68 Year Old Male: Chest Burning – Part 1

A 68-year-old male presents with a chief complaint of chest discomfort. It started at rest approximately three hours prior as has been constant ever since. He describes it as a burning sensation limited to the central portion of his chest. Nothing makes the pain better or worse and he rates it at about a 6 out of 10.

At a glance the patient appears pretty healthy. He is well-nourished, only slightly overweight, does not smoke, and feels fine aside from the nagging discomfort in his chest. There is no evidence of rash or discoloration over the area of discomfort. He denies nausea, vomiting, shortness of breath, diaphoresis, lightheadedness, syncope, or near syncope.

His skin in warm, pink, and dry and his radial pulse is strong, fast, and irregular.

Vitals are as follows:

  • HR  approx. 125 bpm, irregular
  • BP 110/58 mmHg
  • RR 18 /min and unlabored
  • SpO2 96% on room air
  • Temp 37.1 C (98.8 F)

Past medical history is significant for well-controlled hypertension, DVT/PE two years prior, and incidental coronary artery disease noted on a chest CT performed for the PE.

His medications include only amlodipine for hypertension and ongoing warfarin therapy for the prior PE/DVT.

Because of the patient’s chest pain and irregular pulse you perform a 12-lead ECG and see the following…

You also have immediate access to a copy of the patient’s ECG from two years prior, at the time of his PE/DVT…


How are you going to treat this patient?

Are you going to activate the cath lab?


Check out Part 2 for the rest of his initial course and management.
The case conclusion and discussion are in Part 3 (coming soon!).

created: 2013.12.30  last modified: 2017.08.29


  • Chris Touzeau says:

    Critical legion of the left main or LAD.

    The diffuse ST segment depression represents reciprocal change to the STE in aVR.

    This is a STEMI equivalent requiring emergent surgical reperfusion.

    Patients who present with this constellation of symptoms and EKG changes have a higher incidence of mortality if they are treated only medically.

    Neat case.

  • Sanders says:

    LBBB , Afib , anterior hemi block. STEMI ! Cath lab.

  • James says:

    The old left main occlusion.

  • Michelle says:

    I don't see ANY AFIB, I would call this Acute Pericarditis. IV O2 Monitor, Asa, closest appropriate hospital. Monitor him for changes, priority 2 transport….I don't see a LBBB either

  • Jason says:

    I'm thinking CAD with the wide spread depression and elevation in AVR.  Rapid transport to nearest facility.  ASA, O2, IV, possible Fent for pain relief.  Pads on and ready just in case.

  • devkrev says:

    I would treat this as a rate problem/possible new onset A. fib. Vagal, 6mg then 12 mg of adenosine, if no conversion then max of 20 mg cardizem super slow IVP to get the rate around 100, I would take another EKG at that point and see if the ST depression/chest pain improved. Probably some fluid too. If the CP didn't go away at that point maybe consider ACS at that point. I'm not activating the cath lab though. I would probably give him 324 mg of ASA too, for good measure.

    • Kyle says:

      Curious if you’re treating for afib why are you doing vagal and tx with adenosine. These treatments are for SVT. Adenosine in this case is actually quite dangerous. Respectively a CCB or BB would be the treatment of choice should you be going down that route.
      But I’m curious if maybe I missed something that you see 🙂

  • Chaz Justet says:

    Posterior MI – Diffuse ST depression, flip the sheet and you'll see elevation.  Run posterior leads and your elevation will show up as well.  Yes I would activate cath lab.

  • Steve S. says:

    Acute left main ACS with stenosis which causes subendocardial ischemia. Pt. needs CABG. Not a STEMI

  • Mia says:

    I would get a better history to see if any thing else is going on, like a stressful situation . O2, Asa, monitor,closest facility. 

  • Cathy P says:

    With ST depression acquire posterior ECG treat with MONA inform receiving facility of STEMI and inform cath lab. With patients history and current 12 lead the possibility of posterior STEMI is very proble 

  • Matt says:

    first off, adenosine would not help afib…2nd, the heart rate is only 125…incomplete lbbb…left axis deviation..st depression…ACS protocol would appropriate

  • Scary Medic says:

    Look around back and right side.  Determine where this STEMI shows up then consider nitrates, Beta blockade and alert the STEMI Team.

  • Tommy Watson says:

    I agree with the posterior MI. Diffuse ST depression in all leads excluding the expected aVR. Perform a posterior 12-Lead for confirmation. Activate STEMI alert, O2, IV access, aspirin, fluids, titrate morphine and nitro. 

  • Bill says:

    I agree with Chaz… Posterior MI

  • Steve says:

    Posterior 12lead is called for, along with ASA and a phone / radio call to the local PCI facility.  

  • DR Cuong says:

    LM OR serve Three branch, CABG not PCI!

  • Dane Friley says:

    This pt could very well have left main disease, but it is really hard to believe that he has an acute left main occlusion. Other than the afib his vs are stable. If this were an acute occlusion of the lmca I would expect dyspnea, labored resp and probably not a sat of 96% on ra. I would also maybe expect fluid in his lungs. He may very well have a posterior infarction. Obtain a posterior view to confirm. this is most likely new onset atrial fib with rvr. At this time rate is not that fast, but how fast was it three hours ago when it started? Could this be ischemia from a rapid hr? He also meets voltage criteria for lvh in lead avL. Again this pt could have left main disease, but I don't suspect acute occlusion. I would expect this pt to be dead already or close to death if it were acute occlusion. I'm very anxious to here results! None the less pt should be treated with acs protocols. If your posterior leads are negative you are going to have a hard time getting cath lab activated at least where I am located!

  • Dane Friley says:

    Pt also has pathological lad so this is very tough call

  • Chuck says:

    Would use ACS treatments, and transport to nearest hospital.  The rate is only 125 not high enough to treat with meds, nor do I see any elevation in any lead but one.  It is all depression at this time, the elevation was probably when it first started three hours ago and now the damage is already done.  He needs evaluated for prevention of further damage, and to develope a care plan. 

  • Dane Friley says:

    Most likely triple vessel disease

  • Lynn says:

    I agree with the posterior MI call… Perform a 15 lead and V4R. In the meantime, treat according to ACS protocols, but hold off on the Nitro til the patient is better situated. I would also treat the patient with a fluid bolus of NS to see if that would help bring the heart rate down and bring the B/P up so that Nitro might be used, but ASA and O2 first. Fentanyl for pain management. I don't see elevation, but I do see depression all over the leads, particularly the ones that would lead to a posterior MI call. Contact Medical Control and let them compare old and new. As far as where to transport the patient-always err on the favorable side for the patient. (And auscultate the lung sounds to see if you can pick up on a 'pleural rub' sound-just in case..)

  • @devkrev
    Why would you choose to lead with adenosine if you correctly identified the rhythm as rapid atrial fribrillation? What would that offer someone with an irregular narrow-complex tachycardia?

  • @Dane Friley
    I just wanted to say that I like where you head is at in how you would handle this case.
    In regards to the high voltage in aVL and left-axis deviation you spotted, there's a specific entity that can explain both of those findings plus the poor R-wave progression seen across the precordial leads. What you're seeing here isn't LVH, though it's possible this condition can hide pre-existing LVH, so we can't rule out it's existence based on the EKG alone (but what else is new?).

  • @Everyone calling LMCA/triple-vessel disease
    Demand ischemia secondary to a rapid HR, as is commonly seen in atrial fibrillation w/ RVR or SVT's, can produce a picture of subendocardial ischemia with diffuse ST-depression and ST-elevation in aVR.
    How do you know that's not the case here? Can you still make the call in light of the patient's tachycardia? Even if the rate was slower and demand ischemia wasn't in play, is diffuse subendocardial ischemia something you are actually able to activate the cath lab for in your region?

  • Greg says:

    Patient does not present with enough symptomotology for STEMI Cath lab activation and would best be treated monitoring and with pain management. Agreed new onset AFC but only symptom is pain. HR and patients mental status dictates his treatment.

  • Jason says:

    There is STE in lead AVR. This does not occur in demand ischemia from rapid afib. As Mark Josephson likes to say, "AVR points to heaven!" This is a left main or proximal LAD occlusion. There is more than enough here to activate the cath lab, especially with that history. This man is relatively yound and active. Would be a shame to sit on his MI. 

  • David says:

    Likely LMCA occulsion; less likely LAD occulsion / 3VD. 

    Diffuse ST depressions (I see depressions everwhere but aVR [which has significant elevation] and V1). Almost global depressions indicate subendocardial ischemia (producing reciprocal change in aVR) and probably not caused by an isolated posterior STEMI. 

    STE in aVR > V1 favors LMCA over LAD. 


  • Chee Yong Chuan says:

    Interesting tracing you've got there. Here's my 2 cents worth

    1) Not a sinus rhythm. No upright P waves seen in all limb leads preceding QRS complexes. Rhythm is irregularly irregular beating at a rate of about 120beats per minute. QRS complexes narrow. 

    2) Pathological left axis deviation. rS complexes with deep S waves seen inferiorly with qR complexes observed in I and aVL suggestive of left anterior fascicular block. R wave althought tall in aVL(satisfied criteria for LVH) is probably due to presence of LAFB.

    3) Marked ST coving and elevation seen in lead aVR followed by T wave inversion. 

    4) Marked horizontal ST segment depression observed over the inferolateral leads: II,III,aVF,I,aVL,V2-V6. A pattern suggestive of extensive subendocardial ischemia. ST segment isoelectic in V1

    5) No definite sign of infarction yet, no Q waves, QS seen in V1, but a definite R wave is seen in V2

    6) QRS alternans(subtle variation in the height of QRS complexes) common in Afib with RVR

    7) Poor R wave progression in comparison to the baseline ECG

    Impression: Afib with RVR with evidence of severe subendocardial ischemia. The presence of STE in aVR coupled with diffuse ST segment depression over the inferolateral leads may suggest left main disease, severe triple vessel disease or even critical proximal LAD stenosis! 

    Comparing this tracing with the previous one(2 years ago), things which are new:
    1) New atrial fibrillation
    2) New LAFB
    3) Although subtle STE in aVR was already present previously, this time, it is more marked
    4) QS complex in V1 was new
    5) Poorer R wave progression over the anterior precordial leads

    Taking all into consideration. This might be a presentation of left main UA/NSTEMI, very unlikely to be left main STEMI. Patients with left main STEMI usually present with global STE instead of widespread ST depression. And they don't usually survive to the hospital, usually a victim of cardiac arrest en route. Such patients with suspected left main disease should be sent to a PCI capable hospital, as urgent(not emergent) PCI for revascularisation is usually needed and medical therapy is usually futile. Should be managed as high risk unstable angina/NSTEMI

  • Ryan Lord says:

    Had the exact same last night but a known AF patient pain commenced after 2 hours of palpitations and described as like a previous MI. Her rate was up at around the 160 mark… Had the widespread depression but elevated aVR and V1. Discussed with Cath Lab and preceded to A&E next door for review, on route pain reduced with treatment of asp, gtn, morphine and palpitations stopped, rate reduced to 110 and ST changes reduced… Segment changes in that case very similar to this and rate related as confirmed by cardiac nurse on arrival but always worth a call… We are lucky though as A&E and cath lab right next door to each other…

  • It’s the big one Weezy! LAD

  • michelle says:

    i see some depression and slight elevation in the st segment in the avr. i would alert the stemi crew to stand by.

  • Chris Newman says:

    I have to admit I am torn between a STEMI equivalent due to the aVrSTE[+] or a P.E. As someone else has stated if this was due LMCA occlusion the patient would probably present as an arrest.
    Global STdepression is indicative of subendocardal ischemia, and as this patient has a history of CAD we can assume some degree of insufficiency exists in his coronary circulation.
    I would be looking at treating with Anti platelets, nitrates and analgesia. I would then consult with the cath lab and conduct some shared decision making with the cardiologist as my differential would be either ACS or P.E. However I would at the very least head to the A&E with cath lab facilities on site.

  • Kyle says:

    I gotta ask. Why is everyone arbitrarily giving 02? It’s not overtly indicated with sats at 96% and no obvious signs of respiratory compromise. New ACLS guidelines oxygen isn’t considered as part of the acs treatment unless their saturation is below 92% or they experience aggressive dyspnea.

    This is quite possibly a LMCA stenosis/occlusion. Possibly a posterior, I’d obtain a 15 to get a better view.
    The rate being 125 is technically tachycardia but I wouldn’t give BB/CCB in this case.
    I’d go with ASA and NTG SL with caution. Ensure IV and consider thrombolysis if PCI is not available/close. Serial 12 leads are a definate must.
    Consider analgesia if required.

2 Trackbacks

Leave a Reply

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