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One of my favorite quote  about Happiness from Buddha !

 

Happiness quote from Buddha

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Most of my students were  struggling to answer this  seemingly simple question . I  realised  later it is indeed a difficult one !

tall t waves

Some thoughts

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 .

Summary

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.

 

Read further

https://drsvenkatesan.wordpress.com/2012/02/10/basic-lessons-in-stemi-does-dying-myocytes-release-potassium-into-the-circulation/

 

 

 

 

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  • CRT -Cardiac resynchronisation is done  by putting multiple wires and electrically organizing the contraction  sequence and improving mechanical function.
  • ICD-Implantable cardiovertor defibrillator shocks whenever VT or VF occur and suden death is prevented.
  • CRT-D (Combo device which functions as both )

CRT is done for advanced heart failure to improve exercise capacity and hence the quality of life .It does not do any thing significant in prolonging life .ICD is again implanted  in advanced LV dysfunction with either documented VT/VF or patients who are at  propensity for VT .It has dramatic benefit in preventing  sudden cardiac death.

Both CRT and ICD has some overlapping indication in cardiac failure. Attention young cardiologists,   please realise among these two the value of ICD is many  many  fold higher than CRT.This fact is rarely discussed and disseminated.

 True benefits of CRT is realised only when it is combined with ICD.

Summary

  • Ideally all advanced cardiac failure patients should receive both ICD and CRT (CRT-D)
  • ICD as stand alone therapy has a  distinct role in patients with severe LV dysfunction (LV EF<30%) without  wide QRS in ECG
  • There is no role for  CRT  as a standalone procedure in cardiac failure  .it should  always  be combined with ICD (ie CRT-D) *

*Except  in patient with  degenerative complete heart block , both ventricles are paced  the term Bi-Vi pacing is used  instead of CRT.Since LV function is normal here , there is no de-synchrony in the first place .The synchronised  BIVI pacing is meant to prevent future heart failure

Final message

Always use a combo device in advanced symptomatic heart failure which  is refractory to medical therapy.

After all , there need to be a life in the first place  so that we can improve it . ICD ensures life while  CRT tries to improve it.

http://europace.oxfordjournals.org/content/14/9/1236.long

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The correct  answer could be any of the above , depending  upon the level of your knowledge.

Ever since Herrick reported coronary thrombosis as a cause for MI and Davies documented it by angiogram many decades later (1980) ,the fate of thrombus  and the mechanism of its dissolution is the key to our understanding of ACS.

Even though we are now able to take on this thrombus in a direct fight  by aspiration techniques ,still the hematological  aftermath  and the aberrant coronary behavior  can fool us at any time ! The major lesson learnt  in recent times  is the  success of pPCI  is not in clearing the thrombus but ensure it never accumulates again  at the site  in the future .This is why there is whole big industry working on post PCI anti coagulation and anti platelet strategies .

Clinical correlates of poor  perfusion in micro circulation.

Plugging of micro circulation is the most under-recognised  issue.This results in no reflow in acute fashion or LV  dysfunction and micro-vascular angina in long term . Late recovery of LV function is attributed to late clearance of thrombotic debri.

RCA vs LCA thrombus load.

*One interesting observation is RCA thrombus clears more slowly as it has no well formed venous circuits .most RCA blood drains through thebesian veins which traverses  RV  myocardium .this can be hemodynamic hurdle unlike the LCA venous drainage

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A tense anesthetist  calls for help !

I had an unusual cardiac consult last week .A middle aged man who was to undergo routine ortho surgery wanted  a cardiac clearance.

It was  a through and through fracture of clavicle , why do they need a cardiology opinion , it seemed a  simple  procedure I asked over phone

The anesthetic  fellow who was  in charge of the patient told me ,”There is a wire just going parallel to the clavicle sir .I  believe it is pacemaker lead” I agreed to see the patient immediately

This was the X-ray

pacemaker lead clavicle fracture electro cautery surgery

It was obvious why they got tensed up  as the pacemaker wire criss -crossed surgical field . His ECG showed own rhythm of 80/minute but occasionally VVI pacemaker was capturing his ventricles.

I suggested

General precautions

  1. Strict Intra-operative  ECG monitoring
  2. Keep another temporary pacer ready .
  3. Hold a cardiologist on call and  pacemaker programmer on site.
  4. Surgical field  kept small with  minimal   manipulation .
  5. Issue of cautery : Free to do as long as it’s  bipolar and good earthing plate.
  6. Ensure the cautery is  applied in one or two second pulses with a gap of 10 seconds pause in-between
  7. Wiring the clavicle – Signal interference  are  very rare  as the wires are inert

Use of magnet in such situations  (Link to magnet and Pacemaker)

Keeping a magnet over the pacemaker generator removes the pacemaker sensing function and is an option if  prolonged electrical interference.

*Caution : Response to magnet can be quiet variable .Should be done only with cardiologist supervision.

What happened to this patient during surgery ?

Nothing alarming.When anesthesia was induced he was entirely  on pacemaker rhythm . limited cautery was used with ease. Patient  tolerated well.

Final message.

One need not  panic when a pacemaker patient is taken up for non cardiac  surgery .It is not a major issue .Few precautions are required .

Read a related article in this site .Electrical cautery  in pacemaker patients.

Reference

pacemaker and electrocautery diathermy

 

 

 

 

 

 

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Primary VF is the arrhythmia that occurs within minutes to few hours after acute coronary ischemia .This is most common fatal arrhythmia following STEMI accounting for 90% of all pre hospital deaths.

It  occurs within  4 hours after onset of symptom and the risk rapidly fade as the hours go by.One variant of primary VF is the re-perfusion arrhythmia after thrombolysis  .This  can occur up to 12 hours or so.Primary VF responds  well to prompt defibrillation.Follow  up anti arhythmic drugs are not required in most situations.

What is secondary  VF ?

  • As a rule secondary VF is  not related* to  index event of ischemia but to the anatomical substrates of Infarcted myocardium or pump failure
  • It generally occurs after 24 hours .Response to defibrillation is less favorable .Continued anti- arrhythmic  drug therapy  is required.
  • Few of them may end up with ICD.

(*However,a role for ongoing ischemia can never be disproved ! What about a small re-infarct  trigggering another episode of primary VF ? )

 

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A 76 year old man with history of recent stroke presented with acute chest pain  and his ECG  showed ,

ischemic rbbb

It was diagnosed as Anterior STEMI .Since he had co-exciting renal dysfunction also he was not considered for thrombolysis (Primary PCI not feasible !)

IV  Heparin bolus followed by infusion was started. Patient  had a comfortable night stay. The ECG taken on the morning  looked like this.

 

ischemic rbbb 001

Do you call this aborted STEMI or a simply an Ischemic RBBB ?

Transient RBBB due to Ischemia in  LAD territory(with septal compromise ) is very much possible during ACS. But , it is a rarely discussed entity unlike ischemic LBBB .

We know qRBBB  complicating anterior STEMI is much commoner than LBBB , still transient ischemic RBBB in non STEMI setting seems to be uncommon .Is it possible propensity for  Ischemic RBBB is different from necrotic RBBB ?

 

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Cardiology as a filed has been the epitome of progress of medical science in the last century .Most research  in cardiac science  has grown and transformed with a definite clinical purpose.

The cardiac pharmacology has grown many fold and various drugs play a distinct role in relieving symptoms and prolonging life .

Which drug , do you think has  the maximum impact in the clinical outcome and overall cardiovascular health of our population  ?

My vote is for  the old warrior . . . yes the the drug ,  which is used atleast a  million times a month to unload the heart the meanly loop diuretic Frusemide ! Heparin came very close  second !

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Today , we  post cases for coronary angiogram , just like sending clients to breakfast table ! Close your eyes. Think for a moment. It is heartening to know how cardiac catheterization grew from a humble beginning . We know , Forssman , Cournand  and Richardson  who shared the Nobel price  for Inventing  cardiac catheterization in 1930s .

Soon after it’s  invention it was criticized by most, few ridiculed it outright , few others wondered about it . One man from the iconic  Grady memorial hospital  , attached to Emory silently  adopted this  procedure and almost single-handedly  did more than 1500 cardiac catheterization procedure. (Between 1940-50s)

How many of us know this man  from  Atlanta ,Georgia  ?

Some times history appears unkind. He is Dr Steads . . . to be precise Dr.Eugene Anson Stead Jr. ( 1908,  –  2005)

stead_eugene

Born in a humble background in the suburbs of Atlanta , became a great medical teacher , researcher and educator . He is one of the founding  fathers  of cardiac catheterization . Defined it’s usage in  clinical cardiology . The other major  achievement was his strong conviction that  medical science is indeed simple  but made complicated by complex concepts .This  thought transformed  in him ,  as he found the concept of physician assistant . He believed focused medical knowledge in young and enthusiastic  mind can make huge  difference in the way medical knowledge  is disseminated, applied and consumed .What a stunning truth even today !

grady_hosptial_pc

The legacy of Grady continues which is one of the largest public hospital in USA with special affinity to poor and low-income population.

The lab which Dr Stead worked was later taken over by Dr  Noble O Fowler* , another great cardiac physician continued the research and wrote the famous book on cardiac diagnosis and treatment.( * I think it should be in early 1950s when Dr Stead left for Dukes)

Final message

Invention of a concept is one thing . Accepting it , trying it ,  improving it ,  disseminating it , is an equally important  contribution to science. Dr Stead did exactly that .He remained  a positive force in  propagation of medical knowledge, made it  available for those  people who need it .

He passed away on June 12, 2005 at the age of 96 leaving behind a huge legacy .It will be  an  error if we don’t teach our  young students history of such great men , in medical  schools today  !

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