74 year old male with chest discomfort, right bundle branch block, and ST-segment elevation

It’s a sunny winter afternoon when EMS is called to a doctor’s office for “an adult male with possible heart problem.”

When you arrive you are led into room #3 where you find a 74 year old male in no apparent distress. His color looks good.

You introduce yourself and find out that your patient was suffering from left sided chest discomfort, 4/10, that radiated to his right arm.

“I can’t believe I have to go to the hospital, I thought it was something minor”, he tells you.

He admits that he has had short episodes like this for the last couple of days, but that today’s is worse. It doesn’t seem connected to exertion, and nothing makes it better. He can’t quite localize the discomfort, and it doesn’t change with breathing.

He denies any shortness of breath, diaphoresis, lightheadedness or nausea/vomiting.

His past medical history is significant for: Prostate cancer, high cholesterol, peptic ulcer disease and chronic back pain.

Vitals are as follows:

  • HR: 84 and regular
  • BP: 152/84
  • RR: 18 and regular; SpO2 98% on supplemental O2
  • Skin: warm and dry

You acquire the following 12 lead ECG.

ECG18

You package the patient and acquire a second 12 lead ECG.

ECG18-2

Decision time!

The local community hospital is 20 minutes away by ground. The PCI center is about 30 minutes away by air. As you ponder your decisions, he tells you again that he “still can’t believe he has to go to the hospital!”

What is your interpretation of the 12 lead ECG’s?

What do you want to do with your patient? What are your transport and treatment decisions?

Are there any significant changes between the first and second ECG?

Updated: 02/26/2016 TLB

8 Comments

  • Caleb Seavey says:

    This is the real one.

    Interpretation: Normal Sinus Rhythm with a borderline 1st degree AV block (PR is slightly over 200ms…maybe), right bundle branch block (widened QRS with positive terminal deflection in V1) and, left axis deviation (possible LAFB). So to start out with he has a trifascicular block. Then to the glaring ST elevation in the anterior and precordial lateral leads suggesting acute anteriolateral MI. In addition, the T-wave morphology in the ischemic leads is wide and symmetrical, further confirming MI. The most important difference between the two EKG’s is that in the later EKG, the T-waves appear even more ischemic (tall, wide, symmetrical) and you can see the start of pathological Q-wave formation, suggesting the development of infarction.

    Treatment: Activate STEMI Alert, O2 NC 2L, Asprin 324 mg PO, IV 18 Gauge (probably 2), NTG .4 mg q 3-5 minutes x3 to complete relief of pain (if blood pressure holds), Consider Morphine if pain remains refractory and blood pressure holds, Transport Fast Lights and Sirens to PCI center.

  • Darren says:

    “Sir, I’m sorry. Not only do you need to be at the hospital, but you need specialized care, and you need it faster than we can get you there by ground. It will be in your best interest if we send you to a PCI equipped facility by helicopter.”

    Bifascicular block in the presence of an active STEMI equals a 4x greater mortality rate than an STEMI without complications. Regardless of how this patient presents or acts, it is our job to give him the best treatment and transport possible. Ultimately, the decision must be the patient’s, but our job is to educate him to make the best decision.

    If he consents, focus should be on rapid transport, aspirin admin, and relief of pain and anxiety. Nitro, morphine, and low-dose benzos are all indicated. In addition, this patient stands an above-average chance of going into VT or VF. Defib pads would be a good idea.

  • Justin Alberson says:

    NSR with borderline 1st degree AVB. RBBB. LAD with LAFB (borderline trifasicular block, definitely bifasicular). ST-elevation in V2-V5 and T-wave inversions in V1-V2. This patient needs to be flown to a PCI center based on his cardiac condition. He is a high risk of complete AVB or cardiac arrest.
    Treatment: Oxygen. Dual large-bore IVs. Aspirin 324mg. Nitro 0.4mg x3 x5 minutes depending on BP. Morphine if pain doesn’t go away. Add nitropaste 1 inch. Changes from 1st to 2nd ECG is the T-wave inversions in V1-V2 are no longer present.

  • This is an excellent ECG. And thanks for maintaining a very informative and challenging website. I teach advanced electrocardiography and I must say I am very impressed by the responses here.

    One word of caution (actually a few words):

    1. Since this patient was retrieved from a doctor’s office, did anyone get a copy of a previous ECG? It would make a lot of difference if the RBBB were old or brand new or if any of the ST segment elevations were present previously. Also, in considering the history (and jumping forward just a bit), as I understand it, we have an ELDERLY MAN, who LOOKS GOOD, pain is only a 4/10, he is in ABSOLUTELY NO DISTRESS, his VS ARE GOOD, his chest pain is UNAFFECTED BY EXERTION, he has NO HISTORY OF DIABETES and he has NO OTHER SYMPTOMS. And – given all that history – we are supposed to believe that he has just wiped out his ENTIRE ANTERIOR VENTRICULAR WALL and PART OF HIS INFERIOR WALL, too (no one mentioned the STE in II and aVF)? Somehow, I just don’t think so. In 40 years of practice I have never seen anyone with this much “myocardial injury” look so good, have so few symptoms or have such great VS. Even long-standing diabetics who have wiped out their pain fibers still have other symptoms and very unstable VS with this much injury – whether they can feel the pain or not.

    2. I would be a little cautious here about calling a LAFB. The mean QRS axis is going to be slightly less than -30 degrees and I really wouldn’t consider calling anything with an axis less than -45 degrees a LAFB without a vectorcardiogram (VCG) – and I can promise you that you aren’t going to see one of those any time soon! In the second ECG, the QRS in lead II is barely net positive and in aVF it is negative. This will locate the mean QRS axis at around -28 degrees or so – certainly slightly more positive than -30 degrees. I would expect to see an rS morphology in lead II if this were a LAFB but there is none. Remember: QRS amplitude really isn’t measured by the relative heights of the R and S waves. That’s just a quick and very dirty shortcut. Amplitude is measured by the area contained within the deflection and sometimes you just have to take a little closer look at that area.

    3. There are septal q waves in leads I, aVL and V6. These usually disappear in any MI involving the septum from the mid-septum distally because they get incorporated into the other QRS changes of ischemia.

    3. When you have a RBBB with a qR morphology, what you are usually seeing is really NOT really a qR but the sR’ portion of an rsR’ in which the initial r wave is very tiny or isoelectric. If you look at the QRS complexes in the precordial leads of both ECGs, you can actually see tiny r waves at the beginning of many of them. The large R’ waves represent right ventricular depolarization and the right ventricle is presumably not involved here. Remember: in RBBB the left ventricle has completely finished depolarizing before the right ventricle even starts. So if you have RV depolarization, you have to have had LV depolarization just before it. So what we have is very little left ventricular mass exemplified by the very tiny r waves across the precordium. I think it would be very unusual for a patient to have an acute MI and wipe out so much of his anterior wall (it usually takes about 24 hrs or so for the R waves to disappear) and apparently look so good.

    4. The question in my mind is: how acute is this infarct? In addition to the obvious STE in V2 – V6, there is also STE in leads II and aVF. The straight ascending ST segment in lead II is very characteristic of the first stage of epicardial ischemia. These are hyperacute T waves (as has already been noted) and the QT interval certainly reaches the middle of the R-R interval, also suggesting some QT prolongation which can also occur in an acute (or subacute) MI. QT prolongation is a pretty soft call, however, since it can appear in many other situations.

    5. What also impresses me is the lack of STE in leads aVL and V1. This would suggest that the LAD obstruction has occurred distal to the first septal perforator but perhaps proximal to the first diagonal branch. The lack of STE in V1 strongly suggests an occlusion distal to the first septal perforator. But with a lesion proximal to D1, you would expect STE in aVL – or would you? In a Type 3 “wrap-around” LAD (which is present in over 70% of the population) there would be STE in both the inferior leads (which we have here in leads II and aVF) and in aVL. But… aVL and the inferior leads are reciprocal to each other and will typically result in what is called “counterpoise” – their forces tend to cancel each other. I would surmise that in this case, there was probably more STE in the inferior leads than in aVL and they managed to pull the ST segment in aVL down to the baseline while still retaining a subtle STE in II and aVF. Also, good collateral circulation in the high lateral area from a well-perfused LCx or ramus intermedius would certainly reduce any ischemia and concomitant STE in aVL.

    6. Tumor mass and/or amyloid deposition can also create ECGs like this. Both could be present in a man with a hx of prostatic cancer.

    I hope these comments help a bit. Again, the question in my mind here would be: how acute is this “MI?” An old ECG would have helped a lot. This man certainly needs immediate transport, but a CT of the chest may give us more answers than another ECG.

    • David Baumrind says:

      Jerry,

      I appreciate your point of view.
      One aspect you have not mentioned…

      The morphology clearly looks like STEMI in the presence of RBBB. If you are not sold on that, which you do not seem to be, how do you explain the clear dynamic changes from the first ECG to the second? If you were not sold after the first, the dynamic changes into an even more ominous looking STEMI is diagnostic.

      -David

  • A short addendum:

    If this represented a ventricular aneurysm, it would have developed following a massive MI which I seriously doubt would have gone unnoticed by the patient. But there is no history of heart disease, much less an MI, in his PMH.

    I have seen tumor mass PERFECTLY mimic an acute MI, so one would also have to be very suspicious of metastasis here.

  • David…

    A very interesting and valid point, but here is what I am thinking: There are marked ST changes present that would – in any other situation – be extremely alarming. If this patient were having a more severe chest pain (I got the impression from the history that the patient’s pain bothered him only to the extent that he felt he should make an appointment to go see the doctor), if he had associated symptoms (nausea, diaphoresis, dyspnea) and if his vitals were more indicative of a major MI – I would be much more concerned that an MI was in progress. If this is an MI, it would be very acute and in progress – there are no signs of reperfusion with resolution yet. Pain should be maximal at this point (I would expect more than just a calm report of 4/10), yet there is no mention of any NTG or other pain meds having been given.

    Look at how MASSIVE this “MI” is and then look at the patient. Something is just not adding up here. How many very elderly patients with massive MIs look so good and have so few symptoms or signs? While I do not disagree at all with the ECG presentation of an acute MI, the overall picture just doesn’t fit the illness, but would be much more compatible with a STEMI-mimic. I do see the change between the two ECGs, but again, given the overall picture – I’m still not impressed.

    Please bear in mind that I am discussing the eventual diagnosis here – NOT the immediate management of the patient. The paramedics are spot on in wanting to transport this man to facility with a cath lab as quickly as possible.

    Can a person have an MI and not realize it? Sure, but it’s almost never because they didn’t feel it. It’s usually because they attributed it to something else, reperfusion and resolution occurred, and no one ever knew anything like an MI had taken place. They may even have gone to see a doctor or NP and an MI was never considered due to the symptoms/presentation. I do think that students of electrocardiography in the past have been led to believe that it’s not that unusual for people to have MIs and not feel anything – nor even be aware that anything happened. Look at all the elderly patients with Q waves all over their ECGs who maintain they’ve never had any heart problems. Could they possibly really know what they’re talking about? We now know that that is simply not true in many (if not most) cases. What happens is that the natural fibrosis of aging occurs, leaving the same kind of scar that an MI leaves and Q waves eventually appear. This happens very frequently with cardiomyopathy and ventricular hypertrophy and in the past has almost invariably been interpreted as a “silent” or “missed” MI when no MI ever actually occurred. In fact, most LBBB in older people is caused by fibrosis of aging (and the fibrosis associated with ventricular hypertrophy). Left axis deviation and COPD often cause a marked loss of R waves across the precordium which was, for years, incorrectly interpreted as “old, silent anterior MIs.”

    I personally have seen tumor mets cause exactly the same picture with alarming ST elevations and a patient who was uncomfortable but in no more “distress” than this patient.

    What would I have done if I were the physician in that office? First, I would have checked previous ECGs (at age 74 he’s bound to have had several). Second, would I have treated him based on my suspicion that the STE was due to a non-vascular cause? Absolutely NOT!! I would have treated him like an MI, called the paramedics and let them transport him to the nearest CV center (assuming one was within a reasonable distance).

    I’ve had enough experience to suspect something is not right when I see this kind of history, this kind of patient along with these ECGs, but also enough experience to know better than to bet the patient’s life on a hunch.

  • David…. one more thing:

    I think the gist of my posts on this patient was that everyone was so focused on the ECGs but no one appeared to pay much attention to the patient himself or his history.

    Jerry

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