Dil Se Technical: July 2011

Saturday, July 30, 2011

Living with a single coronary artery : Let us trust the nature atleast once in a while !

We are at the mercy of the three major coronary arteries (LAD,LCX,RCA) that sustain our life . Their job is clear cut .It has to perfuse about 300 Grams of live bundle of energy for an average of 6-7 decades.

What are the hurdles it faces , how it overcomes these obstacles forms the fascinating story of "survival of human heart"

When coronary blood supply is confronted with a sudden compromise as in ACS , often the heart has little time to respond . Hence the damage and risk of death is more. Even here there are lots of safety mechanisms and natural lytic process that limit the loss of life to less than 30 % of all STEMIs. This implies nature protects against the death in 70 % of individuals and help them to reach hospital.*

*Among those who reach hospital , we the cardiologists try to reduce the mortality to about 6-7 % (20% without treatment ) with all those hi-tech gadgets .It is a different story and will be addressed elsewhere .

When it comes to chronic insults , the heart has a unique potential to stage long haul battles. It has many tricks under its sleeves when challenged in a slow fashion.

The main weapons are two

1. Coronary collateral circulation.

2. Ischemic preconditioning.

Here is a patient who fights his life even after all his three coronary arteries totally blocked and surviving with one of the branches of left main -Ramus intermedius .

If you have thought his RCA was the savior you are mistaken .

To every one's surprise his RCA was awful as well !

He had angina which was troublesome but manageable .Was able to live a life with acceptable standards (Indian standard ) After the angiogram he received CABG. A turbulent post operative course ensued due to various reasons . He struggled but fully recovered . . . and ultimately reached the previous standard of life !

Final message

Modern cardiology is all about not trusting powers of nature .

But youngsters should realise the enormous potential of those invisible powers.It may sound philosophical , but please remember . . .after all . . . philosophy is nothing but search for truths. Atleast believe in them once in a while !

Dr.Anil Kumar Gangotia
Sr.D.M.O.( Indian Railway Medical Services)
Former President I.M.A.Gwalior.
Former Director IMA CGP ( M.P.)
District Coordinator for Physicians Trining Initiative ( HIV/AIDS)
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Can you diagnose diastolic dysfunction by ECG ?

We presume ECG fails miserably against echocardiography for assessing hemodynamics , while echocardiogram has little value when it comes to studying electrophysiology . Ironically , we often ignore the fact , ECG can provide important long-term hemodynamic data . The pattern of chamber enlargement give us vital clues to the prevailing hemodynamic stress and loading conditions. While echo can be termed as an anatomical and physiologic modality , ECG apart from its unique capacity to record cardiac electrical finger prints , it provides useful , anatomical , hemodynamic information too !

While Doppler is a fascinating modality to measure hemodynamic data in a moment to moment fashion it can never ever tell us , what has been going around in the preceding months or years. This is were chamber size helps which give us chronic physiological information (Chronic Doppler ?)

A simple E:A reversal in mitral inflow doppler can be a innocuous finding in isolation . If it is associated with even minimal grades of LAE it gains huge importance. That is why left atrial size is funnily referred to as HB A1C of diastolic dysfunction ( A marker of chronicity of diastolic dysfunction)

If LAE is so important to diagnose diastolic dysfunction , why we are so obsessed with doppler filling profiles of mitral valve ,pulmonary veins, mitral annular tissue Doppler and what not ! .Many of these sophisticated doppler methods are extremely operator dependent and are subjected to technical and mathematical errors. Especially , with tissue doppler where we magnify the errors as we filter extremely slow tissue motion .

For many decades we have failed to impress ourselves , about the importance of subtle P wave abnormalities in the ECGs of hypertensive patients.

In fact those innocuous looking slurs and notches in P waves , suggest the left atrial stress and a definite marker of underlying LV diastolic dysfunction .

P wave is the only electrical wave that occur in diastole .Hence there is no surprise ,i gives us enormous information about this phase of cardiac cycle .

If only we look at them carefully, zoom it (Now it is made easy with so many softwares) analyse critically we can find a wealth of information about the atrial behavior in hypertension.

Experience from our hypertension clinic with periodic echocardiograms suggest , the following ECG findings can be good markers of significant diastolic dysfunction .

Notched P wave
Wide P waves
Slurred P wave
Bi-phasic P waves

* Surprisingly , these abnormalities correlated with at least grade 1 diastolic dysfunction even in the absence of for LAE or LVH by echocardiogram.

** In an occasional patient P waves can widen due to inter atrial block or conduction delay. This a rare exception for wide P waves without LAE.

Final message

A well recorded and analysed ECG can predict diastolic dysfunction with fair degree of accuracy .This fact need to be emphasized by every one . Next to ECG , LA size and volume by 2d echo are excellent parameters to assess diastolic function in a long term fashion. Sophisticated but error prone , momentary doppler parameters are getting too much attention at the cost of simple , shrewd ECG and 2D echo !

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How does Beta blockers help in vaso vagal syncope ?

It is a well proven concept beta adrenergic blockers have a useful role in controlling the frequency, and intensity of vaso- vagal syncope .

One may wonder how an anti adrenergic drug help to counter hyper vagotonia syndrome !

This is because during vaso -vagal syncope , the inital trigger is sympathetic . A sudden hyper adrenergic surge occurs that stimulate the vagus, ( Which overshoots the initial quantum of adrenergic signal) and cause a systemic vasodilatation , hypotension and bradycardia.

How does adrenergic surge stimulate the vagus?

By two ways

Brain stem spill over effect in medulla (Vasomotor to tractus solitarius)
Cardiac stretch caused by hyperadrenergic activity . This stretch initiates a vagal reflex especially from the base of the heart (Similar to Bazold Zarish reflex ). This mechanism is thought to be more important than brain stem spill over , that's why it is referred to as neuro-cardiogenic syncope .

How does beta blocker help?

It sedates the adrenergic centre which modulates the trigger .It also blocks the sympathetic afferent limb of the syncope circuit.
Anxiety and panic reactions are close associate's of vaso- vagal syncope. They are not only considered as prodrome for syncope but also act as important triggers.This is effectively tackled by beta blockers .
Finally , beta blockers soothes the mycardial stretch receptors by reducing the ventricular shear stress (Reduced contractility and wall stress ) hence neuro-cardiogenic axis is pacified.

It is important to remember beta blcokers can only prevent/ reduce episodes of vaso vagal syncope. It may aggravate the situation if administered shortly after the event , as bradycardia and hypotension is dominant in the recovery phases.

*During an episode of vaso vagal syncope atropine group of drugs is most useful .

Which beta blocker ?

Propronolol is the prototype as it has non selectivity and good penetrance of blood brain barrier , which is the most appropriate site for suppressing hyper adrenergic drive.

Cardio selective beta blockers do have a role as cardiac stretch receptors is one of the two target sites .

Final message

Ironically , in the long term management of vaso-vagal syncope , anti adrenergic drugs have a major role rather than atropine like drugs .

Poor R Wave in precardial leads would indicate old anterior MI , why can't poor R waves in inferior leads reflect inferior MI ?

Can you diagnose inferior MI with poor R waves ?

No , you need a "Q " that's for sure ! Do not diagnose inferior MI without a q wave . ( The luxury of diagnosing MI without q waves is available only for LAD region )

Any axis deviation ( even 30 degrees) from base line can alter the inferior lead qrs morphology to a great extent. R wave amplitude is primarily determined by the initial septal depolarisation . So if the inferior septum is intact it will never allow to inscribe a q wave . Further , limb leads are bi polar leads and they are sum-mated potential reflected along the entire bottom half of the torso . Hence it is not reliable to attribute significance to presence or absence of r wave (Unlike chest leads).

The lung and diaphragm exert not only electrical insulation but also mechanical alteration of septal profile with phases of respiration.

Counter point

Not really . . . you do not need a Q waves to diagnose inferior MI , electrically diminutive R is same as "Q"

There is an alternate way of reasoning too . R wave is muscle , We diagnose LVH with tall R waves so muscle loss should be equivalent to R wave loss .We have innumerable examples where low voltage R waves are recorded in inferior leads after a well documented inferior MI.

How do you diagnose old inferior MI by ECG ?

Near normal ECG with degeneration of q waves and regeneration* of R waves
Residual T wave inversion
Simple low voltage inferior leads
Slurred or notched qrs complex in 2 3 AVF
Rarely with atrial abnormalities and AV nodal prolongations

The concept of regenerated R is well established . And it brings to the age-old debate of R with live muscle Q is dead muscle

Regeneration is salvaged muscle (Natural salvage , awakening from hibernation etc)

How good is Echocardiogram in diagnosing old Inferior MIs ?

Surprisingly , echocardiography do not help much either .Technically inferior transmural MI is expected to leave a residual wall motion defect. But many times it do not. Many non q inferior MI (Is there such an entity ?) do look perfectly normal by echo .

The primary reason for this is , infero-posterior surface is anatomically remote and it makes wall motion analysis difficult .Newer tissue motion analysis (Velocity vector imaging) could aid us better.

Some times a trivial or mild mitral regurgitation is the only sign of old inferior MI as the pap muscle lags behind in it's functional recovery while free posterior wall is fully salvaged and contracting well .

Final message

It needs that extra bit of of knowledge to expose our ignorance.

Even in this maddening scientific era we have valid reasons to go back to fundamentals of R wave and Q wave genesis in MI , where clarity is lacking .