Posts Tagged ‘betablockers in stemi and hyperkalemia’

Human life is a bundle of energy orchestrated by ions coming  in and  going out  of  every cell . Potassium is the life sustaining ion which  determines the  resting membrane potential  of our cells.

When the  heart  suffers a massive necrotic attack  what  would  happen to the potassium dynamics  inside the  myocytes ?

K  + is the dominant  intracellular cation  ,  when  about  100 million myocytes   die  suddenly ,  a chaos in the  potassium  metabolism  is expected  is it not ? .

When skeletal  muscles dies  it  releases  potassium  . We  know   this  from typical crush injuries and rabdomyolyis.

It is  more of a  common sense  to expect this   . . . from myocardium as well .

Which ion is responsible for the current of injury ?

We know a  strong and continuous  negative current that  emanates from the necrotic zone after STEMI  .  (It is so powerful it  shifts the baseline  itself  !), We do not know yet what exactly  is causing this current of injury .  It goes without saying sodium should sustain the depolarisation wave but  potassium will  also have a major role in the  propagation  of this injury current.

Do dying myocytes   excrete the potassium into the circulation   ?

Is    k+  a marker of extent of MI  ?

What is the mechanism of hyper acute tall T waves in  MI ?

Questions  galore  . . . Answers struggle !

When a  large  area of  cardiac muscle goes for necrosis  it  leads to  leaking   of   K +    . If it is true  , it  is expected to be a marker for extent of  infarct. In reality it is not . Why ?  This is because cardiac  potassium pool is much  small . A  leak from  an organ which weighs   400 grams   do not elevate the ECF  potassium .  Still , there is ample evidence  for   K + to accumulate  in the local  intracellular milieu. (Myocardial hyper-kalemia ) In fact ,  one of  the mechanisms  suggested  for tall T waves in  hyper-acute MI phase   potassium excess .

Image courtesey hqmeded-ecg.blogspot.in/2009/02/hyperacute-t-waves.html


Potassium levels and incidence of  ventricular tachycardia.

Many of the primary ventricular arrhythmias  are  due to acute ischemia .  We  have conflicting evidence  for  the effect of ischemia on QT interval. How does ischemia trigger VT  ?
The answer to this question  remain as a missing link !  . Grossly simplifying ,  one could suggest it is  due to   ischemic cell membrane damage that alters the ion channel function  , resulting  in intracellular accumulation of calcium and triggered  activity  .

What is the effect of potassium  on cardiac contractility  ?

Myocardial paralysis.  (Please note  it is the  hypokalemia  that primarily  causes paralysis in skeletal muscles !)

It causes  myocardial  stunning  a manifestation of local potassium  leak ! A temporary myocardial paralysis.

What does the current guidelines of ACC/AHA state about potassium hemostasis  in STEMI ?

It suggests   a fairly aggressive  maintenance of potassium levels  to  upper normal levels. Traditionally we are worried more about hypokalemia than the hyper. It is  surprising   we had the facts wrong . . .  for so long !

What is new in the regulation of potassium level during STEMI ?

This landmark paper from JAMA seeks  to set right the misconceptions about potassium during STEMI. It suggests  K + levels  has a U shaped  morbidity curve in STEMI . One need to be cautious in  correcting borderline hypokalemia .  Serum   K +   is   absolutely useless  surrogate marker for myocardial K +   . We do not know how  K  +  behaves in the vicinity of MI  zone . So  extreme caution is required  when giving IV  K +  supplements in coronary care units .

Watch out :  Beta blockers /ACEI   may worsen  hyperkalemia

Early introduction of ACEI and ARBs   is a strong risk factor for systemic as well as myocardial  hyperkalemia . This  is  especially true  in diabetic individuals  who have  low rennin  levels due to diabetic micro circulation defect in kidneys .(Hypo-reninic  hypo-aldosternosim )

Beta blockers are also known to raise potassium by two mechanism

1.Blocking rennin

2.Reduced uptake of K + in to  the cells.


Final message

In the management of STEMI  ,   revascularization  of  the myocardium    is  considered as  the only  therapeutic aim . We  need to realise it   is  much more than that .  There are some subtle but important ways of resuscitating and  protecting  myocardium .  Over  indulgence in electrolytic management  in coronary care  is to be avoided.


Importance of sympathetic drive and  potassium levels



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