Archive for January, 2010

Vasovagal syncope is the commonest cause for syncope in our population.It is also referred to as simple syncope .The mechanism is thought to be  an abnormal overshoot  response  by the vagus  in response to a  sudden surge of  adrenegic activity  usually occurring  in erect posture following   , often an emotional or physically stress full situation .The  receptors for  this  reflex pathway is thought to be located  left ventricular myocardium .

There are  two components  for  the VV syncope

  • Cardio inhibitory
  • Vaso depressive.

The quantum of contribution  by each component in a given episode of syncope varies. Pure vasodepressive or cardioinhibitory forms can occur .

Diagnostic issue

Before labeling  a patient as simple vasovagal syncope all potentially serious , cardiac causes must be ruled out. this may require a fairly extensive investigation in some

Read the related blog  : Why syncope is rarely  fatal ?


Management of vasovagal syncope.

  • Reassurance is the mainstay . By this we mean , V V syncope may never kill . . .
  • Prevention  – Involves  identifying syncope prone situations  & taking precaution
  • Emotional support
  • Pharmacological approach

Some will benefit from beta blockers, fludro cortisone(Increase the intra and extra cellular  fluid space )

Since  these are   simple ,   cheap  treatments ,  we worked over time to innovate  &   find some interventional solutions for this life threatening condition !!!.  Thus ,  the indication for cardiac pacing for vasovagal syncope came into vogue .

DDDR pacemaker was implanted worldwide for thousands of patients with vasovagal syncope .

It took  many years  for our  intellectual brains  to realise ,  there are  two limbs to vasovagal syncope Pacemakers ,  at  no stretch of imagination  is expected to counter vasodepresssive component of the syncope.

And then this article came !


Water ,  (Simple  H2O ! ) administered at right time in right quantity can prevent most  episodes of vaso vagal syncope . When a tumbler of water can be substituted for a  10000 $ misadventure  (DDD pacing)  , and  further  we have  hundreds  of similar examples in modern  day health care  ,   no surprise  why our health care system is  sinking  along  with our economy !

Epilogue :

In this  21st century   medical “AVATAR ”  , we need to realise   in a strong manner,   low cost  medicines  often   provide   high  quality  cure  ” while ,”   many of the  high cost  therapies  may  end up in  low quality  treatment !

It took 50 years of intense research of  medical comunity to realise ,  a good diet , physical activity and quitting smoking has the greatest way to control  and reverse  the cardiovascular epidemic . Please , note all of them come at free of cost .

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Sinus node which orchestrtes the rhythm of life  gets it’s blood supply by a small blood vessel arising from either RCA or LCX. (55 :45%) . The  course of sinus node  branch  is highly variable .

There are three distinct pattern observed.

  1. Posterior encircling  of  SVC .(50%)*
  2. Anterior  encircling  of  SVC(40%)
  3. Form a  “garland like ” anastomosis  on either side of SVC (10%)

* Some refer to as clockwise and counterclockwise course.

SA node is a spindle shaped structure with a length up to 20mm . Extending from cranial to caudal aspect.The pecularity of the blood supply to SA nodal artery is  , it enters the SA node either in it’s superior aspect or inferior aspect never  in  the mid part. There can be water shed area in the either ends depeding upon the entry.This can have  electrophysiological and  pathological significance .

The other consistent feature is that ,  the major trunk of SA node artery courses through the central core of SA node.In fact , many times pathologists recognise ther SA node ,  with the help of   this arterial course.

Is there a collateral blood supply to SA node ?

It is not common  . Rarely  atrial branches of LCX /RCA  can have extensive anastomosis with SA nodal branches .The hemodynamic significance  of which is  not known. 

Ischemic SA nodal disease has become an important entity . As the cardiologists are preoccupied with opening  occluded coronary arteries  in cath labs , it  is not  surprising to note, there is little  ongoing  research  in the anatomy and physiology of SA nodal  blood supply.

We have to go back in time to get some great articles on the  subject

At this point of time ,  we should realise  the 1ooth anniversary of  SA nodediscovery passed of silently  .  Kieth and Flack  found the SA node with bare eyes  in the year 1907 , when none of the present-day investigations  including ECG and X RAY were  not even conceptualised !

With  tributes to those humble pathologists like  M.J Davies, R.H .Anderson, T.N. James,M. Lev ,J.L.Titus  who   followed   the foot steps  of  Kieth and Flack ,

Here is a  link to one of the great articles on the blood supply to SA node


Related point : How do you  recognise  the  SA nodal artery in coronary angiogram ?

During RCA angiogram it is many times confusing  to identify the SA nodal branch . In RAO and LAO views the plane of exit  of SA nodal branch from RCA  will be determined by the  course  it is going to take .(Anterior vs posterior encircling pattern). The conal branch  which is often the first branch of RCA  ,  also behaves aberrantly  many  times. So, we can’t have a rule of thumb in identifying SA nodal branch .

When SA node branch originates from LCX it has to take a long route but once it reaches the SVC/RA junction it takes  one of the above described course. It is not clear whether LCX  fully understands it’s responsibility  , when RCA ignores it 45 % of times .  There is reason to suspect the commitment and dedication of LCX  because it rarely supply  the SA node by a   seperate branch.  It is often the left atrial CX  that comes to the rescue  and give a twig to the  SA node .

Considering the complexity of SA nodal blood supply  , one can understand  why some develop premature sinus node failure. One can never determine with evidence , how much of SA node destruction is due to ischemia and how much is due to age related degeneration and fibrosis.

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ASD is the most common acyanotic heart disease. Clinically distinguishing  ostium primum (OP-ASD ) from ostium secundum (OS- ASD) is not an easy  task . A Wide fixed split pf S2  , a short systolic  murmur and PA pulsations  in left second space, a loud P2 and a hyperdyanmic RV occur in both .  The following features might give a clue for OP -ASD .

  • While  OS-ASD is  often an  isolated anomaly , isolated  OP- ASD is very rare.It usually occur as a part of partial or complete AV canal .
  • Early onset of symptoms
  • Early onset of pulmonary arterial hypertension( PAH )
  • Extra murmur of  1.VSD 2.MR (Cleft mitral valve ) may be present
  • Biventricular enlargement (MR/VSD)
  • ECG -Left axis deviation -Structural defect in left bundle ?

Confirmation is by Echocardiography and angiogram is rarely required today . Documentation of  classical goose neck deformity of LV outflow confirms the diagnosis.

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Assessing   LV function is the most common indication  for doing  echocardiography .Sinus tachycardia is the most common cardiac arrhythmia in humans. So, it is no surprise we encounter the above  situation  very often  in echo labs.

The principle behind echo assessment of LV function is to measure the  left ventricular wall thickening and the resultant reduction in LV cavity size.

The LV wall thickens in  systole and  returns  to baseline  thickness in diastole.When the heart rate increases the  rate of thickening has to be faster,  as do the rate of subsequent thinning in diastole. The endocardial segment of systole and thin segment of diastole tend to overlap at the base . borders are too shaggy and many times the thick So identifying true reference point  for endocardium become a difficult task.

It is  ironical  ,  inspite of  M mode echo  being termed outdated and obsolete by  most Echo schools , it remains the most utilized modality to measure LV function . It is  highly unlikely  , M-Mode derived LV EF   will be  replaced in the near future .This is because   “simplicity will always   prevail”  over  quality and accuracy .

It is all the more important  ,  the already poor index of M-Mode – LV EF %  becomes further  error prone at high heart rates.

It need to be emphasised , the impact of tachycardia in confounding  the true EF is greatest in  patients with preexisting LV dysfunction .

In a normal heart the errors are less and it can be  safely stated , tachycardias  rarely result in clinically important LV function errors

Does 2D derived EF by modified Simpson  overcome the problem of tachycardia related errors ?

To a certain extent ,  “yes ” . Here again the endocardial excursion is so fast one might have difficulty in marking the border.Automated  border detection algorithms are never corrected for heart rate related errors.

Other issues in LV function assessment  during tachycardia

In the presence of CAD  , the coronary arteries  often have varying degrees of obstruction.  Hence ,the  myocardial  segments  also exist  in varying degrees of ischemia.

In patients with significant CAD ,tachycardia due to any cause (Compensatory /Non compensatory -Fever, anxiety etc) can be considered a stress to myocardium . (By all means ,  can  we  consider it   an  equivalent of  dobutamine   stress echo! ?)

We know , dobutamine stress echo , has a variable effect on the contractility of LV. It can either  depress , argument, or  have neutral effect .Different lesions have different response depending upon the baseline viability of myocardium . For example  a 70% lesion  subtending a infarcted  –  viable segment may improve , while a 90% lesion supplying a normal LV segment may either worsen or hypercontractile .

What is poor man’s viabilty test ?

Grossly differing LV EF % in two different echocardiograms at two  different heart  rates may be an indirect clue  for the presence of viable myocardium.(Poor man’s PET or Thallium !)

The final message

The above concepts remind us the complexity of measuring the true EF in the presence of CAD. Purists,  may even question the existence of  a ” true normal  EF” in  a given patient

So, in the presence of marked tachycardia what is the ideal advice ?

  • Aviod measuring EF % during tachycardia , atleast in patients with CAD.
  • Use simpson method whenever possible
  • Atleast attempt it  few times,  you will overcome the laziness !

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T waves  are the most enigmatic waves  in clinical electrocardiography  . This is not a surprise , when you consider a tall T wave  and   a   markedly  inverted T wave both can be normal in  at least in 6 leads out of 12 lead  standard electrocardiogram ( V1 V2 V3 , 2 ,3 AVF, ofcourse the AVR  )

Common T wave patterns that can either be physiological or pathological

  • Tall T wave
  • Inverted T WAVE
  • Notched or Bifid  T wave
  • Biphasic T wave

* T wave polarity is strongly determined by the direction of QRS vector. Generally it should be on the same direction as QRS. In the presence of conduction defect or chamber hypertrophy  this gets  altered and is refered toa s  secondary repolarisation changes . This has to be differentiated  from primary biphasic T waves.

What is a biphasic  T wave ?

A T wave which is inscribed on either side of baseline is called biphasic T wave .

Many of the normal persons can have a biphasic Twave.

A typical biphasic wave can be two types

  • Terminal positivity
  • Terminal negativity

Terminal negativity is more significant than terminal positivity , especially in CAD.

A terminal negativity especially in mid precardial leads would suggest ongoing ischemia in LAD territory .

This happens due to dispersion of repolarisation between endocardium and epicardium.

The other mechanism could be the altered ventricular  gradient between QRS vector and T wave vector.

Why biphasic T waves are important ?

The biphasic T waves are known for dynamic change in polarity . It may either pull down the or pull up the  adjacent ST  segment . Prolonged QT interval is a closely related to the biphasic T wave.

Some times a U wave can be inscribed in such a way it may mimic a biphasic T wave. This is especially common in baseline bradycardia.

LVH is one of the common cause of biphasic T wave (Usually terminal positivity )

Biphasic T wave as mode of presentation of NSTEMI

Even though , ST depression is considered the dominant and classical theme of NSTEMI  , It is now recognised NSTEMI  has another  mode of   common presentation as biphasic T waves.

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A combination pleural and pericardial effusion is more common than we realise .

Here is a patient with  both  effusions.

  • The etiology was tuberculosis.
  • Twin pressure effect   increases the chances of tamponade
  • Careful echocardiography is required to identify both .
  • Large left  pleural effusion can mimic a pericardial effusion some times . A useful clue is looking at  the LV  apex.It is invariably free in pleural effusion.

Unanswered question

Is there a anatomical continuity between pleural and pericardial spaces ?

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Exercise stress testing(EST)  is one of the common investigation modality in the evaluation of CAD.he indication for EST  generally fall into two broad categories.

  • Diagnostic in patients suspected to have CAD
  • Prognostic evaluation in patients with established CAD .9Many times after a coronary angiogram)

Currently there is a major shift in our thinking,  patients with  classical angina  may undergo coronary angiogram  directly .This is understandable as the stress test  has little to   improve  diagnostic  sensitivity and specificity in patents with clinically obvious CAD.

So , it is now becoming clear , the diagnostic  value  is  increasingly  restricted in the evaluation of  o atypical chest pain .

What is a strongly positive response ?

  • Gross ST segment depression > 2-3mm
  • Occurring in stage one
  • Fall in blood pressure
  • Prolonged angina into recovery

What is the angiographic  correlates of strongly positive EST?

  • Critical left main disease
  • Near total proximal LAD /LCX
  • A severely compromised bifurcation lesion

Morphological correlation

  • These patients  often have eccentric lesions with irregular margins.
  • unstable  lesions
  • Lack collaterals

What is the effect of vigorous  excercise on a critical flow limiting lesion ?

The shear stress over the plaque  increases  with  exercise  and  the  transcoronary gradient can reach a theoretical 60-90mmhg .One can imagine the what this stress can do to the  unstable lipid core .This is the reason unstable angina is an absolute contraindication  to EST.

What does a strongly positive EST imply for the patient ?

  • It indicates he needs urgent CAG and  most likely an immediate revascularisation.
  • Often , these patients have prolonged angina , and mandates admission in a coronary care unit.
  • there has been many incidence of ACS in these  patients  within 24hours of EST.
  • Lives have been lost  on their  way back    ,   as  these patients are sent home , as EST is a  OP procedure .

Final message

  1. It need to be realised a strongly positive response to EST  could  be a  clinical equivalent of  unstable angina .
  2. The common response  from a   physician or cardiologist    after witnessing  a  gross ST depression to EST  would be   “Had  I known this  I would have sent him straight into cathlab instead of EST ”
  3. If only , we give little ear to our patient’s  history we can pick the high risk clue in 9 out of 10 cases !
  4. It can be argued ,  a strongly   positive  EST  by itself  is  “A  clinical diagnostic  failure”  ,   ie  failure  of the physician  to recognise  the likely hood of strongly  positive EST ie a left main disease.
  5. These patients  should never be sent home immediately  after the EST .This is fraught with a risk SCD
  6. Most of them will require observation in step down unit for 24 hours  and if feasible they should be posted for coronary angiogram in the earliest available slot.

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