Dr.S.Venkatesan MD

When dyspnea plays a dual act as “Anginal equivalent” . . . extreme caution is required in the bed side !

May 19, 2011 by dr s venkatesan

Angina and dyspnea are the  two cardinal ( classic ) symptoms of cardiac disease . While dyspnea is a manifestation of raised LV filling pressure ,  angina  implies reduction in blood supply to heart .

In other words dyspnea is related to excess blood in the  lungs and angina is due to less  blood in  the coronaries  !

So , it is obvious  even though these  two  symptoms are closely knit entities , patho- physiologically  they are  distinctly different  in real time , when an actual  cardiac event unfolds in the bed side .

This also partially explains  , why simultaneous  presentation   of  angina and dyspnea is  relatively  uncommon in CCUs  , than one would expect .(In a given patient , one of them will be dominant)

Photo courtesy : http://www.sciencephoto.com

Why and how our patients (and also  physicians !)  get confused  with dyspnea and angina ?

When William Heberden described  angina over a century ago ,  he was  so meticulous in his description and observation. In fact , it was,  as if  he felt the angina  himself  and wrote it .One can rarely  expect such a  description from any of our patients .  So , it is not at all a surprise  for mistaking  any mid sternal discomfort as dyspnea instead of  angina . (This error in describing angina  is the commonest cause  for dyspnea  playing this  dubious dual role !)

When to suspect  dyspnea  as an Anginal equivalent ?

Here  are some real situations ( and clues )  where  dyspnea  may be  considered as  anginal equivalent.

• Diabetics
• In elderly with autonomic dysfunction
• Patients with chronic beta blocker and other anti anginal drugs.
• Post PCI/CABG patients (Normal LV function but dyspnea : Denerved heart blocks pain  ?)
• Exertional dyspnea that stops immediately could be anginal equivalent.
• Dyspnea with palpitation is  rarely be anginal  equivalent as palpitation indicate good LV /mitral valve function.
• Dyspnea on  isometric  exercise rather than isotonic exercise .

Mechanism of anginal equivalence

While the trigger for dyspnea is elevated LVEDP  which   stimulates the  stretch receptors in lung .For angina ,  it is the free nerve ending in myocytes that gets irritated and generate pain signals.

When ischemia  presents as dyspnea  two mechanisms are considered. One is myocardial , other is purely neurogenic.

1. It is  believed critical   ischemia  of myocardium  ( Defective Ca ++ uptake  into sarcoplasmic reticulum) induce  “a wide area  diastolic dysfunction” of LV  that   raises  PCWP  to generate  dyspnea. Further , ischemia induced regional LV dysfunction  that  subtends the pap muscle could  result  in ischemic  MR and severe dyspnea. (Exertional Mitral regurgitation is getting major attention now  )
2.  In many patients with diabetes or autonomic dysfunction the velocity of  pain signals  become sluggish  or  blocked  en-route  to brain stem . Often they change track to travel in the nerves  meant  for  carrying somatic siganls  ,  J receptors  , intercostal spindle etc . This spill over and cross talk  creates a  false sense of dyspnea , whenever ischemia  occurs. This is attributed to the  wide and complex  neural network of thoracic sympathetic ganglions.

Some of the known  associations with Angina equivalent .

• Diastolic dysfunction
• Ischemic MR
• Small rigid  left atrium
• Atrial fibrillation

How to  investigate a patient who is  suspected to have  angina equivalent dyspnea ?

• ECG
• X ray chest
• Echocardiogram will settle the issue most times.

Nuclear scan and angiogram in deserving patients

When can  angina and   dyspnea occur together  ?

Angina and dyspnea  if   truely  occur together causes  grave concern for the physician.

This indicates two things .

1. The myocardium is ischemic  and generates  pain (And possibly ongoing necrosis) .
2. Simultaneously its  pumping or receiving function is also compromised resulting in  entry block from the lung resulting in acute dyspnea.

Both are ominous signals . This situation occurs  most often in  STEMI with LV failure .

If  dyspnea occur in NSTEMI/UA ,  it is a worst possible complication . GRACE  registry quotes  maximum  mortality for unstable angina with cardiac failure .The reason being the cardiac failure in UA is due to non necrotic global ischemic stunning of LV myocardium with or with out acute  mitral valve failure.(Flash pulmonary edema)

Why angina is rare  in  chronic congestive  cardiac failure ?

The main reason being  , a severely dysfunctional heart  contracts  poorly .In reality , it is never thirsty for blood  . Even if it  is  perfused  well  , there is no good muscle  mass  to burn the ATPs from it .A failed myocardium is  more or less a  sleeping  myocardium .It does not even have the  energy   to cry with pain at times of ischemia ! .However significant the ischemia  is ,   it can often  evoke only  a gasping sensation .

The other explanation  is more imaginative . In cardiac failure heart  dilates .The end diastolic and end systolic  volume is high. The cardiac chamber is always filled with  excess residual blood .This , some how tend to perfuse the myocardium directly and provide a good reserve .This may be  more important in  RV perfusion  .( Trans myocardial laser revascularization is based on this concept – direct myocardial perfusion from the chambers)

While angina is  rare in chronic cardiac failure,   it should also be realised ,dyspnea  is  rare in  uncomplicated acute coronary  syndromes. We know ACS  primarily present with angina.  Exceptions are always there.

In elderly, diabetic , with co morbid   patients ,    ACS  may  present without  angina . Instead  they present with vague dyspnea and shortness of breath . It is here ,  physicians  face a tough task to identify  dyspnea  behaving like   angina  equivalent.  Of course , the  good old  ECG bails us out most of the time.

Therapeutic importance of recognising anginal  equivalents ?

The revascularisation  procedures (CABG/PCI)  are too good  in  relieving  angina , but least effective in providing relief from dyspnea.So  real anginal equivalents if recognised properly can be subjected to early revascularisation .

Can we consider  exertional dyspnea as evidence for ongoing ischemia  in a post MI patient ?

This is tricky question . We do not have answers to it. Readers can try to  answer . The commonest cause of dyspnea following MI is due to physical deconditioning and associated LV dysfunction.

Final message

Coming back to the basic question  , Is  this dyspnea  . . .  an angina equivalent  doctor ?   No simple answer is available .

The first and foremost investigation to do  is ECG .This will settle the issue many times.  Next is the reassessment of  history  clinical  presentation and past history.  Every patient with unexplained dyspnea must undergo a minimum of three investigations (ECG,  X ray chest and Echocardiogram )  If any of these  suggest a cardiac compromise   further evaluation is   indicated.

So, the message here is ,  clinical findings  are insufficient  to rule out ischemic etiology for dyspnea.

References

Nil . Every thing is my random thoughts !

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Posted in Uncategorized | Tagged angina equivalent, dyspnea, dyspnea heart vs lungs, dyspnea vs angina, exertional dypnea, lvedp and dyspnea, mechanism of dyspnea | Leave a Comment »

Why cardiologists would love to outsource history taking and physical examination to para medics ?

May 18, 2011 by dr s venkatesan

Most important MCQ in clinical cardiology

Many cardiologists  would love to do away with detailed  clinical examination because  . . .

1. They think it is an inferior job to do  . By skipping  it , they get a false sense of superiority.
2. It is a time killer  and eat into precious cath-lab  time
3. They no longer believe in  these “perceived – primitive” medical methods.
4. Fear of colleagues making  fun of hem if they  indulge  in detailed clinical examination.( At-least in India ! )
5. To give more job opportunities  to para medics.
6. They are no longer confident about making a good clinical examination as they  are neither  trained  adequately nor interested in it !

Answer :  All of the above can be true .  The 6th response is  likely to be  more  correct !

While cath labs can prevent few deaths occasionally . . . it is the general wards and OPDs that add life every day

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Posted in Cardiology - Clinical, Cardiology-Coronary artery disese, cardiology-ethics, Cardiology-Land mark studies, critical care ccu | Tagged clinical cardiology, mcq in clincal cardiology, medical ethics, outsourcing clinical examination | Leave a Comment »

Discontinuing medical education : Why current medicine is often not the correct medicine ?

May 16, 2011 by dr s venkatesan

One of the greatest medical sermon of our times  is   “Doctors must   constantly update their knowledge , Continuing medical  education is as sacred as their profession  !  If you are not updating your knowledge you cease to a doctor “

It is fashionable , but true  to state  modern medicine lacks humane  care . Modern medicine  is  challenged by a huge  technological ,  commercial  onslaught  where common sense takes  the back seat

Hence , doctors need to renew not only  their  academic competence   but also  their ethical  fitness  every  year !

Aggression  could be the other  name for  modern medical care . For every  new  invention , treatment   or guideline that  is  approved  an equal number  is shelved after few months or years  for safety reasons.

Bulk of  medical updates  for  current age physicians  is nothing , but asking   them to forget  all those wrong things that has been meticulously uploaded in their brains in the recent past  ( Recall the classical story of drug eluting stents )

If this is the  case . . . then  . . .  what for  we  are  updating ?   and  for what  we are  learning and forgetting  ?  and  . . . how frequent we need to forget ?  Of course  , there is a big chunk of   human tribe  who  can never master the art of forgetting ! Some mistakes are permanently etched in their terra byte hard disks .

Is there a place  for backdating and discontinuing  medical  education  ?

What  man- kind needs  at times of  medical  crisis  ,  is  not  the current  treatment  but the correct  treatment    .It is our duty  to  find  all those  trustworthy  drugs  & treatment modalities  that were  sent  to  the gallows by the modern medical forces   for various reasons !

If  some of  the gems in  medicine are  left behind in  past  “time domain”  ,  it is  mandatory  for us  to go  back in time and   catch it , adopt it and disseminate it !

Further ,  whenever  the  hyped   “medical updating sessions ”  turns out to be  synonymous with adding nonsense (It is  becoming all too common these days   !) we should resist   it by all means !

For many . . . Hippocrates and his medicine sounds dirty now !

If  only we back-date  our knowledge   .  .  .

Todays  youngsters  can learn a secret that liver enlargement can be diagnosed easily  with their  hands ,  without  waiting for a  CT scan report !

If only we back-date  our   knowledge  . . .

We can realise  Aminophylline can save so many  lives of cardiac  failure  , which  our newer inotropic agents are struggling to accomplish .

If only we  back- date  our knowledge  . . .

We can calmly manage  acute MI with lignocaine  even in a country side  .  Amiodarone unfairly replaced  this  efficient  anti  VT  molecule  for no academic reasons !

If only we back- date  our knowledge  . . .

We  can  advice simple non pharmacological intervention for  stage 1 HT   than prescribing the  glamorous  sartan molecules  form a  multinational  ARB shoppe.

If only we back- date our knowledge  . . .

We can  promptly recognise  cardiac failure  without  ordering  for the error prone   BNP . Back dating also  helps us to under stand  that post infarct angina is a  glaring sign  for presence of   viable myocardium  and prevent us from undertaking a  2000 $ PET  excursion !

If only we back- date our knowledge  . . .

We can  send  all our uncomplicated , asymptomatic   STEMI  patients ( in class 1 )  straight to  their  home rather than to cath lab  play grounds !

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Posted in Cardiology - Clinical, cardiology -Therapeutics, cardiology innovation, cardiology-ethics, history of cardiology | Tagged art of medicine, cardiology update, cme, continuing medical education, discontinuing medical education, hippocrates medicine, history of medicine, jama, medical backdate, medical ethics, medical update, nejm, revisited | Leave a Comment »

A defiant LAD refuses to die even after hanging !

May 15, 2011 by dr s venkatesan

Thousands of  coronary angiograms are done every day. Cardiologist no longer get excited to see exotic coronary lesions .Still , some images can be striking and dramatic. Here is an angiogram from a middle aged man  with stable angina  , who was  one among the routine early morning diagnostic studies  in our cath lab.

Who chopped the neck of this LAD ?

How this man was able to fill up the distal LAD almost completely? (With a complete cut off  right in the neck of LAD )

Are you sure there is antegrade flow ?

Do you get any clue ?

• Can a trickle of  ante grade flow  sustain  a  TIMI 3 FLOW  ?
• Or is it a  very efficient  instant collaterals  from LCX ?

Yes . The first one is right . An almost invisible antegrade channel  doing a exemplary job !

How is it possible ?

Realize an important fact . The distal flow beyond an obstruction  is not primarily dependent on degree of obstruction but the status of the distal vascular  bed .  If it is normal  even a hair-line patency  can  profusely perfuse the distal myocardial segment. This is what is happening to this man with a stable angina and perfectly normal micro vascular bed.

Lessens  from this Image.

Do not get fooled by the lay man’s logic. Realise there is  no simple relation  between  the degree of obstruction and degree of  blood flow impediment.It can be linear , curvilinear , or even inverse depending upon   the evolution and timing of obstruction  ,  number of lesions , presence or absence of collateral support , finally and  most importantly  the integrity of microvascular bed .

The  distal vascular bed drops its resistance drastically  once it senses  the problem in  proximal segment . This is based on Bernoulli principle and  is akin to how a  garden hose pipe  can simply increase  the velocity  by tightening the nozzle.*

* The garden hose analogy is a gross simplification of   complex factors that determine coronary blood flow.But it effectively clarifies a point ie  coronary blood flow is least dependent on coronary  stenosis (until  very late stages)

**Note further : This  hemodynamic  principle may not apply in acute occlusion as in STEMI  , where   acute  obstruction  often has a linear relationship with the quantum of blood flow.

By the way what happened to the above patient ?

Since he had significant angina there were no debates regarding management.  He  is posted for elective PCI this week-end .(We  can’t  get a stent just like that unless it is a real emergency  .Ours is a  Govt hospital !)

What is your take . Is it a going to be tough cross ?

I feel so , but my colleague Dr Gnanavelu   strongly  differs !

Let me post  our experience during PCI shortly.

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Posted in Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, cardiology innovation, cardiology- coronary care, Cardiology-Coronary artery disese, Hemodynamics, Infrequently asked questions in cardiology (iFAQs) | Tagged 100% lad, 99% lad, bernouli principle in coroanry artery, coroanry doppler, coroanry perfusion pressure, coronary angiogram, coronary collateral circulation, coronary hemodynamics, coronary microvasculature, coronary stump with timi 3 flow, courage trial syntax score, distal coronary resistance, hanging the lad, intra coronary pressure, lad total timi 3 flow, ressitance in series, timi 3 flow | Leave a Comment »

When calf muscles can double up as LV assist device . . .your patient saves a million !

May 14, 2011 by dr s venkatesan

                                                     Every day thousands of  hearts  end their life   due to terminal heart failure . Much more  lives are  confined  to their bed rooms.In refractory cardiac failure and severe LV dysfunction the only  long-term option is cardiac transplantation.

Medical therapy has reached its saturation point.  Neuro- humoral modulation shows some promise. The other modalities like cardiac resynchronisation ,LV assist devices ,  ventricular  reduction surgeries ,  restriction devices , mitral valve splinting  are  still experimental .

Simply watch this Image : Your heart will get Energy

Modern day  cardiology is trying to add life to these dying  hearts  .

There are two aims

• To prolong survival
• Improve functional capacity (Make them at least take care of daily activities and live a fairly independent live)

This is the purpose of the  mushrooming heart failure clinics all over the  world . These clinics , though started with  good intention , ultimately   become  feeding  centres for so many experimental  bridge modalities  , sometimes  with an  infinite wait for  a potential donor  or at the mercy of their insurance companies  . (Many time it turns out to be a  bridge to heaven as the patient fails to cross it !) .

Even though there is strict criteria for terminal  heart failure ,  in practical terms it has many issues .Temporary functional deterioration is misinterpreted   often .

Premature  dependence on LV assist devices and  indulgence  in inappropriate  mitral valve reconstructive  procedures are the currently most important pseudo cardiac interventions .( Myosplint/AV groove tying etc)   Some where along   the  academic  corridors ,   we failed to realise many patients can bridge themselves  to a  transplant (or even   self de-list  from transplant programme  )  provided we are willing to wait and take few   risks  .

It is observed exercise training  programme is awfully inadequate in most centres  who deal with late stages of cardiac failure.

The hidden link  between skeletal muscle and  cardiac muscle

Skeletal muscle  function is impaired in cardiac failure . This impairment is attributable  to both  dis-use and low cardiac output.  Proper training of these muscles can not only improve the functional capacity  but also  sets in  a positive hemodynamic cycle  that   ultimately improves cardiac function as well.

In  our  country we have data  of  thousands of patients  with severe LV dysfunction living with the much ridiculed  digoxin   ,   diuretics ,  ACEI  and minimal exercise living a comfortable life for over 10 years .  It is often said in  cardiology class rooms ,  do not whip a tired horse  as the   failed heart needs rest  .This statement  has  truth  in it even in  this  space age cardiology !

Whipping  a failing heart with electrodes in the name of CRT   could be as  bad as  whipping with inotropic agents . This is not a  personal joke ! This fact has been repeatedly  proved by various inotropic  studies in terminal heart failure(Dobutamine to be specific ) Even CRT  is a suspect .These patients walk for 30 meters  further  with  no convincing survival  benefits .(Of course it requires a ICD -Combo to prevent sudden deaths ) Zero impact in non sudden deaths ?

Can  we propose a  new therapeutic  concept to our  patients   ?

Do you  want to   live with a  low functional capacity (Restricted  life   still  happy  )    for 5 years   or live  apparently unrestricted  life   and die prematurely ?

                         In simple terms,  for all those patients with severe  grades of  heart failure   the  best advice could be . . .to  avoid the levels  of exertion that cause dyspnea / Modern gadgets  may help relieve  exertion for a short  while  , but it  can cut short your longevity * (* This is not a threatening message. This applies to near terminal stages of cardiac failure .All other minor grades of CHF are encouraged to exert up to 70 % of their limits.)

Peripheral mechanism in cardiac failure.

We know cardiac  failure is not a simple  mechanical failure of heart , it activates a complex neuro endocrine system which makes it a systemic disorder .Many of the current research is aimed at favorably modify this. It is now certain Skeletal muscle function is a  major determinant of  cardiac failure outcome and hence a therapeutic target .

If you have good muscle mass ,  good diaphragm and intercostal muscles one can  compensate the compromise inflicted by the heart to a large extent.  We know,   the entire vascular tree has a mechanical function  to do . The stiffness and compliance of aorta , other  major vessels, the muscles  through which these vessels  traverse determine the  ultimate  efficiency  of  circulation.We know  the pulse wave , as it  travels to the periphery , gets amplified. This amplification is not without any significance. It aids in muscle  blood flow . This agumnetation is missing in poorly trained cardiac failure patients. Further muscle respiration is synonymous with  functional capacity . Numerous defects (Both structural and functional )  in skeletal muscle mitochondria are reported.

This is why meticulous  exercise training  becomes an important   intervention in  cardiac failure . There are very good studies that document   muscle respiration defects  getting reverted  with  proper exercise training and  muscle  care  .  Among all muscles the   calf  and thigh muscles show great promise.   We have observed  cardiac failure patients  with good calf muscles ,  outperform others with identical ejection fraction.(Will be published shortly )

Strangely there is no comparative  studies between calf muscle  efficiency   and other available modalities  in cardiac failure .

The concept of  Venous pump vs  Arterial pump

Skeletal muscle mass acts not only as venous pump  it also has a modulating  effect on the arterial pulse transmission .A good venous  pump will activate  vascular  tone . In congestive heart failure  a the RV filling pressure is raised,  blood tends  to  move sluggishly  in right heart chambers .  A proper venous tone  can alleviate this . Well trained  calf muscle  can exactly do this  by a controlled elevation  of  IVC pressure at times of exertion . 

 Dyspnea  of muscular  origin (Peripheral dyspnea)

The symptomatology of cardiac failure has an intimate  realtionship with skeletal muscle integrity  !

Lactate in blood and  hypoxia  in   exercising muscles  can trigger   non hemodynamic dyspnea . Further , there is strong reason to believe  the sensation of dyspnea   is perceived at the chest muscle level  (By muscle spindle length/tension   mismatch ) .It is not known whether lower limb  muscles can generate a feeling of dyspnea  !

But , one thing is certain   by altering the tone of the muscle  spindle and the  optimising the  stretch signals the peripheral component of cardiac dyspnea can be significantly neutralised . This  is what  happens in well-trained   cardiac  failure patients .

How to train the skeletal muscles ? ( In to heart friendly  muscle )

• Passive stretch
• Simple 6 minute walking three times a day will help .
• Muscle massage and toning
• Drugs like Trimetazidine may improve muscle metabolism by better ATP utilisation
• Diligent use of diuretics (Excess diuretic can make your muscle exhausted )
• Chest exercise for improving intercostal muscle function

 

Final message

Skeletal muscle training  in cardiac  failure  could be as important as  the  digoxins  , diurteics   and ACEI .When a 300 grams of heart muscle is struggling  , God  is willing to  help  it with huge muscle mass that lies elsewhere , we should read the silent  signals of nature . Many cardiac failure patients  realise this and live  a happy live without artificial assistance .This applies  in all grades of cardiac failure .

For  all those physicians  out there in modern hospitals who treat cardiac  failure , spend at least  few minutes  for prescribing a good exercise  program with a specific  mention about calf muscle function  . After all , it  may turn out be the most efficient  RV/LV assist device !

References

                                                                     http://content.onlinejacc.org/cgi/content/abstract/30/7/1758

 http://www.uptodate.com/contents/skeletal-muscle-dysfunction-and-exercise-intolerance-in-heart-failure

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Posted in cardiac drugs, Cardiology - Clinical, Cardiology -Interventional -PCI, cardiology -Therapeutics, Cardiology -unresolved questions, cardiology innovation, myocardial disease | Tagged calf muscle in cardiac failure, lv assist device, skeletal muscle function in cardiac failure | 1 Comment »

What is the mechanism of action of Adenosine in AVNRT ?

April 22, 2011 by dr s venkatesan

Adenosine is a  purine analogue. Acts by stimulating outward K+ channel  of AV nodal tissue, more specifically  in the posteriorly   located  slow pathway in the vicinity of  coronary sinus.

Another action of adenosine is inhibition of cAMP , which is similar to beta blocking action may also help in terminating the tachycardia.

Adenosine : A 10 second cardiac miracle

• 12mg bolus is administered , preferably in a central vein (Not mandatory  though)
• Termination is usually abrupt . Transient VPDs are observed during termination.
• Transient flushing may occur.
• If the patient is taking Aminophylline group of drugs (Which are adenosine antagonists) the AV nodal blocking action may be neutralised .

(It may be apt to recall  at this juncture ,  Aminophylline is used in sinus node dysfunction or AV block to increase heart rate )

Reference

A good one from Medscape http://www.medscape.com/viewarticle/585287_2

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Posted in cardiac drugs, Cardiology - Clinical, Cardiology - Electrophysiology -Pacemaker, cardiology -Therapeutics, Cardiology-Arrhythmias | Tagged adenocard, adenosine and slow pathway, adenosine av node hyperpolarisation, adenosine iko channel, adenosine in avnrt, avnrt, k+ channel activation by adnosine, pottasium channel activation, psvt, slow fast avnrt, svt | 1 Comment »

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