51 Year Old Male: Chest Pain

Here is a great case submitted by faithful reader Niels, a Paramedic in Germany. As always, some minor information may have been changed to preserve patient confidentiality.

Our case today takes us overseas, to the German countryside. It's a clear blue Monday morning, 11:40 am, when you and your partner are called to a 51 year old male complaining of chest pain. You are dispatched parallel to an Emergency Physician (in Germany, every ALS call is dispatched with an ALS ambulance and a doctor).

On arrival, you find a male patient lying in bed. He appears to be very diaphoretic an pale. He tells you he is very athletic and fit, but today is "feeling horrible". He says his "chest is killing him", and he admits to being nauseous, with several bouts of vomiting.

O,P,Q,R,S,T: He tells you he woke up with the pain, and it seemingly came out of the blue–he was feeling fine the night before. Nothing seems to make the pain, which he describes as "crushing', feel better. In fact he can find no position of comfort. You seem to be compiling "red flags" as he tells you that the substernal pain also radiates to his left arm. He rates it a 4 or 5 out of 10, and says it began about 15 minutes before EMS was called. You ask if he's ever had this happen before and he says no.

As your partner starts to apply the electrodes, you continue your HPI and vitals. He has no real medical history, although he did smoke but quit ten years ago. He takes no meds. He does tell you that he saw his general physician last week for becoming "short of breath" during his workouts. Pneumonia was ruled out.

  • HR:     67 and regular
  • BP:     92/57
  • RR:    28, a bit labored
  • Skin:  cool and moist
  • Lungs Clear, SpO2 99% on room air

You give him 4 baby ASA, and acquire the following 12 lead ECG:

Ok, this is not what you are used to seeing. In addition, the speed is 50mm/sec. Thanks to the studio magic of Christopher Watford, here is the same ECG "stitched" together in the familiar format, speed adjusted to 25mm/sec:

A few moments later, the Physician arrives. He wants to know the status of the patient, and what you see on the ECG.

What do you tell him?



  • Chee Yong Chuan says:

    51 year old seemingly healthy athlete with sudden onset retrosternal chest pain radiating to the arm. By any means, acute coronary syndrome should be on the top of the list. ECG reveals:
    1) Sinus rhythm with each QRS complexes preceded by P waves
    2) Axis normal
    3) QRS seems narrow, unable to tell the rhythm without a long lead II. Assuming that it is regular with no R-R variation. 

    What is striking here:
    1) Diffuse saddle back ST elevation over most of the limb & pre-cordial chest leads. 
    2) PR depression best seen in lead I and V5
    3) Horizontal ST depression with PR elevation in lead aVR
    4) Anterior R wave progression good with no lost of amplitude. Lateral septal Q waves present
    The above features are consistent with acute stage 1 pericarditis. But however, what concerns me is the ST depression and T wave inversion over lead III and aVF. Althought at a glance the ST elevation does not seem to be associated with reciprocal changes, an isolated ST-T changes in lead III and aVF(inferiorly) would prompt me to think about high lateral infarct. Or it could be ST-T changes secondary to concomitant myocarditis.
    Admission is warranted. Troponin with an ECHO will help clinch the diagnosis(concomitant myocarditis). Field activation of cath lab however i feel is not necessary.
    What do you all think?

  • FB says:

    There are inferior reciprocal changes from an anterolateral STEMI. If reciprocal changes are present it cannot be pericarditis. He is having a rather extensive MI. Candidate for reperfusion.

  • Dave Eastman says:

    Have to agree with FB, this is NOT pericarditis. Reciprocal ST-segment depression in the inferior leads (II, III, and aVF) coupled with ST-Segment elevation in leads V2-V6, I and aVL suggest an anterolateral STEMI – probably an occlusion in the proximal left coronary artery/LAD. This gentleman needs a cathlab.

  • doobis says:

    I believe he experienced an AMI at sometime in the recent past, probably the last week when he saw his personal physician.  I base this on having no significant history and the pathological 'Q' waves noted in the inferior leads.  I believe that this has also caused him to develop a LBBB.
    As to the ST elevation, it is abnormal in that LBBB should be discordant not cocordant and is highly elevated.  However, the ST segments are concave in appearance.  If I go by the Sgarbossa chart that I used as a cheat sheet in my paramedic notes, I believe this PT would have an 88% probability for an AMI.
    At any rate, AMI or not, he is in cardiogenic shock.  I'd listen for L/S and if clear, go with a caution fluid bolus.  I'd also prep the dopamine and admin if necessary.  If the B/P rises, I'd go for the nitro route.
    He needs a cardiac center for eval and treatments.  Would I call a STEMI . . . . probably.  I tend to "pull the trigger" and let the hospital sort it out if it is something serious with all the signs and symptoms and risk making the hospital mad than let something slip by.  I'd also justify it based on my belief he had a major inferior STEMI recently, has severe CP, DIB, & shock, and based on the Sgarbossa chart/criteria.
    Of course all this assumes I read the EKG correctly, which is a big assumption!  : )

  • Aaron S says:

    Sinus w/ 1st degree. Anteriolateral MI with septal involvement. I'd try to get an 18/20 DL when it comes to IV access for this guy. Let's get 4mg Zofran and Dobutamine on board starting off at 5mcg/kg/min, we'll see how it goes from there. I disagree with the use of Dopamine for this case. Hold off on nitro and narcotics until his BP gets above 100 systolic…STEMI alert and rapid transport.

  • Aaron S says:

    Oh, forgot to mention to first start a NSS bolus in 250cc increments based on his lung sounds. Dobutamine admin would probably end up being very effective if his bp isn't improving from fluid.

  • just another medic says:

    I looked at the 12-lead before clicking and said, "eeuuuuuggghhh…"  Looks pretty awful.  My thoughts:
    In favor of MI:  ST-segment elevation in a anterolateral distribution with reciprocal ST-depression, subjective explanation of pain and history consistent with AMI, no pain with movement, previous recent episode of DIB (transient disruption of flow, reperfused, now occluded?)
    In favor of Pericarditis:  saddle-back appearance of ST-segments, possible PR-depression (not 100% certain of this)
    Not sure:  Looks like wide QRS but I'm not certain.
    In my area, the decision of PCI vs. Community hospital is not as big of an issue as most area hospitals are PCI capable.  Not sure about the transport times in Germany.  Other things I would assess:  quick exam of heart sounds, looking for a pericardial friction rub or muffled heart tones, assess for JVD, and also get an oral temperature.  I believe pericarditis/pericardial tamponade could present this way.
    RX-ASA, fluid bolus, ondansetron 4-8mg if N/V persists, repeat 12-leads with transmission, and a rapid transport to a PCI hospital with early notification and transmission of EKG.  Two large bore IVs (500-1000 mL bolus through one, saline lock for the other…)
    Depending on transfer time, I would probably set up a dopamine drip but NOT begin infusing it unless he became profoundly hypotensive.  I have little experience with pressors and epinephrine is the only other one we carry.  Would anyone care to comment on the role of Dopamine on cardiogenic shock with AMI?  A quick google seems to suggest dobutamine is preferred but we don't carry it.
    As always, thanks for the great case study.

  • Robert says:

    I'm with Chee Yong on this one.
    Differential Diagnosis: Acute MI vs BER vs Acute Pericarditis. Most important, Serial ECG's is going to be the absolute most important thing to do in ruling in/out Acute MI!!!!! I'm leaning more towards BER or Acute Pericarditis based on the following reasons. 1. Elevation w/ preservation of normal concavity of the ST-segment v3-v6 2. J notch in lead v2. 3. PR-segment elevation in AvR w/ multiple leads showing PR-Segment depression. Hard to tell w/ all the artificact though. In addition, II & AVF appear to be elevated evern though there is T wave inversion. I measure from the TP-segment. 
    Questions: Family cardiac history? Any recent tooth infections for pericarditis? Cholesterol levels? Did the Dr. do a 12 lead on last vist, any abnormalities he told you about?
    Treatment/Plan: Treat for cardiac ASA 324mg. Get some fluid on board. Cardiogenic shock? Eh, i'm not buying it. This guy is fit and his pressure probably runs in the 90's.Matches his heart rate in the 60's. Dopamine for cardiogenic shock? No way, I'm not even heading any where close to that direction. Clear lung sounds, low heart rate, BP is reasonable given he is a fit/athletic person. I would personally call the Dr by telephone at the receiving hospital and let him know that it is possible cardiac alert w/ Acute MI vs BER. Again, look for evolving changes in the 12 lead and that would give me a definitive answer wherther or not it is a MI.

  • athrombus says:

    Age and smoking risk factors, recent history of shortness of breath on exertion (possibly cardiac, possibly not), pretty much every possible sign and symptom of acute myocardial infarction and minimal S&S directing towards pericarditis – in fact other than “chest pain”, there are no clinical symptoms of pericarditis. Onset, provocation, quality, radiation and duration of pain do not suggest pericarditis but make me highly suspicious of AMI; especially if someone usually so “fit” is suddenly looking pale, diaphoretic and complaining of chest pain without prodromal symptoms (recent viral illness, dental work, musculoskeletal injury, recent surgery/travel, or previous medical conditions which could account for his presentation – although unlikely). If I was attending this patient, purely by the examination and history I’d be thinking AMI even before the 12-lead was on. Now to the 12-lead…

    I’m not being funny, but if it looks like a horse, and sounds like a horse, it is probably a horse… specific (not diffuse) ST-elevation suggestive of antero-lateral MI, reciprocal changes in inferior leads plus history and examination suggestive of AMI – there is no two-ways about it, he is being treated as ACS and transported direct to PPCI. Differential of BER or pericarditis I think would be foolish in this case study (not all, just one as obvious as this). No suggestive symptoms or history (other than chest pain), no PR depression, not diffuse ST elevation, and most importantly, there are reciprocal changes. Yeah, the shape of the ST segment isn’t typical for ACS, but it’s elevated in a manner suggestive of coronary artery occulsion and everything else in the “story” suggests MI.

    I’m not suggesting to discount every other eventuality, after all, we have all had patients who surprise us! This is an acute anterolateral ST elevate myocardial infarction. That, or prinzmetal’s angina (coronary artery spasm) – indistinguishable during an episode but does respond to vasodilators such as nitrates and does not result in necrosis. Either way, leave him at home and refer him back to his GP (JOKE!)

    ECGs are cool

  • forsythfd922 says:

    Antero-Lateral MI trumps Pericarditis in my mind, recording looks distorted after “stitching” to 25 mm/sec, so 100% interpretation is a little….sketchy. If more info was available, would ask about positional changes & recent illness (r/o pericarditis)/ palpation changes in pain if present. Treatment- ASA has been given already, Bilateral IV’s, NS- 250 mL boluses PRN, 4 mg Zofran, talk to the doc about Morphine vs. Fentanyl for pain relief due to borderline hypotension, Serial 12-Leads en route, STEMI Alert for receiving PCI Capable hospital.
    – just another medic- Dobutamine is preferred, it’s more “gentle” on the heart muscle. Dopamine is like smacking the heart with your hand saying “Beat you son-of-a-gun, beat!” But, the service that I work for also only carries Epi and Dopamine for vasopressor infusion.

  • Harrison says:

    I cant believe people are thinking this is anything BUT an AMI.
    AMI clear as day.

  • redwin says:

    i think this is called a widow maker, anterior lateral involvement with reciprocal changes to inferior leads. this is the LAD and circunflex.

  • Mark says:

    Acute extensive anterior STEMI (extensive anterior includes lateral) and old inferior. Aspirin, analgesia (Fentanyl), anti-emetic. Chest clear then 250ml N.Saline bolus repeat X1 then if BP still low commence inotropes and further fluid titrated to perfusion status. Skip GTN due to BP. Straight to cath lab with two large IVs.

  • Bradlee G says:

    If this was my pt, I would take a deep breath and then I would run a second 12 lead and then do a 15 lead to rule out any RVI.  Then I would give ASA, listen to lung sounds, transmit the 12 lead and call medical command to tell them we are coming with a possible AMI and if they call a code R(reperfusion), then I would go through my chest pain protocol.  Start 2 lg bor IVs and give 250cc fluid boluses to get his pressure up checking his lung sounds after everyone.  If this does not bring up his pressure, get orders from the Dr about giving Dopamine drip starting at 10-15 mcg/kg/min.  Use a bolus of diesel to get him to a cath lab. 

  • Dustin says:

    BER??? A patient with sudden onset chest pain, hypotension, shortness of breath would hardly be defined as benign, especially with a12 lead like that.  Unless the patient is lying about medical history I am going with AMI.  

  • Alan says:

    Thank you Bradlee G for mentioning the need for a 15 lead, as this finding will dictate how to treat the patient moving forward. If there is the presence of RVI on the 15-lead then the pt is more or less treated (in my system) with 324mg ASA along with two large bore IV’s and the careful tritation of fluids, maintining a BP in the 90’s, keeping a careful eye on the L/S. IF RVI can be ruled out in the 15 lead I would continue with ASA, CONSIDER NTG assuming an adequate BP can be maintained, Zofran for his n/v and fent. for pain. Tons of great history questions that were discussed here, all of which are very relevant. I also would call this a cardiac alert. Thanks for the great discussions!

  • FB says:

    I'm curious why people want to do a 15 lead EKG. In this case it appears that the infarct is in the distribution of the LAD and the patient is hypotensive. Since NTG has no proven benefit for patients with STEMI is it worth considering giving it (even if the BP increases after a fluid bolus) to a patient that is possibly in cardiogenic shock? Instead of giving fluid just to get the BP high enough to give NTG and drop their pressure again why not just sit on your hands after ASA? Maybe titrate some fentanyl?

  • Canuck Medic says:

    Although pericarditis is a good thought, I don't think this guy would benifit at all from that Dx or mis diagnosis. He is a 51 y/o that has Clear ST elevation on a rough looking 12 lead and you have to treat this as an MI. He is also at that age that is less likely to have any collateral circulation and has a very high chance of cardiac arrest if he isnt treated with asa and a lot of diesel therapy. This appears to be a proximal LAD occlusion. The quick combo paddles need to be placed right after the 12 lead in preparation for this guy to code. I'm not sure what the point of cereal 12 leads would do or how they would benefit him. You have enough info off the initial 12 lead to pull the trigger and treat this guy. All treatments need to be done on route to the hospital. If this is an MI, staying at the scene to start an IV isn't going to save his life. If the Dx of an MI is wrong with this guy at least the theory wasn't put to the test in the field. As much as a good physical would be nice, heart sounds etc, I personally don't think it would change my practice on this guy. After all that, I would say MI as a primary Dx with pericarditis as a DDX.

  • JJ says:

    Ant-Lat STEMI; likely prox. LAD occlusion; prep + direct access to PCI

1 Trackback

Leave a Reply

Your email address will not be published. Required fields are marked *