Snapshot: 64 Year Old Male–Chest Pain

Today we have a short "Snapshot" case…Just the down and dirty.

You are called to an urgent care center for a 64 year old male, CC of substernal chest pain, which radiated to the right shoulder and neck area. He states the discomfort feels a little like "indigestion".

This episode began just after finishing a 30 minute workout on the bike.

He denies any SOB or lightheadedness, but does admit to becoming diaphoretic. However, he does not know how much of that to attribute to the workout.

Frightened, the patient drives himself to the local urgent care center .

Upon your arrival, the patient states that the discomfort had "just diminished", and that he now "doesn't feel too bad at all".

Vitals are within normal limits, and the patient does not admit to any significant history.

You acquire the following 12 lead:

What are your interpretations of this ECG? How concerned, if at all, are you?

The patient's discomfort has "diminished" by the time you arrive. How does this change affect your assessment and risk stratification of this patient?

You are 15 minutes from the local ED, and 40 minutes from a PCI center, although aviation may be available. How do you want to treat this patient?



  • Ryan says:

    T wave inversion in avL and lead I, coved shape ST segment in V1-V3. My impression : anterior STEMI with lateral ischemia. Although the patient feels okay, I would be concerned as even though the ST elevation in anterior leads doesn’t seem too significant, it is indeed a progressing anterior STEMI. Tha patient appears stable so at least it would buy me some time. However, I think there is need for reperfusion therapy by PCI provided that the patient has no any contraindications so that the STEMI does not progress to massive anterior infarction. please enlighten.

  • Sam says:

    Plataeu-shaped depressions in lateral leads (I, II, V4-V6) as well as T-inversion in aVL… so NSTEMI or unstable angina (not STEMI). Diminishing symptoms might point to unstable angina. However, remaining ST-depressions might indicate more serious pathology,
    Would treat with aspirin, clopidogrel (and fondaparinux?) and send to nearest hospital for risk-assement with serial ECGs, troponins and other labs as well as eventual PCI.

  • Brooks Walsh says:

    The truth – since it's posted here, The ST depression/TWI in aVL makes me consider an early inferior AMI.
    The reality – if I was given this ECG without the clinical context (and on a blog post!), I would consider the ST/T changes suggestive of LVH, and not activate nuthin'.

  • Alex says:

    I would say that ECG shows a borderline 1st degree AVB with lateral ischemia.
    If "diminished" = pain free, I would recommend transport to the emergency room for bloods to rule out NSTEMI.
    if there is still chest discomfort, I would treat for ACS: aspirin, nitrates, and analgesia.  This wouldn't meet our criteria for bypassing the local hospital (insufficient ECG changes, and possibly no chest pain)

  • Steve L. says:

    @ RYAN, V-1, V-2 is Septal not Anterior. This 12 lead does not show 1st degree AVB block. .12-.20 is normal finding. This 12 lead is very thin on info. If I activated a Cardiac Alert based on this, I would hear about it. This is an ASA and Nitro treatment, and transport to local hospital. Pain meds as needed. Exertional Angina? Why did the pain subside after exercising? Treat the symtoms. That's what we do. Let the Doctors rule out Stemi. Thats their job.

  • Paul says:

    Has some T wave inversion in I and AVL, no other changes I can see. Treat as exertional angina take to closest ER for observation and labs

  • Nick Adams says:

    The 12 lead is grossly normal other than the high left lateral wall ishemic changes.  SR, PRI and QRS durations are normal, normal axis, no atrial enlargements or ventricular hypertrophy's so there is no TW inversions secondary to LVH.  This patient is showing signs of ECG changes in the form of ischemia during and after exercise (Angina), so that makes this a positive (cheap) stress test.  It is not an AMI, so the patient does not need ASA.  AMI's do not go away without intervention of some sort.  The patient is pain free at this time, so NTG is not needed anymore. The pt should be seen by the ED and followed up with a cardiologist for a scheduled stress test.

  • Joe Stalker says:

    I agree Nick. I’d say stable angina, or exertional angina.

    IV lock, vitals, EKG and monitor.

  • Chris R. says:

    The man's story is a little strange, substernal pain 30 minutes after workout.
    The ECG is suspicious for ischemia: Convex upwardly ST segment V1-V2, small R-wave V2,  Lead I subtle ST depression, aVL negative T.
    Observe, make serial ECG's, take bloodsamples, all at local hospital.

  • DaveOC says:

    Firstly it's not "exertional" angina as his symptoms onset  after his workout not during it. Secondly he doesn't appear to have a history of angina as there's no mention of nitro usage and if he did have angina then his symptoms probably wouldn't have "frightened" him. He has lateral ischemia and Q waves in lead III. I'd take him to the PCI capable facility but wouldn't call a STEMI.

  • Robert says:

    Interpretation: Sinus rhythm w/ T wave inversion in I, Avl. ST segment downsloping in avl can be concerning. Do a serial ekg in 10 minutes and look for evolving changes in the inferior leads and for worsening downsloping in avl. With inferior wall MI's, reciprocal changes can present before the st segment changes. If any changes noted, i'd take patient to cath lab. If not, i'd take to local facility.
    Treatment: Serial 12 Leads and ASA

  • deezy says:

    Needs labs to r/o NSTEMI. ECG is clean with exception to MINIMAL ST changes and flipped T's.
    He was doing cardio exercise just now…purposely putting strain on his heart. I think some people missed that part.
    Talk him into an ED visit for cardiac workup.

  • VinceD says:

    A few general points:
     – aVL is certainly not normal, especially for someone with no prior health Hx. As others have said, I've gotta call it ischemia or reciprocal changes until proven otherwise with old or serial ECGs. I'm also going to be watching the inferior leads like a hawk.
     – I don't agree that V1-V3 demonstrate any signs of STEMI in either morphology or degree of elevation relative to what is normal.
    -The patient stated his pain has diminished, but I will not accept that as meaning that he is pain free unless he tells me so. He may not feel too bad relative to when it felt, well, like he was having a heart attack, but that doesn't mean he is completely better. It may sound like I'm nitpicking – and maybe I am – but I feel that it is essential that we iron out any possible miscommunication with this patient, especially in the scenario of possible ACS, where so much of his clinical course is going to depend on his Hx and Sx. 8/10 chest pain being reduced to 3/10 carries a much different prognosis than if it went to 0/10.
     – This does not sound at all like typical stable angina. His Sx would almost certainly have started sometime during the prior 30min of exercise, and would have been relieved with rest well before he arrived at the urgent care. It may be reflux, but it doesn't sound like stable angina.
     – Even if it was, when you are evaluating someone very soon after experiencing their first episode of stable angina, there's no way you can make that diagnosis except in hindsight after ruling out more worrisome causes.
     – Radiation to the right arm may be more specific for ACS than the left arm pain we are classically taught.
    – @Nick Adams – Witholding ASA in this patient because you don't think it is an acute MI sounds alwfully ballsy to me, especially with the high likelihood that this could turn out to be unstable angina, in which case the number-needed-to-treat is 20 to prevent death or MI.

    What would I do? Transport to the local hospital with serial ECGs en route, scrutinizing for even subtle changes, especially inferiorly. Tx with ASA and nitro if his pain is indeed anything more than 0/10. If I see evolving ECG changes I'm diverting to the PCI center. I wouldn't fault anyone for heading there initially, but I think air transport would be crazy-talk at this stage of the game.

    Looking forward to what everyone else has to say. The ACS spectrum is one of my favorite topics in emergency medicine.

  • gbards says:

    Keep it simple people!! This 12 lead is non diagnostic. Symptoms diminished after 30 minutes… so we are looking at either angina, or it could be a differential Dx of many other things… The things is that this patient is now asymptomatic I assume?? meaning NO ASA, NO MORPHINE, NO CLOPIDEGREL and NO THROMBOLYTICS! Transport, and if you are concerned about an evolving MI, repeat 12 leads dont hurt anyone. 

  • Steve M says:

    I think that there are too many doctor wannabes  in here. The fact is that can you take the chances or not. First off, were are not doctors and we need to realize this. If you want to be a doctor go to medical school and take care of this then you can take chances if you want. Secondly I was not having classic symptoms but there were some suttle changes in my ECG and was taken to the cath lab, I have small vessel disease that was 70 percent a distal LAD block that was 95 percent, I have had patients that showed some ischemic changes that were cathed and were sent for bypass surgery the same day. ECG's are only 1 tool, with this a full cardiac workup would be needed to watch troponin levels the would probably be a 23 hour observation with a stress test scheduled for the next day. This is what has happened to a lot of patients that I have transported in especially those with no prior history. Heart disease is genetic, and there are people everyday having bypass surgery that watch their diet, exercise, and do everything right but there are people out there that are truly sick and they get dismissed. You can never be too careful. Do they get the full stemi treatment no, not if it is not warrented but you do not just dismiss things.

  • Newer EMT-I says:

    I am a bit cautious of the sloping ST in AVL.  That said…there is nothing specific I can point to to call any sort of STEMI Alert or justify a chopper.  I would treat the symptoms with O2, ASA, Nitro, Fent if needed and transport to my closest facility.  

  • doobis says:

    Where I work, the philosophy – for better or worse – is to take the PT to which ever hospital they want, except in cases of Trauma Alerts.  I'd advise the PT to be seen at a hospital and would give then the pros and cons of the two choices between the cardiac and non cardiac hospital.  I'd feel fine based on what was presented in this scenerio to go to a non cardiac hospital.
    I would not be overly worried about the EKG but would monitor for changes.  Is this a normal EKG for them, are ST segs moving downward, upward, or static?  Who knows without serial 12 leads.  Treat with normal CP protocols but I wouldn't go too far in the protocol to morphine or tridal unless there were worsening S/S.
    I suspect this is stable angina but could also be due to heat stess and electrolyte problems (are the T waves a bit flattened?).  Give him some fluids during the transport.
    And not to be cynical (but it is the truth), a lot of the same people call 911 repeatedly for attention or because they have psych issues.  Is this guy freaking out because he worked out a little hard and got sweaty?!?

  • VinceD says:

    I reread my comment and just wanted to clarify a couple of things:
     – When I say aVL  is abnormal, I mean that in addition to the T-wave being inverted, the morphology is markedly abnormal, greatly increasing my suspicion.
     – I'm giving the ASA regardless of the pain level, however the nitro is what I would hold if the patient's pain free.
     – I may have given the impression that unstable angina is the thing I'm most concerned about, but this could also be NSTEMI or a spontaneously reperfused STEMI from a stuttering occlusion.
    – Chance Gearheart makes a good point on Facebook that this patient could very well end up going for cath a day or two from now, so maybe we should consider transporting to the cath facility anyway. Not sure if I entirely agree that we should do that for this patient quite yet, but it's definitely something to keep in mind.

  • Christopher says:

    Steve M,
    Reading an ECG is not a skill limited to doctors.

  • Craig says:

    I am thinking of some occulsion of the LAD with multi vessel disease.

  • smlvl says:

    Finally, someone who know's their stuff. Ever since Chris had to go and become an associate editor, I've had no one to search for when skimming comments to confirm my interpretations. Just letting it be known that your contributions are appreciated, almost as much as the post's themselves!
    On a side note, what about the morph of aVL troubles you? I've seen that morph be normal on many a 12L. A very minute q, septal perhaps, then monomorphic R. Were the inferior leads and circumstances different, I might consider it part of the criterion for a LAFB, but the axis here is holding around 20. Granted its not the biphasic 60 degrees of a pristine textbook image, but I would hardly consider it markedly abnormal. Please enlighten me? Thanks!

  • Jeff says:

    Obviously not a normal EKG, treat with chest pain protocol, would not proceed to STEMI protocol unless I saw progressive changes.  I have consulted ED doctor with even subtle changes in consecutive EKG's and been told to activate cath lab.  It takes 15 minutes from time of onset to permanent cardiovasular tissue damage.  This only worsens with time in AMI, the decrease is pain could have been from angina or a increase in collateral circulation.  Don't rule out AMI because he feels better.  I have seen more then my fair share of syncopal episodes only to find a STEMI with no other symptoms.  To not treat this as a chest pain is irresponsible, the ED doctor is going to, why not start it in the field.  
    Also I am quite suprised to see no mention of a 15 lead EKG, somewhere around 50 percent of all posterior MI's show no change on a 12 lead.  It takes 10 seconds and can easily affect this mans future quality of life if a STEMI was found.   

  • renzo says:

    I absolutly agree wtih VinceD 100%… It worries me that people would activate STEMI with this ECG and patient condition… I would transport give asa and nitro titrate to pain… I would with hold morphine because he is stating the pain is subsiding and I would want him as coherent as possible to talk to the doctor in the er.

  • d brown says:

    treat the patient and NOT the monitor! i am amazed at the amount of people on here that speak in what i would call…cardiologist speak…overcomplicated treatment. treat the patient,he fits into the age group for cardiac risk. how about some O2, ekg/12-lead,asa if no contraindicators. maybe consider a saline lock. transport to ED and observe for any change….for any grammer police,please forgive my typing skills.

  • Brad Jones says:

    Honestly, if I were to get this print out on my patient I wouldn’t be impressed, BUT there is significant ST depression in lead AVL which is indicative of a very early inferior MI. There was a case on Pre hospital 12 leads page a few weeks ago and a physician was giving a paramedic a high five because he saw distinct ST depression in only AVL and called in as a possible AMI.  Well, serial 12 leads revealed that as time went on ST elevation began to appear in II, II, and AVF. Classic case of treat your patient symptoms, but with that being said I wouldn’t transmit or push for the cath lab right away. I would however bring it to one of the ER doc’s attention in addition to giving RN report.

  • ParaGoat says:

    I would immediately don my ppe’s…verbally recite penman and quickly administer the Pneumatic Anti Shock Trousers and transport code 2.9

  • Alton says:

    I agree with Ryan. Transport to ER. IV, O2, Nitro. Let ER get more in to underlying problems. Just don’t sit on scene debating what it is or could be.
    I bet when EMS got on scene to Clinic. They had no O2 or IV and probley had already gave 1 nitro. That what they do around here.

  • VinceD says:

    @smlvl – Thanks for you extremely kind words, and I too used to actively seek out comments from Christopher and David before they got snatched up by Tom to work on the blog, in addition to several others who still pop up with less regularity. Thankfully the expansion of this site onto other social media platforms has introduced a whole new crop of very smart folks, but I'm still learning who's who and how everyone thinks.

    My apologis for the confusion, but when I was discussing morphology it wasn't referring to the QRS but rather the T-wave. It doesn't quite match the downward curve typically seen in LVH's srtain pattern, but rather features a fairly straight downslope. It kinda looks like a STEMI T-wave upside-down. In addition, V5 and V6 lack any LVH strain pattern, pointing me even further away from that explination.
    It also lacks the horizontal and symmetric appearance of more benign T-waves. Ischemia can also produce what I might describe as "pretty" looking T-wave inversions, so seeing that wouldn't be entirely comforting, but seeing this downsloping morphology is probably quite a bit more concerning.
    Cardiac ischemia actually can create QRS disturbances, known as periinfarction block, but I haven't been able to distill some of the more nuanced findings into a simple concept that I can desribe succinctly (proof that I don't understand the topic well enough). But also included under that heading would be the Q-waves classically described in MI, "new LBBB" you see on all the current ACS guidelines, and poor R-wave progression across the anteior precordials commonly seen in anterior STEMI.

    @Jeff – Your quote about 50% of posterior MI's showing no change on the 12-lead is surprising to me, as I've never seen a case lacking precordial ST-depression. I actually feel that ST-depression in the right precordials is probably more sensitive (but less specific) for posterior MI thanks to the tiny QRS complexes you see in V7-9 and the ambiguity when it comes to determining just what qualifies as ST-elevation with such small QRS's. I also believe that Tom happens to have a standing warrant out for any cases of posterior MI picked up by V7-9 without any reciprocal changes on the standard 12-lead, because I think he hasn't seen one either (Tom, let me know if I'm making that up please). Perhaps you mean that 50% of posterior MI's show no ST-elevation on the standard 12-lead?

  • Jeff says:

    @Vince,  Upon rereading what I wrote there I did mix up my numbers.  Here are two studies related to the importance of 15 lead EKG's which im sure your aware of, but thought I'd post for anyone who is interested.  The important thing to note is that the only result shown to be specific in diagnosing a posterior MI is posterior elevation.  Depression in any other lead can make you suspicious however has been proven to be anywhere near specific for determining posterior MI.  Both of the following articles have 15 leads with only posterior elevation, ultimately these patients would be delivered directly to a cath lab if prehospital EKG's would find this.  That is instead of the countless minutes to hours of time wasted in the ED waiting for lab values.   I just find it unbelievable that certain studies out there label 15 leads as increasing STEMI activation 22 percent in comparsion to 12 leads, yet prehospital and ED's are so reluctant to take the extra 10 seconds to look for it.  Thats 22 extra people going directly to the cath lab per 100, seems like a no brainer to me.  I mean no disrepect by any of this but I was just somewhat shocked to see no one mentioned performing a 15 since we agree that the 12 is abnormal.

  • Jeff,

    I think the increase in activation is due to a reluctance to activate off of ST-depression alone. A 15-Lead ECG makes it a much easier "sell" to push the button. This is exactly what the two papers discuss.

    From the Zalinski paper, "…22% of patients negative for ST elevation on 12 leads were positive on 15 leads."

    If there is ST-depression localized to V1-V3 and I had a chest pain equivalent, I would activate on that alone. This is a STEMI Equivalent. Time permitting I would obtain a 15-Lead ECG.

    That being said, there is no harm in acquiring a 15-Lead ECG and likely you can use its findings to bolster your argument to activate the cath lab. I would even argue for you that this is probably a best practice.

    Thank you for these great papers!

  • Floyd says:

    Why should anyone be chastised for giving a detailed description of a ECG and accused of trying to be a cardiologist? If I have to make the transport decision and/or decision to activate the cath lab should I not also be astute? I high percentage of patients discharged from the er are having a MI, one that would have been picked up by many of these trying to play a cardiologist had they been the ones that looked at the 12 lead.

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