Dr.S.Venkatesan MD

A 38 year old man presented with  acute breathlessness  and chest pain .His ECG is  posted  below . The ER in charge   medical officer promptly handed over the patient to   STEMI  alert    group (This is how  cardiologists are   referred to !   in one of the leading corporate hospital in India )

Note Atrial fibrillation , ST segment elevation, in pre-cardial leads

A team of  white coated  humans  in  various  gender and ages  swarmed the patient . ECGs and text where shared  among  the  STEMI alert group  through  I pad 3 which transmitted  HD  quality ST elevation with a  retinal  precision . A senior consultant   insisted   to shift the patient to cath lab direct  . Since he had  signs of cardiac failure , one of  the wise Junior fellow wanted  to correct the failure with Nitroglycerine  and  Dobutamine before rushing him to cath lab . Hence he was put on hold in the side room of ICU .

Echo examination showed LVH and wall motion defect could not  either confirmed or ruled out .  Initial  Troponin was negative . In the mean time the bio chemistry results came. He had a creatinine of  5.2 and Potassium of 6 meq . Hence the patient was diverted to Nephrology unit  and  dialysis was done. The next day morning  his ECG   looked like this .

It  may  sound a  pessimistic , but  still I would consider   the above  episode  is  a rare  example of appropriate care happening  ! This patient was diverted in a timely fashion from cardiology  care  to the  Nephrology . Please note , it is not the  the  clinical acumen that   helped  here.  If  he had  not presented with  LVF   he would have been a victim of inappropriate care  and landed on the cath-lab table directly  !

Final message

Every moment in clinical medicine is important , especially during the genesis of  diagnosis.  Where the patient lands  . . . in a frighteningly  large  hospital is as important  as the disease process itself. In this scientifically arrogant medial atmosphere  most of us, are  tuned  to view every problem as their own  ! This is  the default mode of modern medical  thinking process . How faulty  we are ?

The future is worrisome  as the field of  Internal medicine is  at risk of dying a premature death (or is it dead already !)

By the  way  what is the mechanism of ST elevation and Tall T waves in hyper-kalemia ?

Many factors contribute .

1. Is it a true ST elevation  ? There is reason to believe   the tall T waves drag the fag end of ST segment along with it .
2. Next is  related to QT interval . Hypo-kalemia widens while hypo-kalemia does  the opposite .(  though not classically) .
3. When QT is shortened the segment gets squeezed in within a limited space ,  in order to accommodate the  ST segment it   gets rolled up and elevated . (Like an up sloping ST segment  in extreme tachycardia during stress  testing)
4. Whatever  be the mechanism it is something to do with potassium ion flux .Transient intra-cellualr hyper-kalemia.
5. Another possibility is diffuse uremic peri-carditis , which is a common accompaniment  of renal failure.In fact this patient did have a peri-cardial rub