69 year old male CC: "Indigestion"

Here’s a case from a faithful reader who wishes to remain anonymous.

In his own words:

Presenting Complaint – Chest Pain

History of Present Complaint – 69 year old male, nil cardiac history, none smoker, social drinker.
Complaining of indigestion last 2-3 weeks with noticably increase in belching.
This a.m acute onset of burning heavy central chest pain radiating to neck.

On Arrival – Semi-recumbent in bed

On examination:
Alert, orientated and communicable (GCS 15)

Nil SOB, clear bi-lateral air entry – nil adventitious breath sounds
R/R 16, SpO2 98%

H/R 90 and irregular, Hypertensive 168/110

Temp 36.5 C (97.7 F)
B.M 9.0

C/O chest pain..
O – Acute
P – Nothing makes pain better. Not affected by breathing
Q – Heavy in chest, burning in throat
R – Retrosternal and radiating to neck
S – Pain score 10/10
T – 15 mins
I – No pain intervention sought.

Nil nausea, nil vomit

The cardiac monitor is attached.

A 12-lead ECG is captured.

What is your impression?

*** UPDATE ***

The patient lost consciousness and the monitor showed ventricular fibrillation. A shock was delivered at 200J.

The patient experienced return of spontaneous circulation.

A few minutes later the heart rhythm returned to baseline.

Emergent cath revealed 100% occlusion of the LAD.


  • Geoff says:

    I'm going to agree with the interpretation on this one. ST elevation in the precordial leads, appears convex in nature; most pronounced in V3 & V4. Looks like a small amount of reciprocal depression in II, III & aVF. Interesting (to me) how in V3 the ectopy has a more similar morphology to the underlying rhythm but is a little wider. In V2, there looks to be elevation in the underlying rhythm. Can you say there is concordant elevation in the ectopic complex in V2? Does that mean anything?In terms of treatment, O2 15L via NRB, NTG every 3-5, ASA, Morphine based on transport time. Transport to a STEMI center. Try to get serial ECGs with vitals. Our closest STEMI center will activate if the transport time is greater than 10 minutes and it is up to the ED physician if transport time is less than 10 minutes. They also will activate based on a transmitted ECG if capable.

  • Christopher says:

    Initial rhythm: af w/ unifocal PVCs. 12L looks anterior STEMI. They get the usual and a PCI center w/ STEMI notification.

  • Well, there is definitely something happening in the precordial lead… It looks like the ectopy makes this one hard to read. I honestly am not to sure. There is slight reciprocal depression in II, III, and aVF. QRS looks normal so rule out BBB. EKG is negative for LVH and I don't see signs of pacemakers. Given his presentation and the abnormalities in the EKG, there is obviously something happening. While I can't say definitively if this is AMI, specifically anterior (but I think it is, just a hunch), I would not hesitate to transport him to a designated STEMI center, even if it isn't the hospital down the street. Treatment includes IV, O2 and nitro. I would also drip the ASA and not hesitate to give the Metoprolol. Repeat EKG's every 5. If pressure holds, think about pain management if it doesn't resolve on its own.

  • Terry says:

    A-fib, anterior wall MI with frequent PVCs. Are those u-waves in lead III on the 3 lead strip? IV, high flow O2, ASA, NTG, Fentanyl tx to a cath lab.

  • AJ says:

    ASA, Os, IV, NTG, Morphine, ECG transmission. I would repeat the 12-lead between treatments. I would hold off on the beta blockers as the research is showing increasing mortality of IV beta blockers versus PO beta blockers 24 hours later.

  • AJ says:

    MadHatter,Here is an article you may consider regarding metoprolol use with AMI."Early intravenous then oral metoprolol in 45852 pts with acute MI…."Lancet 2005; vol 366: 1622-32

  • Dan says:

    Be nice, I'm new at this… : ) Although some of this patient's symptoms sound kind of like GERD, the elevation in 2-3-4-AVL seems to indicate Anteroseptal MI, with possibly some lateral involvement. Also some depression in 3 and AVF. Maybe a lesion somewhere in the LAD? There's the underlying A-fib with PVCs, which makes the patient more at risk for clots in general especially since he has no prior cardiac history and is likely not on anticoagulants, though no meds are mentioned.Treatment: O2, ASA PO, IV, Monitor, Nitro SL, serial 12-leads to look for progression/improvement, Morphine or fentanyl for pain management. Pre-alert cath lab and transport to PCI capable facility. I agree that beta blockers should be considered (judiciously) to lower the oxygen demand on the heart, if your local protocols include them.

  • huh, my protocols are heavy in pushing the metoprolol in AMI… Might require some more thought I guess!

  • Anonymous says:

    Looks like anterior STEMI. Treat accordingly. Early notification to the receiving PCI center.Oxygen NC 4LASA 324Nitro Hold morphine unless absolutely necessary. I prefer Fentanyl though.Heparin 5000 units

  • VinceD says:

    ST elevation in V3 and V4, depression in II, III, aVF, T-wave inversion with possibly .5mm elevation in aVL. Acute anterior MI, possible high lateral involvement. The Q waves on the wide complex beats (probable PVC's)in V1-3 bolster my confidence that something is wrong.Tx with ASA, nitro, o2, and transport to a PCI capable hospital. Wouldn't willingly give beta blockers, even though most emergency physicians in my area would give metoprolol on arrival. Would consider analgesia during the trip depending on degree of discomfort and length of our journey, but would probably prefer fentanyl over morphine if we had it (although fentanyl may be just as bad, I haven't run across any studies yet. Anyone else know?).

  • Tom B says:

    Thanks for the comments, everyone! The conclusion is now posted.Tom

  • Dan says:

    Looks like they got to CPR right after the shock if that sinusoidal artifact is any indication. Good work, I see too many people still waiting to see what they have after the shock…

  • Derek says:

    I’m not seeing the atrial fib that some have mentioned and the LP12 identified. There is no fibrillatory baseline and you can clearly see T-waves. If it wouldn’t be for the ectopy interrupting the rhythm it looks like it would be pretty regular.

    I’m seeing ST-elevation in the anterior leads with some depression in II, III, and aVF. Also PAC’s and PVC’s. These ECG findings combined with patient complaint and presentation I would presume AMI and treat as such with ASA, SL NTG, O2 by N/C to maintain SpO2 above 94%, and morphine if pain persistent despite NTG.

    There is mounting evidence of a real danger in giving MI patients 100% O2 by NRB. Several studies dating back to the 1950’s and recently validated using the latest technology found that high concentration of oxygen causes coronary artery vasoconstriction further limiting blood flow and worsening the ischemia/infarction and reduces cardiac output.

  • twoxrifles says:

    Regardless of what the 12 lead says, he is having 10/10 chest pain. Treat the pt. not the monitor. EKG just confirms what the pt. is showing. Wish all pt. turnout was like this guy.

  • Philip says:

    To go along with what everyone else has mentioned, I would treat with 324 mg ASA, IV with fluids hanging, enough oxygen to keep SpO2 >95%, NTG repeated every 5 mins assuming SBP remains conducive, pain management as needed, repeat 12L every 5 mins and call a STEMI alert to a PCI facility. My question and concern remain with the onset of Vfib and the ventricular ectopy at the very end of print three. Would anyone consider 150 mg of Amiodarone over 10 mins?

  • René says:

    Wellens-pattern in V1-2: highly suggestive for critical LAD-stenosis.

  • Notice also the PVC has an RBBB morphology and has concordant ST elevation; another way to diagnose STEMI!

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