Subtle STEMI, New Right Bundle Branch Block, and Cardiac Arrest

It’s a hot summer night in the suburbs, most of which you’ve spent on standby for a local baseball game. After clearing up you’re put on a chest pain call a few blocks from your quarters. The local volunteer fire department has a squad on scene which is advising you to, “continue on emergency.”

Upon your arrival you find the patient seated on the porch, on O2 via a non-rebreather, in moderate respiratory distress. The volunteer EMT relays that the patient, a 59 year old male, is having 10 of 10 chest pressure which started yesterday. He’s administered 324 mg of aspirin and withheld nitroglycerin because of the patient’s blood pressure. You’re handed a quick trip sheet as you take over patient care.

  • Pulse: 50, weak at the radials
  • BP: 80/40
  • RR: 24, labored, lungs clear and equal bilaterally
  • SpO2: 90% on room air, 94% on 15 L/min via NRB

Your partner starts putting on the electrodes for a 12-Lead while you get a quick history.

  • PMHx: hypertension, hypercholesterolemia, GERD
  • Medications: lisinopril, lipitor, omeprazole, “vitamins”
  • Allergies: penicillin, sulfa drugs, levitra
  • Last ins/outs: normal dinner

The patient appears acutely unwell, ashen gray, and diaphoretic. He states the pain is, “pretty constant now,” and that he feels it in, “my shoulder blades and running down my spine”. Your partner hands you the initial 12-Lead:

Uh Please Standby - Initial 12-Lead

The EMT helps you and your partner place the patient on your stretcher and move the patient to your unit. Your partner asks you what you think about the 12-Lead and if you’ll need a driver.

  • What does the 12-Lead show?
  • Should this patient be taken to the local hospital, about 10 minutes away, or the cardiac center, about 25 minutes away?
  • Do you need a driver?


When we left off, we’d loaded our 59 year old male patient with 10 of 10 chest pressure into the back of our unit with the help of a local volunteer EMT. The patient appeared acutely unwell and was hypotensive and bradycardic.

Before we discuss the ECG in depth, let’s show a serial 12-Lead the crew obtained shortly after leaving the scene.

Uh Please Standby - 12-Lead 2

The importance of serial ECG’s cannot be overstated. Using only one prehospital ECG could miss nearly 20% of all STEMI patients!

At this point we can see an obvious inferoposterior STEMI, likely due to an RCA occlusion. Also of note is a new right bundle branch block, which is an ominous sign. These changes were not lost on the crew, and the receiving facility, a PCI center, was made aware.

However, during their radio report a rhythm change was noted on the monitor:

Uh Please Standby - Rhythm Change

A single R-on-T PVC is seen initiating ventricular fibrillation. Thankfully, the crew elected to use a driver and had two sets of hands in the back. The defibrillator was charged while CPR was initiated, and a 200J shock was delivered after a period of chest compressions:

Uh Please Standby - Rhythm Defibrillation

A rhythm change was noted, however, as no pulses were present chest compressions were continued:

Uh Please Standby - Rhythm Post Defibrillation

Within a minute the patient awoke during CPR, and regained full consciousness. A repeat 12-Lead was obtained:

Uh Please Standby - 12-Lead 3

This ECG shows sinus tachycardia, right bundle branch block, and the evolving inferoposterior STEMI. Upon arrival at the PCI center, the patient was pit stopped in the ED’s resuscitation bay due to his recent ventricular arrhythmia. While there, he experienced another VF arrest. He was again resuscitated and moved to the cath lab for PCI.

Could we have predicted this series of events from the initial ECG? Yes and no.

Yes, the initial ECG provided all of the findings necessary to determine that the patient was experiencing a coronary artery occlusion. Reciprocal changes or T-wave inversion in aVL is an earlier and more sensitive finding than inferior ST-elevation during acute inferior STEMI.

No, the VF arrest is not as predictable. The R-on-T PVC which initiated ventricular fibrillation was the only PVC found on the full cardiac monitor report prior to the arrest! However, it is a best practice to place multifunction electrode pads on any STEMI patient in anticipation for these events.

Sometimes it pays off to read the computerized interpretation.

Looking back the initial ECG we can see why the arbitrary criteria of 1 mm ST-elevation is not nearly sensitive enough to catch every coronary artery occlusion:

  • Hyperacute T-waves dominate the inferior leads
  • T-wave inversion in aVL
  • ST-depression in I, V2, V3, and V4
  • Subtle ST-elevation relative to the PR-segment in III, aVF, and V6 (the actual isoelectric baseline)

Remember, ST-depression due to ischemia does not localize. Localized ST-depression is a reciprocal change until proven otherwise!

During PCI the patient was found to have a 99% occlusion of the LCX and received one stent.

99% occlusion of LCX

99% occlusion of LCX

Post pPCI.

Post pPCI.

Even with two VF arrests, the time from first medical contact to balloon was 61 minutes! If you do not believe in a system of care which begins with dispatchers, first responders, and EMS, travels through the hospital, and ends up back with EMS through continuous quality improvement feedback, perhaps this case can change your mind.


  • Verbeek PR, et al. Serial prehospital 12-lead electrocardiograms increase identification of ST-segment elevation myocardial infarction. Prehosp Emerg Care. 2012; 16(1):109-14. [PubMed]
  • Smith SW. Inferior Hyperacute T-waves. Dr. Smith’s ECG Blog, published 26 August 2009. [Free Full Text]
  • Smith SW. Inferior hyperacute T-waves. The clue is T-wave inversion in aVL. Serial ECGs evolve to ST Elevation. Dr. Smith’s ECG Blog, published 8 February 2011. [Free Full Text]
  • Smith SW. A Male in his 60s with Chest pain. What is the ECG Diagnosis? Dr. Smith’s ECG Blog, published 13 December 2013. [Free Full Text]
  • Smith SW. Five Primary Patterns of Ischemic ST depression, without ST elevation. Some are STEMI-equivalents. Dr. Smith’s ECG Blog, published 12 February 2012. [Free Full Text]
  • Hanna EB, Glancy DL. ST-segment depression and T-wave inversion: Classification, differential diagnosis, and caveats. Cleve Clin J Med. 2011; 78(6):404-14. [Free Full Text]


  • Ekaterine says:

    inferolateral AMI, the patient should be taken to the cardiac centre, A driver is needed..

  • patrick says:

    Right sided MI go to cath. Take adriver watch pressure.

  • In a patient with chest pain – this ECG is of definite concern. I see Sinus Bradycardia ~50/minute – with more-peaked-than-usual T waves in inferior and lateral precordial leads. These are probably “hyperacute” T waves – especially since lead aVL shows the “mirror reflection” of an inverted T wave with the same broadening. The R wave in V2,V3 looks a bit taller-than-expected in association with an abnormal flat ST in V2 and subtle but definite ST depression in V3,V4 and lead I. IMPRESSION – this may be an early acute infero-postero-lateral MI (possibly early stemi-in-the-making). Clinical correlation and serial tracings are needed. With 10/10 chest pressure – acute cath is desirable for Dx/Rx. The bradycardia & hypotension are consistent with ECG findings. V1 is not particularly suggestive of acute RV MI – but given the overall picture – right-sided leads would be helpful in diagnosis since hemodynamics do suggest likely right-sided involvement.

  • jason buc says:

    So I see some worrysome signs in the EKG. The flipped T-wave in AVL, the STD in V3. Nothing says STEMI (yet). Serial 12-leads are a dead horse, no sense in beating on that. I’m taking them!
    This pt’s presentation sucks! 80/40, brady, looks like shit. for me this guys goes to the cardiac center. I think he needs it. But I can’t pin that decision to this EKG.

  • ermedic5553 says:

    Probable Inferior posterior STEMI developing. Posterior leads appear to be meeting millimeter criteria based on computerized measurements listed. With clinical picture, I don’t think this would be a “hard sell” for a receiving facility to open the lab. However, his presentation has me concerned for an aortic dissection. When is the last time you heard a patient c/o pain migrating down their back with cardiac symptoms? Wondering if a dissection at the aortic root is hitting the RCA (probably a zebra with dissection). Take a driver (if authorized), probably going to need the help. Definitely going to cardiac center. Personally, I would skip the R sided EKG at this time. We have enough already to strongly suspect R sided involvement, and not going to change pt care (unless needed to get cath lab open). Serial EKG’s, couple of big lines, apply pacer pads, consider cautious fluid boluses (250ml each w/ reassess), hold off on NTG, if O2 sats drop, consider early intubation (CPAP might drop pressure significantly). Watch for change in neuro status or limb weakness (Sudden weakness in limbs or neuro change would really up my suspecion of dissection).

  • Iain says:

    Developing inferior-posterior MI, based on V3-V4 ST depression and presentation. Needs a full right side and posterior (V4-V9) 12-lead done quickly. Treat it like a STEMI (bilat IV, morphine), though I wouldnt necessarily call for field activation unless my additional EKGs are more interesting or it changes.

    Definitely transport to cardiac center, definitely take a 3rd. Transmit and have a talk with a doc since you have 25 minutes.

  • Darren says:

    The patient is in sinus bradycardia, with a normal axis and narrow complex. R wave progression is ok. Little bit of wandering baseline can be tricky, but the morphology of the ST segments, along with the patient’s symptoms, cannot be ignored. There appears to be a slight amount of ST elevation in the inferolateral leads; whether it is enough to call a STEMI, I don’t know.
    My treatment would start with further investigation. A strong likelihood of RVI exists, so right 12 lead is a big next step. Also a good possibility of posterior involvement, so a 15 lead is needed as well. We have clear breath sounds, so bilateral large-bore IV’s with volume therapy is needed now, since ASA has been given. We also need to anticipate the possibility of worsened bradycardia; if this is an RCA occlusion, the likelihood of SA or AV nodal blocks is high. Be ready to pace if necessary. A driver wouldn’t be a bad idea at all, and this patient needs to be at a PCI equipped facility. If I’m able to get blood pressure up, I might consider LOW dose IV nitrates to attempt to relieve the patient’s pain, as well as fentanyl. Morphine is too vasoactive in this case.

  • Floyd says:

    I agree with everything Dr. Grauer stated. I would think of the r wave in v1,2 to be the posterior q wave. I am also concerned about the st depression in I&avl. Certainly likely to be reciprocal changes. While I would like to activate the cath lab I don’t think it meets the “official criteria”. I would contact my local pci capable facility and express my concerns to the er physician. He may disagree but Im sure serial 12 leads would tell the tale soon enough.

  • Jason says:

    I don’t like his presentation at all. First off..the non-machine findings…ashen, unwell, diaphoretic, pain…BP, Pulse, all put together tells me this guy is VERY sick. I might consider a chopper to the PCI facility at this point. I know it’s hard to pinpoint with the wandering baseline, but, elevation in II, III, AFV, with some depression in I and AVL (plus the downward sloping inverted T wave in AVL), and I’m calling the STEMI to the hospital. ASA, O2, Fentanyl, fluid challenge, and a FAST transport.

  • Matt says:

    Infero posterior stemi. Elevation 2, 3, avf. Depression V2, V3. Classic clinical presentation hypotension , bradycardia, pain in shoulders down back, explains posterior wall. 324 aspirin. Access will be tough due to bp IOs, ACs and/or Ejs lots of fluid. Dopamine, preferably levophed, drip to stabilize bp. He probably code in front of you be ready.

  • Lucas says:

    Besides MI and Aortic Dissection, this presentation of acute chest pain and hemodynamic compromise, associated with important dyspnea would concern me for PE, which I think should be properly investigated.

  • Inferolateral MI, not RV (T-wave down in V1)

  • mustafa alalwan says:

    How we can predict the culprit artery ?
    The sTE inlaed III>II with ST depression in lead I
    STE lead III> V6
    all this lead me thinking to RCA .
    But How it’s LCx?

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