71 year old male CC: Chest pain

EMS is called to the residence of a 71 year old male with a chief complaint of chest discomfort.

On arrival patient is found standing at the front door.

He appears anxious and acutely ill.

Skin is cool, pale and diaphoretic.

Onset: “Fairly sudden” 30 minutes prior to 9-1-1 call
Provoke: Nothing makes the pain better or worse
Quality: Pressure in the center of the chest
Radiate: When asked if the pain radiates the patient states “I don’t know”
Severity: 10/10
Time: Less severe episode yesterday lasting approx 15-30 minutes

Past medical history: Dyslipidemia, mild HTN

Meds: Zocor, Norvasc

Vital signs are assessed.

RR: 20
Pulse: 64 R
NIBP: 131/85
SpO2: 98 on RA

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

No JVD or pitting edema.

Oxygen is applied via NRB mask @ 15 LPM.

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is loaded for transport and another 12-lead ECG is captured.

What is your impression of these ECGs?

What is your treatment plan?

See also:

71 year old male CC: Chest pain – Conclusion


  • Brandon O says:

    ASA, nitro, emergent transport to PCI with field activation. Monitor closely for risk of decompensation. Obvious acute, evolving anterolateral STEMI.

  • Harrison says:

    Sinus Rhythm @ 65. Normal Axis. No ectopy. Hyperactue T waves noted in lateral leads with clinically significant upwardly concave ST elevation in anterolateral leads. ST depression noted in III.

    I also want to say slight ST depression in avF, but tracing quality hampers this assessment.

    It looks like hyperkalemia is elevating this T, however the first stage of an AMI on ECG will show hyperactue T’s followed by elevating the ST segment. Thus….
    My DDx in order

    To further the case of AMI and to r/o hyperkalemia, we have actual T wave inversion in V1 and III. Also, the lack of global hyperacute T waves strengthens the case of AMI and not hyper K.

    Stemi alert. Treat/transport per protocol.

  • Jukka Kettunen says:

    Hi Tom, and thanks for the great blog!
    I’m gonna take my first shot here: the impression I’m getting here is that of a SR with anterolateral MI (ST elevation V2-V6, I and aVL, resiprocal III).
    I would treat him according to our local protocol: O2, 2x large IVs, ASA 250mg po, iv NTG, iv oxycodone. Betablocker would probably be too much, but if the pulse rate doesn’t drop too much, maybe 1mg iv.
    Now, since we operate in a region where cardiac cath labs are hard to come by (and are operating only during office hours), I’d probably do a thrombolysis using tenekteplase (Metalyse)and enoksaparine (Klexane). (Sorry if they sound weird, I tried to translate the generic names from finnish!)
    Get all this started and then load the patient in the chopper. The distance to our closest hospital can be up to 500km. Outside office hours the closest cath lab can be up to 750km away (via road).
    How about that?
    Jukka Kettunen
    Flight Nurse/Paramedic
    Rescue Helicopter ASLAK
    Sodankylä, FINLAND

  • Ryan says:

    Agree with Brandon, it’s clearly an evolving global infarct. Though, I’m puzzled why L3 is inverted. Not that it really matters, specifically to this case. And it’s early for me so I might not be clicking on all cylinders yet. Lol.

    But yes, ASA, for sure, id actually like to get a right sided EKG too just to see if this has more inferior involvement. Then after that, bilateral IVs if I can, fluids for pressure support, and nitro the snot out of him. STEMI activation, and rapid transport. Watch for decompensation. I’d like to get a good history of the illness too just to rule out pericarditis, which, I doubt this is. At some point a blood glucose. V3 is quite peaked and aberrant, makes me wonder about hypokalemia…

  • Jukka Kettunen says:

    Oh, and the (reciprocal) ST-depressions in III and aVF seem to be deepening in the second EKG, along with the Q-waves in V2 and V3. The situation seems to be getting worse…

  • VinceD says:

    Extensive acute antero-lateral STEMI. ST-elevation V2-V6, I, aVL.
    ST-depression III and aVF, maybe 0.5mm in II. Hyperacute T-waves V3-V5.

    STEMI alert. Treat with O2 @ 12Lpm per protocol, 324mg ASA, IV access, 0.4mg SL nitro q 5min x3, reassessing BPs. Call med control for 5mg morphine, further dosing if no effect. Would not request metoprolol since his BP is fine where it is (if my nitro and morphine doesn’t tank it, hopefully) and I don’t feel it would add anything to his care. Serial ECG’s en route.

  • Troy says:

    Anteriolateral MI. ASA, O2, Nitro, Morphine, Heparin (4000u bolus then drip 12u/kg), and diesel fuel! Also I would place some fast patches because in my experience its usually the LAD occlusions that like to slip into V-fib. Oh! And serial 12’s.

    Go finland!

  • Christopher says:

    Extensive anteriolateral MI. I’m a fentanyl man for pain in ACS these days, otherwise I’m game with everyone’s routine.

  • Dave B says:

    agree with anterolateral MI… nothing much more to add to the other comments..

  • Matt says:

    ASA, Nitro x 3, Morphine, Send 12 Lead to receiving hospital for consultation and then TNK (Tenecteplase ) in the patients living room. Transport.

  • Mariela says:

    Anterolateral MI. Prehospital inmediat treatment: ASA, Nytroglicerine and continuous monitoring until the arrival to the closest center for PCI.

  • Troy says:


    I read a study recently on how fentanyl causes less damage to the coronary vessels than morphine. Ill try to find it and send it to you!

  • Stephen says:

    A question for those of you that give thrombolytics. Are you giving the full does of the thrombolytics of half does and still transporting to the cath lab for PCI afterwards?

  • VinceD says:

    Troy – Can you post a link to that study on here? I would love to see it.

    I’ve seen a few cases for the association between morphine and worse outcome for MI, but nothing convincing so far. The most prominent I’ve encountered, from the CRUSADE initiative(I had to google it, I don’t carry this stuff around in my head), only looked at NSTEMI. Because most NSTEMI is managed medically for the first day or two, and treatment can to be dictated by the continuance of pain, it’s possible that the pain masking effects of the morphine resulted in the ‘morphinized’ patients receiving less than maximal therapy, leading to increased morbidity/mortality. If that is the case (which it’s just as likely not to be, I admit), these ill-effects wouldn’t matter in a STEMI patient going directly to PCI. If this patient had chest pain and a non-diagnostic ECG, however, it’d be a different story.

    All that being said, if I had both drugs available I too would use fentanyl, but I don’t, so morphine’s plenty good enough for me at this point in time.

  • Ben says:

    Interesting to hear the comparison of fentanyl and morphine, will have to look into it. Id go 300mg ASA PO, 2mg buccal gtn, morphine and thrombolytics as we arnt lucky enough to have a ppci centre within 2 and a half hours. repeated 12 leads and the drug of choice… Diesel

  • Jukka Kettunen says:

    Regarding thrombolytics – full dose. If it doesn’t save the day (relieve the pain, ST-elevations going down, etc), only then rescue-PCI (when we reach a cath lab).

  • Troy says:

    Also I forgot to mention was seems to me like pathological Q waves in the septal leads.

    Also I don’t agree with the axis being at +9. I would say this guy has a left axis deviation that’s close to 0 degrees but there. Also I believe he has a LAFB. Correct me if I’m wrong

  • Troy says:

    Correction….negatory on the Q waves

  • Barry says:

    Anterial-septal MI with lateral involvement (extensive anterior). reciprical changes to the inferior leads.
    ASA, pacer-pads. high flow O2.IV x2-3. NTG preferable in drip. Fentanyl for pain and anxiety (morphine increases mortality, also fentanyl has no histamine response like morphine, no drop in B/P, and slight decreases in resp. rate). Zofran. rapid transport. thrombilitics (TNKase 1mg/kg). fax 12-lead to ER.

  • Barry says:

    Troy this is normal axis and here is why: lead 1 up, AVF up. axis number +16, normal between 0- (+90). For this to have a left axis lead 1 up, AVF down, and the axis number between 0-(-90). pathologic left is between (-30) – (-90)depending on the book you read. I also do not detect a LAFB.

  • Troy says:


    The book I learned axis out of called an isoelectric (equal R and S wave) aVF with a Q1S3 indicitive of a borderline Left axis deviation with a LAFB. Also this book stated look for the isoelectric V-lead (in this case V2). If normal between V3-V4, the rotation is normal, but since this rotation is right, this makes a borderline Axis deviation even more relevent.

    I could just be blowing smoke…..

  • Troy says:

    Geeze that sounded a little arrogant of me….

    More or less how I interpreted my reading (thus far) is that you look at the rotation to see if there is a possiblility of compensation for an axis deviation to go from pathological to normal variant.

    I AM NOT SAYING HE FOR SURE HAS AXIS DEVIATION. I’m just saying with the Q1S3 id be a little more leaning that way. And with the LAD occluded (only supplier to the LAF where as the LPF is also supplied by the RCA) its definitely a possibility

  • Christopher says:

    I think the computerized axis is spot on, somewhere between 0 and +10 degrees in the frontal plane. For LAFB you need LAD as everyone has pointed out (-30 to -90). If we look at lead II (+60) we see positive polarity without question (Rs), which all but rules out LAFB I believe.

    I will agree that there is a rotation in the Z-axis, but not a terribly surprising one given the infarct and its potential size.

  • Troy says:

    Well then…. I guess I need to study that a little harder. Evidentally that part of the book is not spot on o_o

  • halil gölcük says:

    electro cardio graph is common in ischemia, MI

    1. an on-site security
    2. A-B-C
    3. blood pressure normal nitrate 5mg
    4. aspirate
    5. morphine sulfate chest pain does not go
    6. appropriate equipment
    7. transferred to hospital the most recent and most accurate

    turkey – paramedic

  • alex says:

    extensive antero-lateral wall mi' he needs pci as soon as possible

  • Scott says:

    take him off the oxygen, his sats are good and it can cause harm due to increased cardiac workload.
    aspirin, GTN and analgesia en route to PPCI, for the anterior lateral MI, monitor en route.

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