“Bad heartburn” – 82 y.o. female without chest pain.

This case is courtesy of paramedic Jason Cameron, who works for Stratford EMS in Connecticut.

The ALS unit had been dispatched for an older female with “chest pain.” Upon arrival, however, the 80 y.o. patient denied any pain or pressure, and only endorsed some mild “heartburn,” localized to the epigastrium, non-radiating, and rated it at a 2/10. It had started about 30 minutes prior, and had not been relieved by Maalox. Her husband had called 911. The patient denied all other symptoms, and specifically denied any jaw, arm, or back discomfort, and denied any dyspnea or sweating.

Her medical history was significant only for mild hypertension and elevated cholesterol. She took a statin and an ACE inhibitor

Vital signs

  • HR – 40
  • BP – 118/72
  • RR – 18
  • SaO2 – 98% RA

The physical exam was unremarkable.

The paramedic obtained an ECG:


Aspirin was given, but nitroglycerin was withheld. An IV was established, but the patient did not became hypotensive.

Suggested Discussion Points:

  • Do you believe that this patient requires PCI for acute coronary occlusion?
  • If so, what was the likely site of the occlusion?
  • Are there any other management concerns, given this ECG pattern?
  • Should you routinely obtain ECGs in patients who complain of GI symptoms, but who deny any chest pain, pressure, or discomfort?
  • Lastly, although the local protocols do not require that the computer interpretation display ***MEETS ST ELEVATION MI CRITERIA *** in order to activate the cath lab, they limit activation to patients with “active chest pain and/or dyspnea.” In that context, how should the paramedic have proceeded?

I will have follow up posted within 48 hours!


  • Jessica says:

    Here goes nothing….

    The medics did the right thing; a 12-lead is absolutely appropriate for ostensibly GI symptoms. Many people present with atypical cardiac symptoms (GI discomfort being a common one), especially females, diabetics and the elderly.

    I would call this an inferior wall MI/RCA occlusion. No rhythm strip, but judging by rate and lack of P-waves the rhythm appears junctional. O2 via nasal cannula, 324mg ASA, get V4R, withold nitro because in the setting of inferior MI it would dump the BP and reduce preload to a dangerous degree. I’m ok with a heart rate of 40, so long as the patient is mentating.

    I’d present the case as I found it: an elderly male experiencing epigastric discomfort not relieved by antacids, and the 12-lead obtained shows ST elevations consistent with inferior wall MI. The cath lab docs should know that chest pain isn’t the same for everyone.

    • MB says:

      Ok so I’m a little curious as to some peoples thought process on this one. Yes obvious this is a inferior MI and possible a Right Ventricular infarct. Fact that the patients Brady really makes me think about the right ventricle. But why would anyone consider nitro in this patient. The patient is pain free first off. In right sided MIs the heart is preload dependent which means nitro could kill the patient. This patient needs fluid and a 250 bouls isn’t significant enough to do jack for this patient. Next if the patient was experience pain fentanyl would be more appropriate then Nitro. Only would I consider giving nitro after I’ve given at least a liter a fluid. And you wouldn’t give atropine either because it can worsen myocardial ischemia and farther damage the heart. Also you’d withhold oxygen unless the patients spo2 was below 94 percent or showing signs of hypoxia. All of this info is new in treatment because of new research and studies but to be a proficient provider you must stay up to date on research and information..

  • Jessica says:


  • Earl Phelps says:

    With a few different suggestions, I agree with what Jessica say: I would not withhold the nitro, I agree sublingual nitro is not the best route but a nitro infusion isn’t a bad idea. Agreed that you need to be cautious with it in the presence of a inferior MI, but not to the point of withholding it. Start it about about 15mcg/min roughly and adjust as needed. If you are worried about dumping the preload then give a fluid bolus to help offset the vasodilation. Remember time is muscle in this situation and we need to restore blood flow to the hypoxic area of the heart to decrease the perms at damage. I also think that distance to an interventional cardiologist should play into treatment, as for me, I work for a dept that is very rual and we could have hour transport times to our hospital and a hour and a half to two hour aircraft ride to a cardiac center so restoring blood flow is a priority for us. This is my humble opinion only, I’m sure there are hundreds of treatments all of which are right in their own way.

  • potatoes, potatoes. heartburn, pain.

  • Razvan A. says:

    Inferior STEMI (ST Elevations in DII, DIII, aVF)
    ST Depression in V1-V4
    I would do posterior and right derivations. 325mg aspirin, 600mg clopidogrel.
    I would withheld NTG due to the low HR and the possibility of RVI. (RVI is preload dependent, remember?)
    If pain increases I would administer a small dosage of Fentanyl to relieve pain.
    STEMI code regardless of computer interpretation.
    Culprit artery is either RCA or LCX.

  • Daniel says:

    We are lucky in my area to have a “Code 37” alert (STEMI alert) that puts the cath team into action. I would call a “Code 37” due to inferior STEMI, then a right sided ECG to look for right ventricular involvement prior to NTG administration for treatment decision reasons, then do a posterior 12-lead en route to present to the cardiologist when we arrive.

  • Jonathan says:

    ST elevation II, III, aVF

    Inferior Infarct requires repeat ECG with V4R to check for right ventricular infarct. If this is the case then a fluid bolus may be indicated to increase venous return to the left ventricle. RCA occlusion is the most likely cause. Right ventricular infarcts can present with symptomatic bradycardia.
    Aspirin, GTN with caution, clopidogrel. Usual ACS protocol.

    In my area we would transmit both ECG’s to pPCi and call them up to get secondary assessment of ECG and advice on treatment from the cardiologist. Usually a 250ml bolus of fluids.

  • Paul says:

    Screw it. I’m giving NTG/GTN. I give everybody at least 1. Not every IWMI will lose their BP from NTG. Likewise, I’ve even had a few RVMIs that I gave NTG/GTN to who actually improved quite a bit. Don’t withhold treatment “just because.” Use clinical judgement. I don’t think you can do that by withholding medications, even when there is an increased incidence or likelihood of side effects. You can’t look at one thing in isolation.

  • Sassy says:

    Our local protocols prevent administration of GTN to RVI, Inferior STEMI with BP less than 160 systolic or HR less than 50bpm. As more than 50% of inferior MI’s have RV involvement you walk a very fine line between preload and none. The HR could possibly indicate RCA occlusion so there’s one side of your CO equation kaput. Aspirin, pain relief, transport and call for MICA back up (prehospital thrombolysis is now part of their management if indicated) is my ALS management.

  • Very interesting discussion – I had not anticipated the degree to which giving/not giving nitro would be controversial! I had my own agenda in presenting this case, but I think it would be better to follow the interest of our readers.

    I’ll add a few pearls about ACS, nitro, and inferior STEMIs in my discussion (which should be up in < 48 hours).

  • Dan August says:

    ST elevation in all leads is caused by early repolarization. That’s why the Q and T are mashed together. Could be a stemi, but you can’t tell with this going on.

  • Dan says:

    I’m on board with most of the convents so far. No need to elaborate.

    I would add maybe a dissection into the aortic root causing RCA occlusion. Not going to know without imaging. Call cath from the field regardless.

  • Al says:

    Good treatment by all. Well done Jessica for being the first. …. I would use morphine instead of fentanyl due to BP dump and future use of amiodarone but very small doses 1-2 mg. Two good reasons two steer clear of GTN 1. Inferior AMI 2. HR 40. Both Will reposition the Pt on the floor and complicate the day.
    Thrombotic agents will also be helpful, providing it’s not contra indicated . PCI for sure….. and early organisation will save Cardiac tissue.
    The days of ECG recognition should be gone. We as professionals should be able to read this as we as the reciprocal changes. ST elevation > 1mm limb leads > 2 mm chest leads (contiguous leads).
    There are usually more reasons to withhold medications than are indicated especially the one’s talked about in this setting, it never hurts to get other opinions and further diagnostics but time is money/tissue in this area.

    • Al says:

      oh I forgot one more thing, where are the P waves ??
      hard to see on this phone but is it junctional or a block ?? If it’s a heart block then there is more evidence of ischaemia to the Node. …… which is isn’t good…..

  • Christopher says:

    I’m shocked the computer missed this one! Pretty clean baseline, easy to find J-points…I think the incorrect QRSd tripped it up.

    Should send this to PhysioControl, especially if this is from an LP15. I’m sure the Glasgow folks would love to get their hands on the data for this tracing.

    • Chris – two thoughts.

      First, what’s the best data on sens/spec for STEMI in the lp-15?
      Second, welcome to the >= 30 club!

      • Christopher Watford says:


        Firstly, thank you for the warm welcome to the club.

        Secondly, the Glasgow algorithm’s only published sens/spec for AMI is 51.6%/97.6% respectively (Tuscon STEMI Database). I’ve not been able to find any other publications. The GE Marquette 12SL algorithm has been widely studied, but is much older, and ranges in sensitivity from 48% to 69% (depending on the study), and in specificity from 98% to 100%. Due to its age the 12SL algorithm has the benefit of being field tested and thus these numbers are probably believable in the general sense. The Glasgow algorithm in the LP15 does not seem to have any published results from the field.

  • Austin says:

    There’s not much I think I can add at this point, but I will comment on a couple of things. The reciprocal changes indicate to me that there is likely RCA involvement. Also, I’ve recently been hearing quite a bit about withholding O2 in ACS patients like this. Dr. Walsh, do you have any opinions (informed or otherwise?)

    • My uninformed opinion? I pretty much agree with AHA – if they aren’t hypoxic, no need. I’m not sure how terrible superoxia really is, short-term, but why bother if it doesn’t help?

  • jason says:

    Chris Watford- as you probably know the “acute MI suspected” detection function in the LP12/15 is a programable option. I suspect the software didn’t miss this but rather it wasn’t turned on.
    As for treatment everyone has pretty much got it down.
    Finally as for activation. Absolutely! Don’t real care if the protocol allows for activation in the setting of stemi w/o CP or if the protocol allows for aniginal equivalents in place of CP. Activate now deal with any repercussions later. You’ll be alright- I promise. And if not you probably don’t want to work there anyway.
    Finally Dr. Walsh- you don’t let your medics activate w/o CP?!?! 😉

    • Austin says:

      You took the words right off of my keyboard, Jason! A little bit of critical thinking works wonders when faced with “protocol versus best interests of the patient” type decisions. Not to encourage deviation from protocols and such, but it is a much less severe trespass if you bend the rules a bit as long as it is clearly in the patient’s best interest.

    • The option was indeed turned on!

      As for non-CP presentations of ACS, I absolutely believe that these warrant the same level of urgency as the “typical” presentations. Both men and women, young and old, all commonly present without classic chest pain. Besides, how much difference is there between “burning in the epigastrium,” and “pain in the chest?” About 2 cm and and a modestly different adjective.

      OTOH, we see pretty dramatic examples of early repolarization, and the computers get fooled by those fairly often, so the patient should have some sort of anginal equivalent. Figuring that out is the medic’s job!

  • Jared says:

    Not much to add but my 2 cents…I’d definitely be careful with the nitro, not saying withhold it completely but absolutely use some common sense. I’d have to say probably RCA occlusion, and catch team needs to be activated for a stemi alert immediately. Treat it like a stemi until proven otherwise. If it walks like a duck and quacks like a duck odds are its a duck. Treat for the worst case scenario

  • Bryan Laviolette says:

    In addition to the above treatment consensus (ASA, Plavix, judicious NTG, fentanyl, fluid bolus, right sided leads), I would absolutely transport this patient to a PCI centre. Culprit artery is the RCA (STE lead III > II) leading to AV nodal ischemia and junctional bradycardia. In addition to the above treatment I would give 0.5 mg atropine and place the combo-pads in preparation for pacing and/or deterioration.

    My local protocol does not allow direct transport to the PCI centre without “chest pain”, would contact medical direction for authorization to bypass local hospital.

  • Mary says:

    I, for one, would really like to read a response or two, to Dr. Walsh’s question to BV about why give atropine at this time. Why give atropin at this time? Thanks.

  • Billy Bob says:

    I’m a bit late and curious to read the conclusion (coming after this) I agree with all and again to beat the dead horse but yes I agree with 12 leads in the setting of GI symptoms (specifically here) as it is quite common to have “heart burn” as the C/C for IWMI due to the close proximity of the inferior portion of the heart and diaphragm (or so I’ve been told). IWMI with probable RVI we could do the 15 lead but everything is already telling us. STE > in III than II points to it and STD in lead I tells us the culprit artery is RCA vs LCX and given the rhythm (hard to tell as there is some artifact) but it appears junctional (rate goes along with it as well) so probably a proximal occlusion effecting our nodes. The STD in V1-4 is more than likely not reciprocal this points us to the posterior STEMI. So ASA O2 is good I’ll with hold that along with the NTG yes her pressure is good and the diastolic is well but I wouldn’t risk it (consider fentanyl for pain) no need to increase the rate she is doing just fine and again this could even be cardioprotective (I.E in the setting of BJR if it were applicable here). Call the cath lab.

  • michelle says:

    i agree with jessica most women especially start with heartburn symptoms.

  • iliyas says:

    Inferioposterior mi

  • Kevin Dittrich says:

    S-T (J-Point) elevation in II, III, and AVF are clear. There are no repol abnormalities. There are even reciprocal changes. IV with fluids is a must but beyond that, what else is there. Females, especially, present with atypical symptomologies. Be ready with fluids, but treat with standard AMI protocols. Presentation, ECG, age, sex, it’s not too much of a stretch to treat regardless of QT/QTc abnormalities.

  • IGDon says:

    I kept feading this thread to see how long it’d take for someone to call it as it is ‘inferioposterior MI’ and the prize goes to iliyas on Sept 11.

  • Nick says:

    It’s most likely a RVMI because the ischemia/infarction has effected the SA node. IWMI with bradycardia should highly suspect a RVMI. Not all RVMI’s are preload dependant. Do a 15 lead ecg to verify V4R elevation. Have 2 IV’s established with a bolus of at least 1L of fluid before giving nitrates. If the pt dumps her/his pressure, lay them down and give fluids. Fentanyl will not provide vasodilation to get blood and oxygen to the tissue. You can also use IV nitro in place of SL NTG, because the pt does need NTG to get circulation passed the blockage. Of course you’re going to activated the cath lab at the nearest PCI center.

  • Dominic says:

    I would do a v4r to see if right side involvement as well as posterior v8-v9. Based on the pt not presenting hypotensive this can be RCA occlusion caused by disection of thoracic aortic aneurysm! Debakey type 1 aneurysm! No catch lab however surgical intervention would be required!

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