Found on the LIFENET 05/2011

Found on the LIFENET.

What is your impression of this ECG?


*** UPDATE ***

Consider this recent case from Dr. Smith's ECG Blog.

ST-elevation in aVR, with widespread ST-depression

"ST elevation in aVR is often thought to represent left main occlusion. However, it really just signifies widespread and diffuse subendocardial ischemia which could be due to left main or 3-vessel disease, or severe proximal LAD disease. Left Main occlusion generally causes rapid death; most who survive left main ACS have some flow and thus often have widespread ST depression."

See also:

63 year old male CC: Chest pain

An unusual case of left bundle branch block


  • VinceD says:

    Hmm I agree with the computer; diffuse ST-depression with elevation in aVR, likely ischemia. On paper that sounds like a recipe for left-main disease, but it's the clinical picture that sells that call if the patient is "sick" and in distress. The rate varies from 100-150, which probably factors in somewhat, but with an average of 118 bpm, I'm seeing just a bit too much ST-depression to attribute it entirely secondary to the rate.
    Maybe it's just recall bias because I had a patient with this exact tracing a few weeks ago, but I'm imagining a guy who's been having chest pain for a couple of days and is the clinical picture of unstable angina. In this imagined case the patient's response to treatment will likely dictate if/when they go to cath, but I don't see any need for a STEMI alert.

  • chris t says:

    Not me. aVR the forgotten lead with more elvation than V1. LMCA occlution. no es bueno!!!!

    (24 Jan 2012 ed: updated to correctly state aVR per the comment author.)

  • Harrison says:

    Atrial rhythm w/ RVR @ 118
    Normal axis, irregular r-r. Marked global ST-Depression (except V1).
    I'd like to know some vitals/history, especially any recent exertion. The patient probably has a blocked coronary artery if this was a sudden onset.

  • WilliamM says:

    Atrial fib with rvr as evidenced by

  • WilliamM says:

    Atrial Fib with RVR as evidenced by lack of P waves and irregular R waves.  Also, the LP12 does not note a PR interval.  The ST depression is most noticeable in V-4/V-5, also present in II.  Not a cath lab activation for my service, but this patient is most likely going to be headed to cath or for a CABG considering the correlation of avR elevation with three vessel or left main disease.

  • Troy says:

    Aside for the patient having a LMCA occlusion I don’t see anything else wrong 🙂

    Elevation in aVR, diffuse depression is 86% specific for LMCA occlusion or 3 vessel disease. IV, O2, ASA , very sparing if at all nitro, no plavix, fentanyl, serial 12’s and haul A$$! Although STEMI, call ER and tell them to get a team ready for an emergency CABG

  • PHRNguy says:

    Is anybody thinking a little more outside the box?  Possibly pericarditis or blunt cardiac injury?  Also a few differing QRS heights (certainly not electrical alternans), but begs the question of tamponade physiology as well…

  • chris t says:

    Harrison  I doubt i know anything you do not. There is some baseline wander/quality issues but i believe i can comfirm about 1mm elevation in V1 and with aVR and global depressions im confident in LMCA. paricarditis – depressed p segments, i dont see those. cardiac tompnade seems unlikely with such a high voltage and qrs is consistant sometimes with fluid around the heart i have seen the qrs apmlitude increase and decrease each beat as it "swings" away from the electrodes. Dont know if that all true but With both taken into consideration i do not see that here either.


    (24 Jan 2012 ed: updated to read aVR per comment author.)

  • Christopher says:

    AF w/ RVR, possibly demand ischemia due to existing stenosis of the LMCA. I think Chris T meant aVR not aVF. As for the change in voltage, it could also be explained by the respiratory cycle as it appeared to have a decrescendo-crescendo appearance to it (and the voltages in general are normal).

  • Andrew Okey says:

    I don't see any P waves? and are those u waves in V1? The electrical condution from V1-V6 through the heart looks normal to me, so I wouldn't think tamponade. I have to learn more about LMCA. I see the elevation in AVR and V1 and depression in I II III AVF V2-V6. I would want to do a V7-V9 and RV4 to see if the reciprocal changes follow. O2, treat Pt. .

  • chris t says:

    So you do not think this is acute Christopher, perhaps just a rate exacerbation with the stenosis to LMCA?

  • Blake says:

    With all the ST Depression in the anterior and lateral leads, I would like a posterior view.  I have to wonder if these are reciprical changes for something really nasty going on from behind.

  • Steven says:

    A-fib with RVR, LMCA, Cardiogenic shock AEB rate.  Sounds like this is one sick patient.

  • VinceD says:

    While I agree that it could very well be left-main/triple-vessel/proximal LAD disease, I think I didn't make my point correctly. The real question I'm trying to raise is, "does this ECG truly warrant the status of STEMI-equivalent?"
    While it's very easy to make the argument, "obviously left-main lesions are a bad thing and should be fixed immediately," I wonder if that is actually the case. We call STEMI alerts because patients with ST-elevation MI's have been proven to benefit from revascularization therapy (be it PCI or thrombolysis) on an emergent basis, but is this the same scenario? If left main disease is the culprit, as others have stated, the patient would be receiving CABG as PCI and tPA are ineffective. If the two definitive treatments for which we tailor our STEMI system do not work, is left main disease really an equivalent? If the LMCA was 100% occluded, the patient would be dead, but because the patient is alive, there's still collateral flow. Assuming the patient is not unstable, do the cath lab and ultimately CT surgery need to be called in the middle of the night, or could he/she be managed medically until cardiology has their morning tea?
    Now I'm not saying we could manage this patient with some aspirin and cath after the weekend, I just wonder if an emergent cath is really the best answer, or an urgent approach (there's a difference) would suit the patient just as well. In the end I suppose it's up to the receiving doc how he or she would like to mobilize their resources.

  • C.E. says:

    A-fib & possibly LMCA, but i expect additionally a coronary insufficiency because of the DESCENDING st depression. Possible? What do you feel about it?

  • dbaumrind says:

    I agree with both Christopher and Vince… just to add, from what i understand, it is important to note that ST elevation in aVR and diffuse ST depression elsewhere does not represent occlusion of the LMCA, but rather "LMCA disease", or 3 vessel disease… i think that is what Vince is getting at, but still an important difference regarding the need for prehospital activation of the cath lab…would it fit STEMI criteria, probably not, although clearly the patient needs emergent care.

    on a side note regarding Christopher's comment, why not demand ischemia from the AF with RVR?

  • On The Road says:

    I think we're all agreed on the rhythm as AF with RVR, but I'm seeing inferior, lateral, and high lateral ST depression, with little if no change to the anterior leads. I think that I'd like to see a right sided tracing, as I figure that if the depression were reciprocal changes, we'd find the infarcted tissue on the right hand side.
    What I don't quite know is does the STE in AVR mean the same as STE in the other leads, or is it more likely (as I suspect) to equate to seeing ST depression in any other lead?
    Regarding the concept of tissue ischaemia, I guess it would be important to know how long since onset of symptoms.

  • Mark says:

    ?LVH, strain pattern. A.Fib

  • Lance says:

    Septic patient or SIRS which has progressed to ARDS.  You are seeing evidence of globabal ischemia due to hypoxemia.

  • Mark says:

    Looking forward to a conclusion on this one – soon please?

  • Yojo says:

    It looks like Sinus tachycardia…. casuing ST depression …is not it?

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