63 year old male CC: Substernal Chest Pain

Today we're presenting a case from our friend Dr. Brooks Walsh of Mill Hill Avenue Command and Doc Cottle's Desk. In fact, this case is being presented both for his readers and for ours! We hope you like it.

You're working ED triage when a 63-year-old man walks in complaining of substernal chest pressure that had awoken him from sleep 2 hours prior. He denied any radiation of the pain, but complained of some mild presyncopal symptoms. His wife reported that he had had intense diaphoresis at home. He reported having a similar episode 1 year ago, but a subsequent stress test was negative. 

You obtain a quick history:

  • PMHx: HTN, type 2 diabetes mellitus
  • Meds: irbesartan, insulin
  • Allergies: NKDA 

A quick set of vitals are obtained:

  • HR: 90 
  • BP: 145/123 (NIBP)
  • RR: 16, unlabored
  • SaO2: 98% r/a

The physical exam reveals a patient with mild sweating, but no JVD. His lungs are clear, there are no cardiac murmurs, and he does not have any lower extremity swelling or tenderness.

You obtain a STAT 12-Lead ECG:

I Think Your Segments are Upside Down - Initial 12-Lead

The patient is taken back to a bed, 324mg of aspirin is administered, an IV is started, and labs are drawn. The patient receives 0.4 mg SL nitroglycerin and 5 mg morphine, both without relief. Metoprolol is given for the patient's hypertension and a heparin drip initiated. Cardiology was consulted and believed the ECG to be non-specific. 

Per the ED physician, an ECG is performed 15 minutes later to assess the right side of the heart. Note that all of the precordial leads were reversed (e.g. V2R = V1):

I Think Your Segments are Upside Down - Right-Sided 12-Lead

Due to persistent chest pain, a nitroglycerin drip is initiated and titrated up to 132 mcg/min without improvement in chest pain. A loading dose of clopidogrel is given.

An hour after presentation the ED physician asks for a posterior ECG:

I Think Your Segments are Upside Down - Posterior 12-Lead

Labs return a troponin of 0.05 (normal is < 0.04). A CBC and basic chemistry panel were essentially negative.


  • What does the first ECG show? Is it diagnostic?
  • Do the right-side and posterior leads help with diagnosis? 
  • If this is a STEMI, what coronary artery is likely involved? 


  • Chase says:

    High Posteriolateral? LCX

  • Brooks Walsh says:

    LCx is always a good bet.
    Would you call a STEMI based on the intial ECG? The second or third?

  • Travis K says:

    First EKG( highly suspicious of ACS/Posterior stemi)
    1) ST-D in the inferior leads made me look at the high lateral leads for ST-E, which none was seen.
    2) ST-D in v1-v4 made me think of a posterior stemi
    3) we do have symmetrical T waves
    Second ekg (stemi):
    Now we have ST-E in avL.  
    Third EKG (stemi):
    You can see ST-E in the posterior leads
    Great case! 😀 

  • Paul says:

    1.) ST depression as noted, but ST elevation is present in AvL and arguably V6, as per Smith criteria. I would have done a posterior 12-lead at this point. Serial 12-leads are advisable, but it wouldn’t change my treatment any.

    Posteriolateral STEMI. Good on them for giving clopidogrel and all the treatment above being commenced early on. I really have nothing to contribute other than when I would have called this a STEMI. Their treatment was par excellence. I would cath this patient.

  • haitham farid says:

    high lat mi & post involved 

  • David Eastman says:

    First ECG suggests posterior MI (morphology of V1-V3 with reciprocal changes in II, III, and aVF)
    Third ECG confirms posterior MI and shows I and aVL with slight ST-segment elevation and developing pathologic Q-waves.
    Probable proximal occlusion of the LCX.

  • Andre Ruby Medic 912 says:

    After viewing this 12 Lead, It is presumed as a possible posterior…. Inferior is not depressed but in retrospect the depressing in V1-V3 leads me to believe an MI but this does not indicate a STEMI in my opinion. The other aspect of this case I would like to know is the CKMB, due to Troponin being an longer onset. Follow-up Troponin as well as CKMB is really the determining factors for me.

  • Andre Ruby Medic 912 says:

    I will agree to a Posterior MI due to the ECG finding as well

  • 3adamjoe says:

    has anyone checked his blood sugar. i have seen alot of cases where a low blood sugar shows signs of ischemia.
    i dont know if i would call a stemi but for sure a cardiology consult and the boy needs a cath… just for the fact of recurrent pain. would like to see an ekg from previous cases beings we are in ER for this case.

  • SHUCKS says:

    v1 is pathologically wide and has a negative deflection.  New onset LBBB, didnt need a 2nd or 3rd 12 lead.  should have been treated as an MI just like that.

  • Christopher says:

    The QRSd calculates to ~100ms, but isn't 3 small blocks or greater. Additionally, new-onset LBBB is not a reasonable indication to activate a cath lab nor is it reason to suspect MI. LBBB with primary ST/T-wave changes is a reasonable indication to activate the cath lab and Sgarbossa's criteria with Smith's modification is your best bet.

  • VinceD says:

    I've gotten to the point where I'd feel very comfortable calling it "STEMI" based solely off the first ECG, but maybe I'm getting a bit over-confident, having reviewed a lot of confirmed posterior STEMI tracings recently.

    Thanks for sharing, Dr. Walsh!

  • Medic Gregory says:

    If I had this pt pre-hospital, I would immediately do a 12 lead EKG, apply O2 via NC at 2 LPM.  I would than do a VR4 lead and a 15 lead from my findings of  the first 12 lead.  I would transmit this to the hospital, give him 324 mg of ASA, start a line, and get him to the cath lab pronto.  Since I am in the field alos, I would not have given him nitro until I had the VR4 reading due to possible right sided involvement.  I think this pt is definitely cath lab bound and a code R would be called pre-hospital.  I would also get command orders for possible Morphine to help with the pain since giving nitro would not be advisable at this time.

  • Brooks Walsh says:

    3adamjoe –
    The sugar was normal.
    Fascinating comment though. I actually hadn't heard of hypo-/hyperglycemia causing ST segment changes.
    5 seconds with Google, however, and I found a few studies looking at glucose levels causing ST elevation in patients with Brugada syndrome. Kind of a special case, not generally applicable, but pretty interesting!

  • posterolateral mi,? LCX IS the culprit lesion

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