Masters Case #01: 50 Year Old Male – Severe Chest Pain

***Update: The conclusion for this case is now posted here.***

Most of our cases here at EMS 12-Lead are designed to strike a balance between challenging experienced prehospital providers while also highlighting a couple of specific teaching points for those seeking to learn. It’s a difficult line to walk. We want to showcase EKG’s with specific findings that are apparent enough to make good teaching tools, but we also want them to be subtle enough to make our practiced readers work.

At this point I’m sure there are a few folks out there who have been following us (and related blogs) for long enough to be familiar with a lot of the major tropes we often discuss, so to keep things challenging I’m starting up a new case series: the Masters Cases. These ECG cases are designed to challenge even our most advanced readers, with no limit to how subtle or multi-faceted the findings can be. While no-one here at EMS 12-Lead claims electrocardiographic mastery (holo-chat us in 30 years, maybe…), this series will feature some of the toughest diagnosable EKG’s we’ve come across after collectively reading tens-of-thousands of tracings.

To kick things off, here’s our first “Masters Case” courtesy of Dr. Bojana Uzelac from Serbia…


A 50 year old male presents with a chief complaint of sudden-onset severe chest pain x 45 minutes. The pain began at rest and has been constant, if not worsening. He is pale, diaphoretic, and fairly lethargic; although he still answers questions appropriately. He states he feels weak, short of breath, and just can’t find the energy to move. His radial pulse is weak but present and you hear rales in the lung bases bilaterally. Past medical history is significant for type II DM, heavy smoking, obesity, and hypertension. He has never been diagnosed with COPD, coronary artery disease, or MI.

Vitals: HR 90 bpm and irregular, RR 22/min, SpO2 94% on room air, BP 90/50 mmHg, and temp 36.5 C.

The following EKG is captured upon first EMS contact.

Masters Case: 50yo M - Severe Chest Pain


Here’s the rub: your job is to read this EKG as completely as possible. If you leave me a one-sentence comment I’m just going to delete it. Whatever abnormalities you find should be supported by reasoning. If you think the patient has pericarditis, you’d better list the findings supporting your diagnosis. If this patient is having a STEMI, I want to know where the lesion is and your rationale. I’d also like a brief overview of your treatment plan, though not as in-depth as the interpretation. Take your time and be thorough; these aren’t spot-diagnoses.

As a final general hint, when it comes to these Masters Cases you can rely on the EKG to tell the story. We aren’t going to try and trick you by slipping small clinical clues in the case description. For example, in the above case you would be right to consider aortic dissection if you met this patient in real life, but this is an ECG blog and I promise you the patient is experiencing acute coronary syndrome. Don’t over-think the descriptions but do dive deep into the ECG.

Good luck!



  • Jenny Moncur says:

    Atrial fibrillation at rate of 90 to 150 bpm
    STE aVR greater than STE in V1 with widespread ST depression in 1, 11, aVL, aVF, V2-V5 indicate probable LMCA obstruction.
    Short run of irregular WCT most likely RBBB (Ashmann’s Phenomenon) associated with increased rate and shorter RR interval with first aberrantly conducted complex.
    Treatment – urgent PCI if within I hour or thrombolysis and then transport to angio centre.

  • Mohamed Wafiq says:

    Inferno posterior MI . Dominant LCX , the anterolateral chest leads showing ST depression. Frequent VT , 2nd AVB mobitiz II , ptn in cardiogenic shock . Lidocaine IV bolus then infusion, activate the Cath lab for PPCI of culprit lesion .

  • Daniel says:

    Atrial fibrillation with runs of VT, and signs of right ventricular infarction due to elevation in aVR, however i would want a V4r, could possibly be non STEMI with signs of triple vessel disease. ECG lacks reciprocal changes. Rhythm of atrial fibrillation (If new) suggests the occlusion is high RCA, affecting perfusion to the SA node hence atrial fibrillation and runs of VT. Pt in cardiogenic shock, needs legs raised, IV access and judicious fluid challenge as well as ASA. Cath lab activation and pads on. continuous reassessment

    • RV MI is certainly a good thought I didn’t give much consideration when I first saw this tracing, and fairly isolated RV MI would make a good Masters case, but it’s not what we’re seeing here. Thanks for a unique idea though, I like where your minds at!

  • Paul says:

    Rate – 90bpm
    Rhythm – irregular
    P-waves/ PR – not present
    QRS-.14s, not a normal lbbb or rbbb morphology, pt presentation)
    Interpretation – AF at 90bpm with evidence of LMCA occlusion and runs of VT.
    provisional diagnosis – acute cardiogenic shock secondary to LMCA occlusion causing ischeamia to left ventricle leading to left ventricular pump failure
    Treatment – oxygen, IV access, analgesia (fentanyl), Aspirin, defib pads on pt, consider small fluid challenge, rapid transport to pCI capable facility with early prenotification, draw up adrenaline 1:10000 for inotropic support if required and prepare other resuscitation drugs in preparation of cardiac arrest.

    • Most importantly, I like your plan but my final read on the ECG is a bit different. Note how there’s a ton of ST-elevation in aVR but not so much ST-depression in the precordial leads… something doesn’t fit our typical picture of subendocardial ischemia.

  • Carlos Moreno says:

    The first there is not sustained ventricular tachicardia thats common in a MI because of reentry macanism induced by ischemia, second there is in DI and DII an oposite side lesion image that suggest that there is a lesion i the oposite side of the electrode that can be the sub epicardial in inferior wall or subendocardial in any , besides there is in AVR the only lead with and intracavity view thats suggest subendocardial MI, in that case there is not t wave inversion instead can be high t waves .
    Dx NSTMI

    • The notion that aVR is somehow unique because it is positioned opposite most of the other limb leads is rather misguided. All of the ECG leads “see” not only what we consider their labelled angle (i.e. aVR is 210 degrees), but they also see what’s going on 180 degrees away (i.e. (-)aVR is positioned at 30 degrees). For this reason, (-)aVR isn’t special because it’s just sandwiched between I and II, and regular aVR isn’t special because it’s just sandwiched between (-)I and (-)II.

      Expect another post on this notion soon.

  • ermedic5553 says:

    A fib with 3 beat runs of VT. ST depression I, II, AVL, V2, V3, V4. ST elevation III (1/2mm), AVR (2mm), V1 (1mm). L axis deviation (approx 0 degrees i believe). No LVH(AVL Cardiogenic shock. Strongly suspect LMCA. Tx: ASA, NO plavix (in case of 3 vessel disease due to similar EKG findings), apply defib pads, rapid transport to nearest cath lab. prep equipment for code.

  • đình đạt says:

    in my opinion ,there is a atrial fibrillation with intermitten can see that the 4th,5th,6th rhythm have subtle different morphology and you can see a delta wave .in addition ,the ecg have Q in DIII,possible Q in aVF,and the aVR morphology help us think about ischemic in inferior wall.

  • Carlos says:

    EKG: Fibrilacion Auricular con respuesta ventricular “adecuada”, Salvas de TV monomorficas.
    Por las caracteristicas del dolor y por no haber otros cambios electrocardiograficos podria plantearse un IM sin elevacion de ST en Killip Kimball III, a menos que la misma FA esté causando todos los sintomas y descompensacion hemodinamica. Segun los datos del paciente se encuentra con signos de bajo gasto cardiaco, por lo que yo plantearia cardioversion electrica y luego iniciar el tratamiento para IM.

  • Brian says:

    Atrial fib with triplets of PVC’s (aka VT). There is likely a LMCA Occlusion. The rhythm may change back to a sinus rhythm with a first degree av block, best seen before the last qrs complex in v3-v5. Is that a P wave about .30 before the qrs? I’d need a longer strip to be certain.

    Regarding the ectopic beats- There is a possibility of an Ashman phenomenom with re-entry, if that is possible. But the axis change in lead one, the positive monomorphic R wave in aVR ( without the q wave in the baseline beats seen in aVR) and the entirely negative complex in V6 points to a ventricular origin for these triplets.

    There is nearly global ST depression in the limb leads, with the exception of lead III and aVR has 2.5mm of ST elevation. This points to a LMCA/3 vessel occlusion.

    Treatment- this is bordering on cardiogenic shock. i woukd give ASA, some fentanyl for pain. I might try O2 @1-2l/min, keeping spo2%<99 to see if the ectopy goes away. I would administer small fluid challenges (200cc at a time) to try and increase perfusion. I'm not going to chase the pulmonary edema yet as he is oxygenating okay….and CPAP would probably tank his BP. Nitro is a maybe….but not without a a right sided ecg. No antiarrythmics yet as his BP is questionable.

    • I’m right on board with your management here, which is the most important part of the whole case anyway.

      For those following along at home, Brian and I continued our discussion regarding the EKG findings on facebook. Sorry for jumping between social media platforms, I know it’s poor form.

  • I think Jenny Moncur is right on

  • ris says:

    … for 3 vessel disease,… when do you cabg vs. pci?

  • Peter Hammarlund says:

    Atrial fibrillation with three abberantly conducted beats due to Ashmann phenomenon (I don’t think it’s VTach since the rhythm is irregular). Widespread ST segment depression which is also apparent in the abberantly conducted beats (that have an RBBB pattern with way deeper ST segment depression than expected). I would give the patient 2L/min of oxygen (target >95%), ASA 300 mg, atorvastatin 80 mg, morphine 5-10 mg and UFH 5000 units. I would probably give Ringer’s lactate 500 ml. I would withhold P2Y12 inhibitor (where I work we use ticagrelor) because of the high likelihood of urgent CABG.

    • Good call on the patient eventually needing CABG because he does indeed have diffuse coronary artery disease, but there is a culprit lesion that can be fixed at PCI first and no one has properly identified it yet.

  • I see AFib as the underlying rhythm. There are 2 salvos of wide beats which are VT. Despite the “long-short” – this is NOT the “Ashman” phenomenon, which is not reliable in the setting of AFib (due to unpredictable presence of concealed conduction on subsequent refractory period duration). QRS morphology in these salvos is diagnostic of VT because: i) monophasic upright R wave in aVF; ii) almost entirely negative QRS in V6; and iii) Fusion beat for the 3rd complex in the first salvo.

    Getting back to the 12-lead – there is LAHB – with fairly diffuse ST depression in multiple leads with the exception of marked ST elevation in aVR – plus ST elevation to a lesser extent in leads III and V1. In addition – the T waves in V4-V6 look a bit more peaked and a bit broader than usual (? hyper acute). This pattern is suggestive of severe (3 vessel or left main) coronary disease – though not diagnostic of a stemi. The lateral precordial T waves bring to mind DeWinter T waves (possible prox LAD lesion) – but they are not as tall and don’t start from as depressed a J-point as is usually seen with DeWinter T waves. Left main disease is high on the differential given markedly greater ST elev in aVR compared to V1.

    • As anyone familiar with the man would expect, Ken Grauer has probably come closest to my final answer at this point.

      As a kind of side note, there’s also only one salvo of WCT here. If you measure everything out you realize that the limb and precordial lead intervals are exactly the same. Some prehospital monitors have a setting where, given the high amount of artifact induced by working in the field, you can have the machine select the best 5 seconds of overall data and it will use that when printing both sets of leads. It’s tricky if you’re not used to it because it gives the illusion of a full 10 second strip, but it sacrifices some rhythm interpretation in favor of allowing us a better chance to see a clean baseline for ST-analysis.

      You’re really on to something with those precordial T-waves there Ken! Consider, however, how most subendocardial ischemia presents in the precordial leads in terms of the magnitude of the ST-depression. Compare that to what we see here, which features an admittedly huge amount of ST-elevation in aVR (in the range of 2 mm) but the precordial leads just aren’t that impressive. There’s a specific reason why, and it’s a reason that will respond will to immediate PCI!

  • Fritz Fuchs says:

    ischemia to the AV node with resultant second degree type two AV block. The beat after the pause is triggering a preexisting accessory pathway, (delta waves). ASA, CPAP w/ high flow O2, Dopamine at 5 mg/kg to start, and cath lab. I suspect that increased profusion will help keep the irritability down.

  • James A says:

    A-Fib at 62-110. Left Axis Deviation. Run of V-Tach. St Elevation in AVR, reciprocal depression in Leads I and II. Suspect left main coronary artery blockage. Maintain SpO2 >94%, 12 Leads Q5min, ASA, definitive care is cath lab.

  • Lucas Spillman says:

    elevation in AVR would always prompt me to get a 15 lead to look at the posterior wall. If he has significant hypertension history, and elevation in AVR, V8-V9, and V4R, i would suspect a possible Debakey type 1 aneursym. I would hold off any thought to nitro or pain control, and support the B/P with fluids or pressurs as needed. Any thoughts?

  • Carrie says:

    AF rate 80 with runs of PVC’s, LBBB and extreme RAD. ST elevation in aVR >V1 and ST depression in L I & II – suggest LMCA occlusion and VSS suggest cardiogenic shock with developing APO. Prehospital Management – rapid transport with early notification, 300mg Aspirin PO, GTN not advised due to hypotension, IV access, consider Fentanyl for chest pain, administer O2 to maintain SpO2 94-98%, consider small fluid challenges to maintain cerebral perfusion, consider small increments of Adrenaline to optimise CO if BP drops further altering GCS and radial pulse, 15 lead inc posterior leads, prepare for cardiac arrest. We don’t have a Cath lab in my region and Pt doesn’t qualify for pre-hospital fibrinolysis due to LBBB but I would ensure checklist is completed to facilitate ED/CCU management.

  • Carrie says:

    Sigh – Pt has L axis deviation D not RAD. Also, having read the comments on other’s suggestions am looking further at the possibl culprit artery. At this stage am thinking proximal LAD occlusion rather than LMCA. Will read on!

  • James Combs says:

    Atrial Fibrillation with LAD is correct. I do not see any IVCD. This is a burst of VT, anytime You have fusion beats with wide complex tachycardia you have VT. There is in fact ST elevation in AVR and V1. As a 30 year veteran Paramedic with the last 18 years in the Cath Lab as a senior Cath/EP technologist every ACS with ST elevation in AVR has had surgical left main disease. Although with this patients risk factors he probably has multivessel disease. With his presentation of chest pain, dyspnea, hypotension, VT and heart failure, he most likely has poor LV function with significantly reduced EF. Have seen crazier things with this presentation and EKG like Takusubo’s or spontaneous coronary dissection. Prehospital care requires oxygenation, CPAP, IV access x 2 if possible, ASA, judicious fluid challenge, pain management if BP improves, consider Amiodarone, repeat 12 lead enroute, and without question transport to a facility that provides 24hr PCI with early activation of the cath lab. I agree with comment above as well prepare for impending cardiac arrest.

  • rmoyle87 says:

    I see:
    1. A-fib (irregular without p waves)
    2. a left axis deviation (up, down, down)
    a run of V-Tach
    3. ST elevation in AVr with no contiguous tracing (this seems like junk to me)
    4. ST depressions in the anteroseptal leads indicating ischemia
    5. The T wave in AVf seems to be half as tall as the QRS on AVl indicating posterior MI (if I remember correctly). The ST depression would be the recip-rocol of this.

    1. a 15 lead
    2. oxygen
    3. Amiodorone for the V-Tach
    4. Depending on result of 15 lead, call STEMI and activate the cath-lab

  • michelle says:

    first pt. sat’s are to low at 94% for just room air pt. needs hi-flow o2 at 15 lt. min. i see a-fib. with runs of 3. st depression. there is also a chance of pheumonia. after o2 administer fluids, a chest x-ray, monitor the heart and ekg especially where bp is low.

  • 1. L.A.D
    2. De Winters (ST Elevation aVR, ST abnormality V2-3).
    3. Non sustained VT
    4.Poor quality ECG so cannot say about p waves or whether A.fib.

    Pre alert for ppci = evolving occlusion of LAD artery.
    Aspirin. Pain relief. Diesel

  • iliyas says:

    Short runs of V.T
    Widespread st depression with St elevation in avr
    Lf msin / three vessle disease
    Not sure about rhythm

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