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    24 yo patient comes in with diabetes mellitus and you suspect they have an episode of DKA. You order an ECG.
    What are you looking for? answer is T wave inflation.

    But I don't understand why, I believe T-wave inflation is linked to hyperkalaemia, but how is hyperkalaemia related to diabetes??
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    (Original post by acetylcholinee)
    24 yo patient comes in with diabetes mellitus and you suspect they have an episode of DKA. You order an ECG.
    What are you looking for? answer is T wave inflation.

    But I don't understand why, I believe T-wave inflation is linked to hyperkalaemia, but how is hyperkalaemia related to diabetes??
    What do you mean by T-wave inflation?

    DKA, however, tends to cause HYPOkalaemia. This is because with high plasma glucose, you get a a high urinary glucose and therefore an osmotic diuresis - losing water, Na+ and K+. Furthermore, the low Na+ leads to a compensatory secondary hyperaldosteronism which means also increases urinary K+ excretion.

    The ECG changes associated with hypokalaemia are explained well here: https://lifeinthefastlane.com/ecg-li.../hypokalaemia/
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    (Original post by Asklepios)
    DKA, however, tends to cause HYPOkalaemia.
    It can be high too. You will almost certainly have whole body potassium depletion due to the reasons you state. However, you've also lost all the insulin which drives potassium into cells. So your intracellular space will be very potassium deplete but serum might be normal or high. But when you start insulin therapy, you will need to replace potassium.

    However I don't think an ECG is a core investigation in a routine DKA presentation in most hospitals. You'd probably get a VBG, see the potassium and only if it was high do one for ?severe hyperkalemia. MI can trigger DKA, but you'd expect something in the history.
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    (Original post by Asklepios)
    What do you mean by T-wave inflation?

    DKA, however, tends to cause HYPOkalaemia. This is because with high plasma glucose, you get a a high urinary glucose and therefore an osmotic diuresis - losing water, Na+ and K+. Furthermore, the low Na+ leads to a compensatory secondary hyperaldosteronism which means also increases urinary K+ excretion.

    The ECG changes associated with hypokalaemia are explained well here: https://lifeinthefastlane.com/ecg-li.../hypokalaemia/
    You get both, actually. The serum potassium at initial presentation can often be dangerously high, as the normal insulin drive to push it intracellularly is gone, plus there is some exchange of K+ for H+ to try to offset the acidosis. However, total body potassium is usually actually low, hence once fluid/insulin therapy is started, and it starts to shift back from the plasma to the intracellular compartment it can drop dangerously low very quickly.
 
 
 
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