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