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Archive for the ‘Cardiology – Clinical’ Category

The LV ejection fraction ,  is  the most revered medical parameter for both physicians and cardiologists.There are anesthetists and surgeons , who  do not  operate  a  cardiac patient  without knowing it.There are  physicians  who  do monthly assessment of EF in their patients  with dilated  cardiomyopathy.

Now ,every one is interested to know what is their EF ?  Thanks to the global  information highway .We witness ,   patients who are extremely delighted when their  EF increases from 45% to 48% . Similarly , they get depressed when it falls by 2% .

Why this hoopla around the LV EF ?

Every one knows EF is nothing but a LV contractile force at a particular  beat of the heart . It is possibly a crudest possible way to screen for   LV function.( Of course it can still be useful  in patients  with established myocardial disease to follow up  LV dysfunction)

The  most important caveat in  EF is it’s dependence on the loading conditions  of heart .It is   also  heavily influenced by the  heart rate.We now, even a severely dysfunctional LV can contract vigorously with inotropic stimulation  like dobutamine  or whenever local catecholamines.

Our obsession with EF is complete and it is not expected to get cured in the near future.

There are many hundreds of articles in cardiology literature  which  ridicules the EF as sole parameter for assessing LV function. Still ,  it is the number one parameter to asses LV function  in real world as well as in  vast number of land mark clinical  trials .  Are all those trial  results to be doomed ?

Even as  the  LV EF is   being labeled as  futile index  ,   we  also  realise we have not traveled  far from our great clinical   ancestors . Thousands of  years ago   the Chinese  yellow  emperor  of medicine  found  the cardiac contractility  by pulse volume  and predicted death accurately  ,  probably  better  than the live 3d echocardiography   derived EF   guided by LV volume rendering algorithm !

The purpose of this article is to tell the current generation physicians  there are some simple and probably  accurate  clinical tips  to rule out significant LV dysfunction.

One can confidentially tell  the LV  EF  would  be > 50%  in 99% of population if they have the following !

  • A brisk upstroke of carotid pulse.*
  • A well palpated tapping apical impulse**
  • A Loud  first heart sound(S1)
  • A  totally normal ECG (Even a normal QRS complex  is suffice !) ***
  • Normal CT ratio in Xray chest
  • A  comfortable brisk walk of  at 6 km/hour for 10 m .

* A brisk central arterial pulse is nothing but the reflection of LV DP/DT a sophisticated echo parameter assessed  with much hype ! A good thumb with an   alert brain can accurately tell a given patients dp/dt is within normal range.

** A loud S1 and tapping apical impulse indicate the velocity of closure of  anterior mitral leaflet.Which is in turn reflect the force of contraction of the antero lateral  papillary muscle of LV .So what you hear a loud s1 is nothing but the contractile function of the most important  part of LV namely the pap muscle of LV.

*** A normal ECG ,  generally tells us  all is  well with LV myocardium . Finally,  it makes  immense sense to correlate the functional capacity to EF. (90% correlation)

Final message

Mind you ,  all the above modalities come either  free of cost or a fraction of  echocardiography  . It is estimated up to 90% echocardiography scans to R/O LV dysfunction can be avoided . The global health care costs can be saved and be utilised for some better purpose like protecting our atmospheric shell  from the  hazardous   gases

Note of caution

While ,one can rule out signficant LV dysfunction by above mode  ,  it can miss  other forms of LV dysfunction like relaxation defect etc . (ofcourse the EF also misses it !) .Judicious use of functional  imaging modalities are adviced in those who require it.

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Even though it is a great vein , often the imaging pulmonary veins by echocardiography is a not a pleasant excercise.

This is due to the following facts

  • The pulmonary veins are posterior structures
  • They occupy the far field of echocardiographic window
  • The pulmonary veins often enter obliquely into the LA
  • The course of PVs are highly variable ( Like RCA origin !) especially in ASDs ,where identifying PVs becomes all the more important

Hence no fixed imaging angle can be advised . But generally a pattern is observed.

  • Right pulmonary veins are best viewed in apical 4 chamber or 5 chamber or in between (Especially RUPV is  seen best in 4.5 chamber view !)
  • Left pulmonary vein , best visualised in  Para sternal  long and short axis view.

Other modalities for imaging pulmonary veins

TEE : Can be  very useful since it is brings the vein closer to the probe .But needs more expertice.

Contrast echo :Probably a simple and best modality often underutilised.

Very useful to clinch the diagnosis when PVs take abnormal course as in PAPVC .

MDCT , Spiral CT, MRI  are the new age modalities that can provide us  with dramatic  3d images of PVs.

The  echocardiogram will always prevail over these sophisticated gadgets for its simplicity and also it’s ability to give us the physiology of pulmonary venous flow which is vital in many diseases(Constriction, Diastolic function etc)

The following illustration is a gross attempt to simplify the imaging of PVs.Please note the rules may not be applicable in all.

Left upper and lower pulmonary veins in short axis view will be posted shortly .

Reference

The images are  based on  personal observations and  an  excellent insight  on the topic from  Department of Cardiovascular Medicine, Guangdong Provincial People’s Hospital, Guangzhou , China

http://ejechocard.oxfordjournals.org/content/9/5/655.full

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Are the drug eluting stents really better than bare metal stents ?
A million dolor question ? , No . . . a billion dolor question
A study which answered most convincingly with a huge data base  published in LANCET 2007.
  • 38 trials  , Metaanalysis
  • 18 023 patients with
  • 4 year follow-up of up to 4 years.
  • No mortality difference from bare metal stent vs DES
But unfortunately there is  no takers for this  study . The usage of DES continue to  surge ahead  .
The problem facing the medical science in the current era
It takes years  of research to get  into  the truth    and  still   longer time  for  us  to  accept it ! Ironically  falsehoods have immediate patronage and there is no incubation period !

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Human body is a collection of trillions of cells.  Life  is nothing but , a bundle of energy flowing across each of these cells  .Every  organ  has a  specailised mode of communication among themselves and others. When a cell is in an excited state , there is a  likelihood of spontaneous electrical activity.This can happen in nerve cells, cardiac cells , GI tract,  or virtually in  any cell  which has a porous cell membrane and ionic fluxes across it .

  • Each cell membrane has a resting membrane potential . It  varies between -60 to – 90mv in most cells. When this potential increases there a propensity for  arrhythmias in heart  and convulsions in the brain , peristalsis in intestines and so on .
  • Drugs  like local anesthetic lignociane acts by blocking the  Na+ channels and there by neural activation .Similarly magesium  acts on these channels to reduce the excitability of these cells.
  • We know,  the sharp ascending stroke of cellular  action potential is mediated by Na + .Blockage of this channel blunts the action potential voltage and thus  the  early and late after depolarisation is prevented
  • Magnesium sulphate’s anticonvulsant action is directly  attributable  to this membrane stabilising action

Thus , membrane stabilising action  can be termed as “membrane sedating”  action

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Cannon Sound

A loud first heart sound (S 1)   which is  heard intermittently in patients with complete heart block (CHB)  is  often referred to as  cannon sound .

What is the mechanism of loud S1 in CHB ?

We know , the intensity of S 1 is  mainly determined by the  relative position of mitral leaflet (To be precise, the  anterior mitral leaflet(AML) )   at the onset of systole.  We also know the  PR interval  has an intricate relationship to  mitral leaflet  position .

The shorter it is ,  wider the leaflet separation  and a longer PR interval makes a mitral leaflet assume a almost closed position   by the time the ventricle contracts.this happens because  a long drawn PR interval fills the ventricle more completely and LVEDV  reaches the maximal levels and LV blood column lifts up the mitral leaflets , and hence the LV  contraction  which follows does not close it with a  bang. In a short PR interval the opposite happens and hence a loud S1 .

In CHB we have variety of PR intervals ranging between  very short to long   ( falling just before the qrs complex) It is not difficult to understand this , as P waves are totally dissociated with the QRS complex  in CHB.In fact p waves have a liberty to fall any where in the ECG tracing , some call this as marching through the qrs complex !.

Hence typically the S1 is variable in intensity , varying between loud to soft.  When  P wave falls just behind a QRS complex , it generates a very  loud S 1  that is called cannon sound .This happens intermittently.

Cannon wave

This is entirely different phenomenon except that it shares the word cannon . Cannon a wave is  a visual finding on the jugular venous pulse.(JVP) .It is a systolic event . It is also seen in CHB as like a cannon sound

This is a giant a wave  in  JVP  when the right atrium contracts against a closed tricuspid valve. In physiological situations atrium contracts with an open AV valves , so that ventricle gets  filled . So atrial contraction  does not does not cause any reflux of blood back into vena cava.

But, when the atrium  contracts and  finds , the AV valve closed  there is no other option   for the incoming blood  to reflux  back into  the neck veins. This is seen as giant a waves called as cannon ” a “waves

With reference to ECG  location ,  this cannon”  a” wave occurs   whenever p wave falls within the ventricular systole ie  the QT interval .The cannon waves also occur intermittently like the  cannon sounds.

What is the  peculiar relationship between cannon a wave and   sound ?

In fact , it is  a non- relationship.  Though  , both the sound and wave   can occur in a given  patient with CHB ,   they can not occur simultaneously .This is because ,  for cannon sounds   to occur  the  P  wave has to fall before  QRS  and for cannon waves to occur the  p   waves must fall after QRS  ie with QT interval .

Clinical significance  of  cannon wave

Complete heart block is the most common situation for cannon waves to occur.

Ironically ,the VVI pacemaker which is used  to treat CHB does not prevent the cannon waves , and atrial contractions continue to occur at random , causing various degrees of intermittent venous reflux into the veins .This may produce, worrisome venous palpitation in some (Usually settles down after few weeks !)

Some attribute , the so called pacemaker syndrome ie giddiness, dizziness to this abnormal venous waves triggering the carotid baroreceptors (Venous -artery spillover )

Will DDD pacemakers  eliminate venous cannon waves ?

We hoped so , it does in fact . But,  it really happens only if the A sense V pace mode . A pace V pace mode with programmed PR interval is not a realiable way to produce AV synchrony. It is  common ,  many of the DDD pacemakers fall back to VVI mode either intentionally or by mode switching  for various reasons.

//

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Thrombolytic therapy was a  mini revolution  when it was introduced two decades ago .It has since evolved  , not only in the  molecular structure  but also in it’s usage pattern.

The first generation streptokinase is continued to be used even today  . While the latest generation thrombolytic agent TNKTPA(Tenekteplase) is threatening  to push the  old warrior out of  CCU.

(Of course the  American Physician & Pharma  community  never  gave the due respect to  streptokinase  !)

The two common indications  for thrombolytic therapy  are

  • STEMI
  • Acute pulmonary embolism

Uncommon indications

  • Stroke( Can be common in few institutions)
  • Prosthetic valve thrombosis
  • Rarely DVT

From the beginning , there has been a controversy  about the thrombolytic  dosage and  the speed with which it is to be administered .Let us recall , streptokinase was initially  used  in  various regimes ( 5-30lakh units between a 10 -3hr infusion )  Later ,we arrived at a consensus at  15L units  in 1 hr infusion . TPA also experienced the same . Which  settled  for front loaded regimen(35 + 65mg)  . The confusion reappeared when we developed bolus thrombolytic agents( TNKTPA) .

In STEMI thrombus formation  is  often a one time process  while thrombolysis is a continuous process. In pulmonary embolism both  thrombus formation  and lysis  is often continuous process  .

The success of thrombolysis depends on the sustained  drug concentration ,  the pressure at which the drug interacts  the thrombus.

Many times it is prudent to administer  intensive heparin after thrombolysis  to prevent recurrent thrombosis. Further ,  most of the pulmonary embolisms  will require long term anticoagulants.

How to maximize the success of thrombolytic agents ?

  • Local catheter based thrombolysis can be tried  within the coronary ostium (Largely unpopular)
  • Within the pulmonary artery for pulmonary embolism (Still considered an useful option )

It  makes sense , to administer these thrombolytic agents over a prolonged period of time so that the lytic process gets wider recruitment of the natural lytic mechanisms.

When a drug is infused continuously , the drug  reach the thrombus in  a pulsatile manner , which facilitates thrombus dessication  (Like drip irrigation ) . A long acting drug even with a high concentration may not be  very effective , since  the  drug is required to produce a mechanical effect  here . (Unlike say a long acting antibiotics !)

TPA in Pulmonary embolism

The inadequacies  of  2 hour infusion of TPA is  glaring in acute pulmonary embolism .We believe   a 48-72 hour streptokinase infusion   has a definte edge   over a short and brief TPA infusion.

Issues need answer

It is yet , not understood why we can’ t infuse TPA as  a   long term infusion like streptokinase .

Advantage  of bolus TNK TPA  in  pre-hospital phase of STEMI

The argument in favor of bolus dose  thrombolytic agent  is  the ease of administration .

The other the major advantage claimed  is ,  a 10 second  TNK TPA   in STEMI  can  substantially  reduce the time window   and facilitate  early completion of thrombolysis .

Counter point

But , the  later concept is hard to prove  . . .

In fact , there  are  no controlled studies  available for assessing the   efficacy of TNK-TPA   vs  Streptokinase   with reference to various time windows. We presume so many things. An  incomplete   early thrombolysis  may not be better than a  more  successful  but  slightly delayed TIMI3 flow .

As scientists,  when  we try  to answer these  question we  ask for data .  Are we getting it any way ?  Are the existing data reflect  fact ?     We  wonder,  will we may never get   an  hourly  angiographic  data base  about the IRA  patency  in  TPA bolus  vs streptokinase infusion .

It is most unfortunate,   with  many of the critical questions   still to be answered ,  the cardiology community believes ,  they  have  reached the  summit  of  knowledge  about thrombolytic therapy . Current perception is , the research on  existing  thrombolytic drugs  is  deemed to have been complete .

In this hyped  era of interventional coronary  care  ,   it is a remote possibility   to have any  further comparative studies on thrombolytic agents .

The greatest threat faced by  us  today  is the destiny  of  modern medicine is   often  decided in  few corporate board rooms  and   hence   research questions  rarely  emanate from bed side !

In this scenario, where we are not likely to generate   genuine  clinical  data ,  the only way to move   forward is   to go  by  our experience – ” Genuine  experience to be precise . . .”

Final message

Ease of administration should never be the criteria in choosing a thrombolytic agent . It   can severely    compromise the quality of thrombolysis  ! especially in pulmonary embolism and to a certain extent in STEMI.  Success   rarely  comes  with ease  . . .

Many believe , the choice  between  streptokinase   & TPA    goes much beyond it’s academic reasons.  TNK TPA (Tenektepalse) has come in a big way to replace streptokinase  even   in developing countries.  Ofcourse it is backed by a huge study  ! (ASSENT) .

The cost effectiveness and worthiness  of TPA over streptokinase  was  never proved comprehensively.

Note of caution :

The observation made above is   based on personal  opinion  in  about   20 patients  . Readers are  argued to do their own  analysis on this issue and come to a conclusion .

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Coronary artery anomalies are relatively common . It can be either in it’s origin, course ,  or termination etc.

There are two major sub groups.

  1. Anomalies associated with other congenital heart diseases (Both cyanotic and acyanotic)
  2. Isolated coronary artery anomalies .

The second category  which we encounter in cath labs frequently  does not have major implications . RCA and LCA arising  away from it’s respective sinuses ,Separate origin for LCX, or conus, RCA from left sinus or a high take off of RCA are the common anomalies.

While  coronary anomalies are commonly associated  in complex congenital heart disease (TOF, DORV, TGV, etc )

Isolated  complex anomalies of coronary arteries are extremely  rare

This happens , when one coronary artery arises from pulmonary artery instead of aorta and   it becomes a fascinating disease !

The ALCAPAs  and ARCAPAs

When the LCA originates from PA it becomes a  rare cause  of  left to right shunt .it is referred to anomalous origin of LCA from PA (ALCAPA) .

The ALCAPA is many times common than the “ARCAPA”

We report a case of ARCAPA (Anomalous orgin of RCA from PA )

The unique features of ARCAPA  could be

  • Isolated ARCAPA is very rare.
  • Only a handful of  patients reported in literature
  • These children present with more of right heart failure as RV function is compromised .
  • A continuous murmur in 2nd LSCS without cyanosis gives a clue
  • Angina is rare unlike ALCAPA
  • Mitral regurgitation is uncommon as LV function is relatively intact.
  • The q waves in V5 V6 we see in ALCAPA is conspicuous by it’s absence
  • ARCAPA is often ssociated with bicuspid aortivc valve, VSD etc
  • Left to right shunting can be significant .
  • 64 slice MDCT is a great investigation in this entity
  • Surgical ostial transfer is preferred so as to restore twin coronary circulation

Image and video of the ARCAPA will be uploaded shortly

Reference

1 http://asianannals.ctsnetjournals.org

2 http://ats.ctsnetjournals.org

3 http://ats.ctsnetjournals.org

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STEMI is the commonest cardiac emergency . Many believe , we  are close to  conquering  it .  It is hardly the truth .

  • The  mortality is  up to  30 % out of hospital and another 6-8  % within CCU  and another 2 %   at  30 days due to recurrent ACS   .This  is followed by an   annual attrition rate OF 25  due to progressive LV failure  .
  • The commonest mode of death is electrical,  ie primary VF.
  • Mechanical deaths are also equally important. Free wall rupture carries 100% mortality . Ischemic MR, Ventricular  septal rupture (VSR ) may also result in deaths.

Here is a case history and ECG of a  patient with STEMI .

After thrombolysis , the paradox happened . ST elevation  increased by 4mm and soon the patient became restless with worsening pain and became silent instantaneously ,  with monitor showing EMD and asystole .A diagnosis of free wall rupture was made.

What we used refer  in our CCU (Madras medical college Chennai .One of the oldest CCU in  South Asia )

as   “Action pontentialisation”  of surface ECG . This ECG finding has  great  clinical significance .

Here is a zoomed up view of a qrs complex of  the patient , which is very

closely resembles an action potential

Picture courtesey  http://ocw.tufts.edu/Content/50/lecturenotes/634488/634591

Pathological basis of  “Action potenial”  Like ECG

  • When the ST elevation is huge and wide it mimics  an action potential .
  • Myocyte action potentials are normally recorded epicardially in physiology lab where a  micro electrode with glass pipettes directly enter the myocyte.
  • A giant ST elevation and a sustained dome indicate , the quantum of  electrical injury is  very large and the  ECG electrodes is picking up the myocyte electrical events like that of a intra cellular electrode.
  • It is to be recognised  ,  ST elevation in chest leads is substantially taller than limb leads   because the exploring electrode  is located just above the myocardium . But,    when a  huge  ST elevation  is recorded  over a limb lead (as in this patient )  one can imagine ,   how intense the electrical  charge  of  the myocardium  should  have been  !

This heavy downpour of electrical energy that  emanate from the myocardium   means two things

  • The area of infarct is very substantial
  • The tissue in question is  very unstable .

Clinical correlates of  action potential ECG

  1. Damage is transmural , the   infarcted area is soft, friable and often hemorrhagic .
  2. The pericardium is also  likely to get involved in the injury process .
  3. The myocardium is  rupture prone or already torn .
  4. Even minor hemodynamic stress can be fatal in these patients
  5. An episode of vomiting, a fall in blood pressure,   an episode of  LVF or a short run of VT is suffice  to result in a fatality.

The death happens by a sudden rupture ,  EMD and asystole .

Can a life be saved  by the much fancied Emergency PCI  ?

Not really. The PCI  can not reverse the myocardial damage ,  so it’s role is little . But , any way it should be done and  .  .  . it  will  be done  in most institutions to give the benefit of doubt (Of course , with  a definite the risk of doubting  !)

What is the risk  of  PCI in these situation ?

The infarct related artery * if opened up can convert a bland infarct into a  “angry red”  hemorrhagic  infarct .This   is as good as  giving  the patient ,  a  farewell  party for his journey to heaven !

Note : Primary PCI  definitely  saves life in STMI . The  * is applicable only in persistent ST elevation , late after an acute MI.

How could  have the above death prevented ?

As one of the comments to this article  suggested, we need to have methods to identify impending rupture early and accurately .This should  followed by a prophylactic  surgical intervention (Reinforcing the friable myocardium – with a patch or mesh  )  .This is again not  a easy decision to make .

Final message

When the ECG  assumes  a shape of an  action potential ,  it is often a sign of  imminent  death  . Even though it may sound a pessimistic  view  it is often the truth  . Of course , an  emrgency PCI or  CABG  are  the only options available , we have  to be remember the above truth  ,   as we   play  those sophisticated  games  within their coronary arteries.

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The bundle of his divides into two

  • Anterior fascicle
  • Posterior fascicle
  • Middle septal  fascicle*

Middle fascicle * Many  dispute  it’s presence .  One may wonder , how  can anatomy be  under  dispute  ? If you cut a heart you should be able to clear the dispute .  But medicine is not that simple . . . What you do not see may be more important than what we see.

The anterior  fascicular block (LAFB) is one of the common conduction disorder. It ‘s significance :  Can  be a  benign  or a  dangerous entity depending upon the clinical situation .The  problem with  LAFB  is , it is diagnosed primarily by the axis shift it inflicts on the QRS complex.

In a strict sense, it is not a ideal way .There is  a tendency to label all significant left axis (> -60*) deviations  as LAFB. This  practice has made diagnosing LAFB very common in elderly, hypertensives, etc. In these situations it may not mean anything ,  except to suggest a  delay in conduction in  left anterior  fascicle.

If we filter out all these  benign  axis shift  ECGs  , the true organic pathological LAFB  may  not be that common .

Organic , LAFB occurs in the following situations.

  • Degenerative  blocks (Part of Lev & Lenegre’s disease)
  • Aortic valve disease .
  • Hypertensive heart disease
  • Post MI (Either alone or part of bifascicular or trifascicular block )
  • In association with dilated cardiomyopathy

Even in degenerative  , ischemic conduction defects LAFB is far more common than LPFB why ?

The traditional explanations are

  1. Anterior fascicle is relatively sub epicardial in location
  2. It is a  long and thin  structure prone to damage easily
  3. Exposed to the mechanical   stress of   LVOT **
  4. Anterior fascicle has  only a single blood supply(LAD)

** Which experiences  the peak LV  pressure  at > 100mhg and a dp/dt  up to  2000mmhg  (While,  the posterior fasicle is located  away  in the inflow portion of LV  , which is exposed  to low pressure – at best 10mmhg filling pressure )

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Human body is  now  approached by many of the physicians as  collection of  multiple  organs . This is  the price we pay for modernity in medical science. The era  of great physicians  in general medicine has gone . Now, a  super specialist  of one organ  is  rarely concerned about what is happening to the patient’s  other organ ,  it is  considered    foreign to him  ! While ,  this is the dominant thinking pattern of   modern-day specialist

Let us  travel intime  and  go to the year 1954 . . .

Three  physicians from Michigan ,USA  published  one of greatest observation in clinical sciences , namely the ECG changes in various forms of stroke .

Now , a shrewd physician  , will  suspect a subarachnoid hemorrhage (SAH) by looking at the ECG when the clinical situation demands . But , what we need is every one should develop that skill . We have seen errors happening  even in big institutions (or is it because it is big ?)  when  an elderly person comes with deep T  inversions with or without  altered sensorium being rushed into  CCUs  & cath labs instead of  neurology units.

We  need to teach  our junior  colleagues  . . .  That ,  ECGs of patients with  acute neurological syndromes  (ANS)  can mimic as acute coronary syndromes (ACS) ( especially in elderly ) .

The following ECG changes * are observed during stroke

  • Deep  T wave inversion –   Sub arachnoid hemorrhage
  • Cerebral thrombosis   –      Prolonged QT interval, U WAVES
  • Cerebral hemorrhage –      ST segment  shifts /T inversion

 

The ECG changes tend to occur very early after CNS injury.May last up to 1 week. They are not useful to identify the type of stroke. But , deep T wave inversions strongly suggest SAH rather than ICH or thrombotic stroke.

What is the mechanism of these ECG changes ? 

It is a clear proof that heart and brain are interconnected by neural network. All the noted changes occur during myocardial repolarisation . (ie ST segment )  The current thinking is  (Ofcourse , it is same as our thinking  in 1950s !)  it is mediated by adreneergic surge  initiated by CNS insult  transmitted to  myocardium by the sympathetic system.

Why should SAH produce more  ECG changes than others ?

It is possible the net adrenegic drive from the brainstem and spinal cord will be greater in SAH as it  spreads the entire CNS  through the cerbro spinal fluid. While localised ICH and infarct is  likely to generate less adrenergic impulse. 

Reference

Read the link to circulation 1964 .With courtesey to circualtionaha.com

http://circ.ahajournals.org/cgi/reprint/9/5/719.pdf

This came 50  years  ago , we still quote their work and no one has improved their work . 

Final message

If  only  we make the  clinical bed side teaching as a  regualr habit ,  we  do  justice to   our  great  physicians of the past ,   who enriched  our  life  with their  clinical  skills  and  passion for knowledge  sharing .

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