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    Since electrical characteristics of the infarcted tissue change, arrhythmias are a frequent complication in STEMI.

    The re-entry phenomenon may cause rapid heart rates (VT and even VF), and ischemia in the electrical conduction system of the heart may cause a complete heart block (when the impulse from the sinoatrial node, the normal cardiac pacemaker, does not reach the heart chambers)
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    (Original post by davey jones)
    A chappy came into resus the other day with nothing on his ECG, unwell, anxious, diaphoretic (no chest pain). As we were getting him sorted out he suddenly went into a VF arrest and jumped between VF and VT (including torsades) for a while. When he came to he had really obvious ST elevation and got rushed to another hospital to get (LAD) stented. Now thats all very good blah blah.

    He must have had a massive cardiac event that triggered this. So why would he go into a VF arrest from it? then VT?

    Am I being really thick?

    yours faithfully
    D Jones.
    You sound like a right knob by saying diaphoretic instead of 'sweaty'!

    Anywho, I'm slightly dubious that there was NOTHING on his original ECG. You don't take some to resus with 'sweaty and anxious'.
    As for the sudden VF - thats what happens in heart attacks. Doesn't have to be large, just in the right place. Especially inferior ones. The VF-VT switcharoo is indicative of the simple fact that the pissed off heart will bounce from one to the other. You will basically treat them the same anyway if there isn't a pulse.
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    (Original post by davey jones)
    A chappy came into resus the other day with nothing on his ECG, unwell, anxious, diaphoretic (no chest pain). As we were getting him sorted out he suddenly went into a VF arrest and jumped between VF and VT (including torsades) for a while. When he came to he had really obvious ST elevation and got rushed to another hospital to get (LAD) stented. Now thats all very good blah blah.

    He must have had a massive cardiac event that triggered this. So why would he go into a VF arrest from it? then VT?

    Am I being really thick?

    yours faithfully
    D Jones.
    An unstable LAD lesion would very readily put somebody into VF. That is apparently the cause in your patient and that would have presumably developed in the same way as the majority of atherosclerotic lesions.

    As an aside - he would have had polymorphic VT rather than Torsades de Pointes which is a particularly type of polymorphic VT.
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    (Original post by davey jones)
    he may well have had polymorphic VT, to cut a long story short, another nurse relieved me in resus as I already had one patient with heart failure, I didn't need a second, it is difficult to comment on all events. But exactly as the paramedic reported when he was phoned through to resus, on arrival the chap had no obvious ECG abnormalities, but he LOOKED exactly how patients having MI's looked and he had lost conciousness which was why the ambulance was called in the first place. Two registrars a CNP and later a consultant agreed the first ECG was not abnormal and that he spent time in torsades, which we has a twelve lead of.


    So If I am not being thick I now get that he had an MI which wasn't yet showing on ECG, it was a big ****** and lots of tissue died, the dead tissue not being able to maintain normal electrolytes etc went spazzy and caused an arrythmia which jumped between various types of VT and VFib. He was shocked and drugged and pumped and what not untill he came about a bit then sent somewhere else to stent and live happily ever after.
    No, you don't get it.
    Because you don't need a big MI to give an arrythmia. All MIs have a risk of it. Thats why traditionally one monitors people for 3-5 days following a heart attack. Its the reason for CCU.

    He was shocked back into life. If he hadn't been (i.e. shocking failed), and there were no stenting facilities on site he would likely have been thrombolysed there and then.
 
 
 
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