66 year old male CC: Chest pain

EMS is called to the parking lot of a local fast food restaurant for a 66 year old male complaining of chest pain.

On arrival, the patient appears acutely ill. His skin is pale/ashen but dry. He is rubbing his chest and there is a grimace on his face. He is not conversant but he answers simple questions with yes or no answers and seems quite content to jump on the gurney and go to the hospital.

Onset: 30 minutes prior to EMS arrival
Provoke: Nothing makes the pain better or worse
Quality: He describes the pain as “crushing” in the center of his chest
Radiate: The pain does not radiate to the arms, back, neck or jaw
Severity: The patient gives the pain a 10/10
Time: No previous similar episodes

Vital signs are assessed.

Pulse: 80
Resp: 20
BP: 126/72
SpO2: 97 on RA

He admits to mild dyspnea but breath sounds are clear bilaterally.

The cardiac monitor is attached.

A 12-lead ECG is captured, which gives the “data quality prohibits interpretation” message.

A second 12-lead ECG is captured, this time with an interpretive statement.

What’s wrong with the patient and what should happen next?

*** UPDATE ***

Here is the 12-lead ECG that was captured on arrival at the hospital.

You will note that we have partial resolution of the ST-segments (although the T-waves still look very suspicious, especially in leads V3 and V4).


  • Christopher says:

    NSR w/o ectopy, STE V2-V5, hyperacute T waves. Extensive anterior MI.Early STEMI notification, IV, O2, 0.4mg NTG SL, based on BP following NTG probably some morphine since he appears very anxious. Serial 12L, grab a 2nd line for the cath lab.Recently I've gone to a system where B-blockers are part of the STEMI protocol. I'm admittedly not familiar with their indication in the face of a STEMI. The few articles I've read don't seem to favor prehospital B-blocker for STEMI. Thoughts?

  • Geoff says:

    I also see the STE V2-V5 and would treat the same way. STEMI alert, O2, ASA, IV, NTG & MS. Serial 12 leads and 2nd line if time.Hard to tell with the wavy baseline, but maybe some early elevation in V6? Also are the T-waves in II & aVF more symmetrical than normal?

  • tony D. says:

    question is after seeing the elevations, does pt have LVH ?

  • Tom B says:

    Thanks for chiming in, guys!@C.Watford – Beta blockers were all the rage for a while. Now? I'm not so sure.@Geoff – Sounds reasonable to me!@tony D. – I don't see any signs of LVH on this ECG using any of the LVH criteria I'm familiar with.Tom

  • Brian T says:

    I like this one. It is a good example of of an anterior MI without any recipocol changes in the standard 12 leads. I have occasionally seen people do a filtered "6 lead" (I, II, II, aVR, aVL,aVF) and only do a 12 if anything appears suspicious on the 6. This is a good example of a situation where you wont see anything on a 6 lead. I'd be curious to see whether he had reciprocol changes in the posterior leads….

  • Brian H. says:

    Agreed that for a while, everyone with a heart and a palpable blood pressure got beta-blockers. Then the COMMIT trial came along, with evidence showing that if you were shocky and in Killip III heart failure with your MI, you did poorly with IV beta blockers (who would've thought?). Now, more judicious use seems to be the norm.

  • Jason Winter says:

    Understandable on this ECG, first impressions will alarm you to think anterior AMI, looking at what the 3rd 12 lead ECG captured shows is quite rightly stated STE in V2-V5… so with this patient with some of the symptoms of an AMI (STEMI) and bear in mind we don't have angiographic evidence of coronary artery occlusion yet from the hospital… so we just have to treat what we see or find, at the end of the day, we can't afford not to in case we make the wrong decision and end up losing our jobs…:( and we all want to be eating our Christmas dinner this year knowing we have a job to go back to…:) Studies have shown in the past that up to 85% of patients with chest pain & STE, the STE is due to non-AMI cause, with up to 25% due to LVH, but we see no evidence of this on the ECG, others p/t's may have both or no culprit artery or negative biomarkers, so we also should think about other most frequent STEMI mimics like myo or pericarditis, stress cardiomyopathy and even LBBB… to name but a few. But we all like to play it safe and treat as AMI, until proven otherwise… If we get it wrong pre-hospital, dispite what our opinions are at the time, we could end up big trouble explaining our actions. Anyway with a pain score of 10/10, we should treat this p/t using Mona… BP is stable so none of the first-line medications we give would be contra-indicated, if I had never met this p/t before I would treat as above. also alerting the hospital, plus not seeing any of the patient's ECG before, but may I say I and in two minds with this case, my six sense is telling me something is not all it appears to me, with the all clinical picture.But due to the p/t's clinical presentation of looking pale, but NOT sweaty and crushing chest pain, red flags for being pale and the CP, but this is non-radiating, and I am also asking myself is the p/t really in that much pain with the HR & BP, being as they are??? I think I would say to this p/t is this the worst pain you could ever experience then?, so if someone say cut your leg off, it would be the same…lol?Anyway, I have been going on for a while…:p, I have given you a few things to think about here guys, so will leave this one with you for now and I will comment further on the ECG's later, we could get some mileage out of this case study, due to the many issues that could be addressed…Interesting case Tom… Many thanks!

  • Jason Winter says:

    Just one final thing whether this is an Pseudo-infarction pattern, Benign early repolarization (BAR) or not, which with NO reciprocal changes in would be very shocked and surprised, or I may learn something interesting today, will wait and see…:) I would be interested in the patient's potassium levels.

  • Why says:

    Could this be a septal infarct extending anteriorally?

  • Anonymous says:

    If we get it wrong, "we could end up losing our jobs" or "we could end up big trouble explaining our actions". …….rather small stuff compared to the Patient losing their life.

  • Tom B says:

    @Brian T – I like this case for the same reason! The 3-lead ECG looks perfectly normal. It's a good example of why the "put the patient on the monitor" mindset is insufficient in this day and age. One of these days I'm going to check the posterior leads and see if it shows reciprocal changes with an anterior STEMI! @Brian H – Thanks for the scoop about the COMMIT trial!@Jason W – Believe it or not this isn't a trick case! 🙂 It's just a horse, not a zebra (this time)…@timm – Or an anterior STEMI extending septally? I don't get caught up in it.Thanks for the comments, everyone! I'll be posting an update shortly with the angiograms.Tom

  • Hillis says:

    Well the ECG isn this case shows hyperacute T wave( symmetric tall not tented T wave )which is the erly sign of acute STEMI the changes appear in anterior leads causing.. the treatment include- Nitroglycerine, O2 suplemment, Aspirin, Morphine, Clopidogrel, if not contraindicated unfractionated heparin or LMWH and immediately trasporting the patient to PCA.

  • Tom B says:

    Dr. Hillis – Thank you for the comment! Does PCA stand for percutaneous coronary angioplasty?Best,Tom

  • David says:

    Antero-Lateral involvement. Very suggestive of a STEMI. Bi-lateral Iv’s 16g if you have them. SL Nito, paste, ASA and morphne if BP holds out, but thats why I use 16g IV’s. Call ahead for a window seat in the PCI lab, serial 12 leads. Continue to monitor for chanegs. Anybody who does not use a 12lead should note that lead 2 isn’t even wide y’all. ” You got no clue in lead II”.

  • Matt says:

    Hi all.  Definitely agree with this being an anterior/septal MI.  I also agree with our standard treatment plan being safe and apporpriate given the patient's current vitals.  Just looking for people's thoughts and opinions on something else.  I realize that these ECGs were taken over a very short time period, but does it look to anyone else like the patient is developing poor R wave progression and a Q wave in V3.  And with that being said, would this being something we could use to solidify our working diagnosis of Anterior Wall STEMI, especially in the absence of recipricol changes.  Just a thought.  Looking forward to reading what other people think.  Thanks.

  • platelet says:

    There are definite ST-elevations on the first 2 12-leads, and the patient is symptomatic, so I would go with standard STEMI protocol, too. The 3rd 12-lead prooves that it is an acute coronary syndrome: the ST-segment moves and there is R reduction, too.

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