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Waited too long?

by on August 23, 2014

Had a call during the night from a local ER transferring a patient to a Cath Lab for Posterior MI.  Pt stated he has had chest pain intermittent all day that became very strong and steady around 5PM.   It is now 11pm when the patient arrived at the  cath lab where a nurse met the crew in the hall way and stated the the Dr wanted to talk to the patient before he went to the Cath room.  The Dr seemed to be irritated. He told the patient that he has had a heart attack and waited too long to come for treatment and  it is now too late for him to do anything and was sending him back down to the ER for another 12 lead and Echo.

He was still showing ST depression in early V leads and still had chest pain 5/10 after 2″ NTG paste, 8mg MS and 100Mcg of Fentanyl.   Seems to me if he is still showing signs of posterior MI with an elevated Troponin level and having chest pain he should have at least done an exploratory cath if nothing else.  What are you thoughts?

Here is the EKG


From → Case File

  1. Any info on what the troponin levels were and when they were drawn in relation to the EKG?

    Sx duration is a terrible marker for whether a patient has salvageable myocardium. Acute coronary lesions can be exceptionally dynamic, occluding and de-occluding at a whim; the EKG is a much better marker of how far along a patient is in their STEMI. I just recently had a patient who had been experiencing “constant” CP for 12 hrs, but while I was monitoring him his ST-elevation suddenly quadrupled in size right in front of me, showing that he did indeed have a dynamic lesion with myocardium left to save.

    That said, Sx to balloon time is still very important to consider as a marker of a healthy system. It can even be more important than door-to-balloon time in terms of how much improvement can be made in a patient’s outcome through intervention, but only because patients typically present a few hours into their MI’s.

  2. Regarding the EKG itself, it’s actually not clear whether this is even a true posterior STEMI. RBBB can be exceptionally good at mimicking isolated posterior wall MI (PWMI) as it typically produces inverted T-waves in the right precordial leads with a modicum of ST-depression.

    To even make the diagnosis in a case like this you’d need a good story, an old EKG (hopefully one with a baseline RBBB), probably at least one troponin abnormal, and a bedside echo to look for posterior wall motion abnormality wouldn’t hurt. You wouldn’t need ALL of those things to activate the lab, but some combination would be nice.

    I’ve spent a lot of time studying and pondering posterior MI, and while I can see the obvious reasons why we would worry about one here (even more than V3, I don’t like the depression in V4, though there’s a bit of artifact), I don’t know if I’d be activating off this EKG alone.

    Still, once the patient’s at the lab and assuming the troponin was positive (it sounds like it was?), there’s no strong reason why he shouldn’t get cathed unless he’s elderly or has significant co-morbidities. It sounds more like the physician was angry about being called and arrived biased, trying to find any reason possible to cancel the case and prove the ED was wasting his time.

  3. Vince troponin was 0.177ng/ml

    • That’s a tough level because it’s not high enough to clinch the diagnosis of STEMI, not low enough to rule it out, but just the right level that a host of other non-type I MI factors could be the cause.

      What it does tell us though is that if this patient is indeed experiencing a STEMI, he must not have been fully occluded way too long at the time of the draw and there would be myocardium left to save (even taking into account the troponin-lag).

      Thanks for the update.

  4. Great information!

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