dynamically exchange with intra cellullar compartment. At times of shock the blood can bye- pass the cells through the alternate circuits in the periphery of micro circulation. So what is circulating in the system may not be taking part in tissue perfusion .This is the concept of  effective circulatory volume.This is especially noted in hepatic shocks and in some terminally ill malignancy.

Is there a venous shock syndrome ?

Cardiologists  often show a  step motherly  attitude to venous disorders. In fact many  of the   cardiovascular  specialists   think their   job is  taking care of  heart ( Of course , a little bit of aorta and venacava !) .It is surprising  to know,  there is little  scientific data on determinants  venular and venous tone (Both small and large veins).

The power of venous system should not be under estimated  as it pumps  many litres of blood every minute  defying gravity ! For this to happen it needs a vigorous tone .Where do it get from ?  : The same  autonomic nervous system that controls the heart. Remember , in pathological states there is a  great chance for this to go out of control. So venous shock is a clinically distinct possibility. In fact inappropriate administration of nitrates which reduces the venous tone has resulted in many adverse events in RV shock.

In a patient with circulatory shock , we would  never know  how much is contributed by venous side and how much by arterial side .This is important as in circulatory shock we administer all vital drugs through veins.Now it is thought  systemic venous  dysfunction also contribute to shock state.

Clinical situations of circulatory failure or shock

Bacterial shocks

  • Gram negative sepsis
  • Staphylococcal shock

Viral shocks

Dengue/Swine flu etc

Others*

  • Dissiminated intravascular coagulation
  • ARDShypoxic shock
  • Elderly,Diabetic  autonomic neuropathy
  • Persistent post operative hypotension due to silent autonomic neuropathy.
  • Some cases of Spinal shock
  • Toxins – Scorpion etc(Intense vasoconstrictive shock )
  • Terminal shock in liver failure/Hepato pulmonary   syndrome

* Idiopathic unexplained persistent hypotension , with difficulty to wean off from vasoconstrictive agents is a commonly encountered problem in any intensive care unit.The exact mechanism is not known.When we are not clear about the mechanism  we  generally blame it on the  the autonomic nervous system !

How common is the mixed shock syndrome ?

This is more common than we realise .The classical description of multisystem failure is a direct consequence of this.

Can a cardiogenic shock transform into a peripheral circulatory shock ?

Such a scenario is  possible  .A  resuscitated cardiac arrest may end up with a recovered heart but a loss of vascular tone  possibly due to hypoxic vascular damage. .Many times cardiac patients are kept (Post PCI/CABG ) on large doses of  vasoconstrictors or IABP that can induce  tachyphylaxis. It may result in difficulty in weaning these drugs.

How can circulatory shock result compromised cardiac function ?

The common effect of any shock is  reduced organ perfusion.So even in peripheral shock , the coronary blood flow gets compromised especially if these patients have a silent coronary lesions which are otherwise not significant , becomes sites of hemodynamic hurdles during hypotension.This may result in global contractile dysfunction, or a coronary event.

What is vasoconstrictive shock ?

Epinephrine and nor epinephrine are  very potent  vasoconstrictors .If levels of these becomes excessively high , the blood vessels go in for sustained spastic state that can impair the micro circulation .Some times  this results  in a  good blood pressure in the major vessels but severely compromised tissue perfusion.This particular situation has been reported after scorpion envenomation , and in  rare cases of pheochromocytoma .

Final message

Primary circulatory failure or shock (With largely intact cardiac function without hypovolemia) is a common problem in critically ill.  The entire  macro and micro vascular tree goes for a  stunning reaction and  goes for  a sleep in a  semi dilated  state  . It can  be termed as  Arterial  or Arteriolar   shock. Contrary to  all those hi-tech   mechanical stuff for supporting a failing heart (LV assist, Impalla, Abiomed , ) the available options are very little here  . The response to vasoconstrictive agents are  also unpredictable. Correcting the multi organ failure  and targeting the primary cause  is the only hope.

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