One of oldest hospital in the world , is now an UNICEF heritage site. Santa Creu , Sant Pau original hospital built in 1400 AD rebuilt in 1900 by Catalonian modern architect Montaner.
Archive for September, 2014
TVI is a hemo-dynamic echo parameter measure from Doppler spectrum usually in the outflow.This parameter is used to calculate cardiac output.
Time velocity Integral
One of the hottest debate in the recent world cardiology forum in Barcelona WSC 2014 , was about how to tackle incidentally detected non IRA lesions during primary PCI.
So far , the dictum is , one should not meddle the non culprit lesions unless demanded by hemodynamic instabilty .The next option is to do a staged PCI for these lesions. (Few days later). or just forget about these lesions unless they are critical.
Now new studies are appearing that suggest doing all “do-able” lesions must be stented in one go ! This is obviously inviting trouble .The worry is not in the concept but with the dubious track record , fragile guidelines and potential ethical debacle of the cardiology community !
Stent “As you want and as you please” has already invaded our mindset in the chronic coronary scenario. Now in 2014 , we want more freedom in acute coronary syndrome as well ! We can’t ask for a referee less game of soccer !
We clearly know coronary arteries are to be respected and do not deserve indiscriminate stenting especially in ACS where the early hazard is more.
A recent story which I heard was a height of futility . A semi experienced cardiologist in the suburbs of a big southern Indian city , opened successfully a LAD which was the IRA and subsequently caused acute LCX STEMI , while trying to tackle an insignificant non culprit lesion due to procedural mishap ! (Some suggested migration of LAD thrombus !)
What a pity , when we are supposed to arrest the culprit, in reality it is simply chased down to another territory !
Here comes unique advantage of thrombolysis , you need not locate the culprit artery the drug chases it wherever it is , even if they are multiple ! Read in this link :
We call it as fate when thrombus suddenly occlude a coronary artery and the IRA becomes a culprit . We need not compete with fate and end up creating potential new culprits.Let the sixth sense prevail over the five .Use judicious discretion when trying to stent muti-vessel CAD during PCI. Please realise ,the concept of multivessel stenting during pPCI is not wrong . How we interpret is the issue !
There is no excuse to indulge as you like , simply because your intentions are good !
One of my favorite quote about Happiness from Buddha !
Posted in Cardiology - Clinical, Cardiology -Clinical signs, Cardiology -Mechnisms of disease, cardiology- coronary care, Clinical cardiology, tagged angina vs infarct, difference between stemi and nstemi, epicardial angina vs endocardail angina, heberden angina, how is chest pain different between nstemi and stemi ?, rca vs lad angina on September 24, 2014 | Leave a Comment »
When a patient comes with angina at rest , it could mean two things .Either a STEMI or an NSTEMI .This , we can diagnose only after seeing the ECG .
Can we differentiate these two by the character of chest pain alone ?
Very tough task isn’t ? But there are some definite clues .
- Is mostly sudden .
- Likely to be crescendo , lasts more than 20-30 minutes .
- Fails to get relived by rest or even Nitrites.
- Sweating due to sympathetic activation is more pronounced.
- Is rarely sudden .Often has a pro-drome.
- UA is mostly precipitated by an increased demand situation or a stress.
- It has a typical waxing and waning pattern . Rarely assume a true crescendo character as myocytes does not necrose (Just threaten to die !)
- The chest pain radiation to shoulder is less conspicuous , instead it tends to reach the jaw area .(* An observation,Is it something to do with multi-vessel CAD in UA ?)
Mechanism of the difference : Epicardial vs Endocardial angina
The pain of UA is due to subtotal occlusion and endocardial ischemia , while STEMI is sudden total occlusion and the resultant transmural ischemia . In STEMI epicardial surface is always involved (Which lifts the ST segment in ECG .).We know epicardium is same as visceral layer of pericardium which is well innervated .Hence pain of STEMI acquires more of somatic character than a predominately visceral type pain that occurs with UA/NSTEMI where epicardial ischemia is absent.
The demarcation between unstable angina and Infarct pain becomes vital when we calculate the time window for thrombolysing STEMI .Many of them have a phase of pre infarction angina which is a type of unstable angina. If we mistake it for Infarct pain then one may falsely calculate a prolonged time window and deny re-perfusion therapy.
It is tricky issue to differentiate the chest pain of STEMI and NSTEMI .A significant overlap can occur in real coronary care scenario . We know chest pain that occurs in both pre and post infarct phase is considered as unstable angina .(With infarct pain sandwiched between them!) Hence differentiating them may even be termed as futile.
Still,clinical cardiology can be made fascinating by indulging in such exercise !
Most of my students were struggling to answer this seemingly simple question . I realised later it is indeed a difficult one !
Tall T waves are observed in very early phase of STEMI .(Within 30 minutes ?) What is the mechanism ? Since ST shifts occur little later than T elevation ( considerable overlap may occur) it may not be related to current of Injury.It is an inherent alteration in the T wave genesis .T wave is inscribed when rapid phase 3 K+ efflux happen (Mainly by Iks and also IKr )
What is the effect of ischemia on K + channels ?
No uniform answer.(Blocks, stimulates, irritates, Bi-phasic, variable ?)
There are 6 important K channels in every cardiac myocyte adding to the complexity.
Does the Ischemic cells leaks potassium or accumulates it ?
Though It does both , predominantly it should leak .If it’s leaking there is local extracellular hyperkalemia . Is that the explanation for tall T waves ?
What is the influence of QT interval on T wave morphology ?
Long QT as occurs in hypokalemia pulls the T down and it may even invert it. .Short QT tends to push it up as in ERS .The effect of ischemia on QT interval is again unpredictable.Further regional and remote ischemia in a given patient can alter this.
Once the ST begins to elevate the T waves losses it power to grow tall .It only can regress. I think this is the time the QT is sort of prolongs .
Effect of reperfusion on T waves
The tall T tend to regress as some form perfusion takes place as K+ Is pushed back into the cells or flushed away from the vicinity.
The dynamic nature of reperfusion makes the behavior of T wave amplitude further complex. But one thing is certain , a well perfused IRA is associated with inverted T wave which we call it as completion of the process of evolution of MI .
Finally and most importantly this hyper acute T phase is not a constant phenomenon. In fact it is uncommon in persons who have baseline T inversion .After analysing many things we are back to the original state of ignorance .
Researchers with intra-myocardial micro electrodes try to decode the mysteries in electrophysiology . Still there is a huge disconnect between clinicians and physiologists.
In simple terms I would believe the mechanism of ischemic tall T waves are almost similar to renal hyperkalemia. (A local , transient extracellular k + excess ) The base of the T waves are not narrow and tented as in CKD because some degree of ST elevation (that always is expected ) widens the base of T wave. Further ,the prolonged QT interval in renal hyperkalemia stretches the QT and encroach the base of the T wave to the left making it appear narrow.
A simplest version for students
Tall T waves are due to transient local extra cellular hyperkalemia , when K + leaks due to cellular Ischemia.
Caution: This is a superficial scientific attempt .I need inputs from more scientific brains and electrophysiologists.
Posted in Public Health, Public health issues, tagged better world, brain death defintion, cadaver organ sharing india, ethical medicine, future of man kind, heart transplantation in India, humane medicine, kidney transplantation india, net work for organ sharing, organ transplant act india, role of who health, sucide and cardiology, sucide victims as heart donors, unos, who, world health issues on September 7, 2014 | Leave a Comment »
I got this alert from World health organisation yesterday .Click over the image to read more .
Why should a cardiologist affected about this ?
When we are fighting in cath lab day in night day out to extinguish the myocardial fire set by coronary thrombosis and the resultant STEMI . . . the solemn attempt to salvage whatever myocardial cells we can !
See . . . what is happening elsewhere every 40 seconds a healthy heart in toto is executed by weak minds !
What should the WHO do ?
Just publish these data and forget . No,they should organise the world leaders to take a resolve !
Either , we should prevent these unnatural deaths or else we should have world organ net work. Why can’t we use these weak hearts for those courageous men and women who lose their life daily with end stage cardiomyopathy who long for living !
Is this possible ?
Why not ? Ain’t the world leaders group together periodically to impose a sanction or bomb other countries for personal reasons !