57 year old male CC: Chest pain

Here’s a very interesting case submitted by FF/medic Tim Porter (c/o a faithful reader).

The patient is a 56 year old male with a chief complaint of chest pain.

Onset: Approximately 30 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: Described as intense pressure
Radiate: The pain does not radiate to the arms, back, neck, or jaw
Severity: 6/10
Time: Unknown whether the patient has experienced previous similar episodes

The patient denies shortness of breath.

The patient’s skin is pink, warm, and dry.

Past medical history is significant for cardiac stent 2 years prior.

Medications: unknown.

Vital signs are assessed:

Resp: 18
Pulse: 1oo
BP: 160/90
SpO2: 97 on RA

A 12-lead ECG is captured.


The patient is loaded for transport.


An additional 12-lead ECG is captured en route to the local non-PCI hospital.


Of particular interest to me, in the absence of an obvious STEMI, this paramedic’s EMS system allows bypass to a STEMI center when 2 of 5 secondary criteria are present.

They include:

  • Obesity
  • Smoker
  • Hypertension
  • Diabetes
  • Prior history

In this case, the patient only had prior history.

So, what is your impression?

More to follow…

*** UPDATE ***

Some interesting comments so far. To help illustrate the changes in the right precordial leads between 12-lead 2 and 12-lead 3, I created a side-by-side comparison.

Take a look and share your thoughts!


After you’ve had a chance to comment I’ll post 12-lead 4 and bring the case to a conclusion.

*** UPDATE #2 ***

Here’s the 12-lead ECG that should remove all doubt about what’s going on here!


The least I can say is: this is why we perform serial 12-lead ECGs! Based on this ECG the patient was diverted to a STEMI receiving center (19 minutes after the first 12-lead ECG was captured).

21 Comments

  • Wow, V1 looks mighty unhappy there…just wish V2 showed the same thing so we could call a STEMI. This is an interesting example to illustrate when transmission of 12-leads to a base hospital might be useful for a further decision by physician. Although the pt only met one criteria (prior history), I would want to talk to the base doc to suggest transport to a PCI facility. I would probably at the very least consider this unstable angina, which might have some recieving docs want PCI anyway. Lung sounds, 02, ASA, NTG, thrombolytic checklist (just in case!), serial 12-leads and morphine if we still have time.

  • Tom B says:

    MIFL – I didn't like the looks of lead V1 either. An R/S ratio > 1 always catches my eye. Assuming lead placement was correct, you have to consider the differential diagnosis, which includes:Right bundle branch blockRight ventricular hypertrophyAcute right ventricular dilation WPW Type APosterior myocardial infarctionHypertrophic cardiomyopathyProgressive muscular dystrophyDextrocardiaMisplaced precordial leadsNormal varient (juvenile pattern)To be honest, at first glance the first thing I did was scrutinize the precordial leads for delta waves, but the cardiac history could explain the R/S ratio in lead V1 (previous MI involving the posterior wall is a possibility).I don't know if any docs would cath unstable angina, but then again, it's clinically indistinguishable from NSTEMI in the first several hours.on the other hand, it's usually a positive Troponin I or T (as well as ST-depression) that NSTEMI "high risk" where early invasive strategy appears to be emerging as the preferred therapy.What do you think about the serial ECGs?Tom

  • SoCal Medic says:

    Tom,I agree with Medic Intern in that I do not like V1, coupled with V5 and V6 and what appears to be slowing in the heart rate in the third twelve lead there is just to much going on. Treatment is going to be the standard mona, the slowing in the heart rate would get him a second line (overly precautionary). I would push to put him in a cardiac care facility because of his previous history but I would also, if time permits, get V3R-V6R just as precautionary since there was nothing obvious on his standard 12. Also I would ask him if he knew about any changes that might have happened in the past with regards to his previous MI and his 12 Lead. I have had patients before tell me that they have had NSTEMI before.

  • Geoff says:

    I also don't like the looks of V1. Is it just me or does it look like aVR is elevated as well? That in combination with the ST Depression I see in I, aVL, V4, V5, V6 worries me. It also appears the T waves in V2 & V3 are getting bigger as well. Could it be a Left Main Coronary Artery blockage? I don't know, maybe I'm trying too hard to place this. I'd treat, same as SoCal Medic, O2, ASA, NTG, MS, right sided 12 lead. Maybe all the depression is reciprocal? I'm fortunate, our STEMI center is also our closest greater than half the time, so we'd either go there anyway or creatively show up. Here is where I got my information on aVR, don't know if anybody has seen it, I get to do more research now… If this doesn't work, google EMRAP 68 and go to episode 68. Any more info out there on this? I've found a few things…http://media2.podbean.com/pb/a7f4db260873695d0848b6457f03f388/4b3816b4/blogs2/37693/uploads/EMRAPTV68-AVR.mp4Great strip, thanks.Geoff

  • Tom B says:

    SoCal Medic -I agree! Lead V1 is very strange looking. Not typical at all. But then again, I also find the positive concordance in the precordial leads to be bothersome. That's why I carefully scanned the ECG for WPW Type A.You're right, sometimes patients are surprisingly well informed about their medical history. Other times? It's shocking they take so little interest! "I've got a bum ticker." What?! That's all the interest you took in your medical condition? You've located it to the correct organ!?Tom

  • Tom B says:

    Geoff – I was unable to download the podcast for some reason. Was that the "Rodney Dangerfield lead" podcast? I seem to remember listening to something like that! I'll try the Google search you recommended.Lead aVR actually looks pretty normal to me in this example, at least relative to some of the other leads! You did, however, nail the observation I've been waiting for:"It also appears the T waves in V2 & V3 are getting bigger as well."Yes, indeed! You will also note the sudden appearance of S waves in the right precordial leads! I'm going to post a side-by-side so everyone can appreciate what we're talking about.Then I'll post 12-lead 4.Tom

  • SoCal Medic says:

    It took me multiple looks I must admit but there is a change in QRS Morphology and the ST segment looks changed as well. The T Wave looks partially bi-phasic but not drastic chaange in morphology from the one to the other. I am still leaning towards some sort of MI, especially with the QRS changes and would love to see the next 12 Lead you have hidden on that computer.

  • Tom B says:

    SoCal Medic -You've got it! 12-lead 4 is now posted.Tom

  • SoCal Medic says:

    Yeah serial 12 Leads is important, and this case proves it. To many times I see crews saying, well the 12 Lead looks ok, we can take him/her off with patients having active chest pain.Kudos to the crew who ran this call and bring on some more.

  • Geoff says:

    Tom, Yes, I was referring to the "Rodney Dangerfield, I get no respect" podcast. I also think you can find them on iTunes, but not that far back.Looking again, seeing the S waves now is very obvious. Just to reinforce something, I understand hyperacute T-Waves in the initial onset of AMI, does the development of the S wave indicates something as well?Once again, thanks for the strip.

  • Christopher says:

    Could the S wave development be a shift in the precordial axis as the vector mean changes with tissue damage?

  • Tom B says:

    Geoff – I've often noticed changes in QRS morphology associated with ACS. For example, often the development of inferior Q-waves is associated with increased R-wave height in the high lateral leads and the right precordial leads.With acute anterior STEMI, I've often noticed the obliteration of the S waves just prior to or concurrent with ST-elevation. Why they were absent, then appeared, then disappeared again could be related to dyanamic supply vs. demand characteristics.Tom

  • Tom B says:

    C.Watford – You're certainly correct in that Q-waves can attenuate R-wave height in the right precordials, but usually when the S-waves disappear it's associated with ST-elevation.This is based on my own anecdotal observations, but it's a topic worth exploring further.Tom

  • Christopher says:

    So it's not necessarily that they aren't there, just the composition of the waves where the ST-segment changes means the S wave gets lost?

  • Tom B says:

    C.Watford – Let me preface this comment by saying, "It seems to me…." Yes, in my experience the ST-elevation often "lifts" the S-wave above the isoelectric line (at which time it ceases to be an S-wave).Tom

  • Tim says:

    Yes, serial 12 leads are very important. On arrival a lot of medics would transport this pt. do the "protocol" thing and that's about it.

  • Tom B says:

    You're right, Tim! That's exactly what a lot of paramedics would do. Hopefully cases like this raise awareness! Quality improvement feedback loops are very helpful, too! Tom

  • john says:

    surprised no one has mentioned the obvious acute posterior wall infarction

  • john says:

    sinus rhythm with acute posterior and inferior wall MI. i will look at the PDA or the LCx

  • john says:

    having said that, i see that the R wave in some of the leads is > 13mm so it is also a possibility that the myocardial injury and ischemia is caused by concentric left ventricular hypertrophy ( r waves in some lead > 13mm) and right ventricular hypertrophy ( the R wave in v1 being deeper than the s wave)

  • Andre says:

    This looks like a very interesting case for the fact that there is some changes noted but not to the point that as a Paramedic we can call a STEMI…. Of course except for the Update 2 where there is an Obvious STEMI going on. This is a patient though with the symptom and PHX that I would consider transporting to a higher level of care. I would think that consulting with an ER physician or even the Cardiologist for further treatment beyound MONA is needed, This patient would benefit from some lopresser and some Anticouagulants. I would really like to see his Troponin and CKMB…. This would at the LEAST be unstable Angina I would think

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