63 year old male with sudden onset shortness of breath

This is an interesting case submitted by Tom Bernesser who is a paramedic from North Carolina.

I got to know Tom through the EKG Challenge forum at the EMS Village where he always posted fascinating case studies.

Here’s the story.

63 year old male presents with acute onset of dyspnea.

He reported 4 previous MI’s with similar presenation, only dyspnea – no pain or discomort as was the case on this morning.

Past medical history:

NIDDM, HTN, MI, CHF, CVA and is bed-confined for the most part. He’s also fairly obese.

Vital signs:

BP of 146/90
HR 104
RR 24
SpO2: 87 on RA, 100 on O2 via NRB mask @ 15 LPM

BGL: 141 mg/dL.

He did have diminished lung sounds bilaterally, maybe some rales in the bases but was able to speak in full sentences.

He also had some pedal edema, but wasn’t taking any diuretics.

He’s at a Skilled Nursing Facility (SNF) but of course there is no old EKG on site for comparison.

Another note, he did have occasional bouts of multifocal PVC’s probably about 10-15/min.

Here is the 12-lead ECG.

Here is the computerized interpretive statement.

As you can see, it’s giving the >>>> ACUTE MI <<<< message.

Would you activate the cardiac cath lab?

Why or why not?

26 Comments

  • RobertB says:

    I'd like to see V4R since this 12 Lead and his physical presentation would make me suspicious of right sided involvement. The STE in inferior leads, and V4-6 is marginal but again I'd want to see V leads on the R side. RBBB usually doesn't obscure STEMI like LBBB, so given his history I'd say yes – activate the cath lab.

  • Tom B says:

    RobertB -Just out of curiosity, why does his presentation make you suspicious of right-sided involvement?Thanks for the comment!Tom

  • Christopher says:

    Q-waves in I, II, III, aVF, V4-V6; perhaps consistent with old MI's, perhaps new. Concordant STE III/aVF (it looks like there is a terminal r', although qrSr' seems odd). Concordant STD aVL, flat T's in I. STE V4-V6.Given pt Hx and the feeling that this is like his old one (and that my STEMI criteria is not altered by RBBB), I'd activate the cath lab. If I could send the ECG along to the receiving facility I'd definitely do so, as they may have an original to compare against.

  • RobertB says:

    I guess it would be the ST changes in inferior leads and the pedal edema. Then again, there's elevation in V5 and V6, so it could be inferolateral. None of this is consistent with the dyspnea and possible pulmonary congestion, unless the patient already had LHF that is now precipitating RHF. Either way, I'd still put the cath lab on a STEMI alert.

  • Tom B says:

    Christopher – Be careful when you see bifascicular morphology! You'll notice that the inferior leads show a QRS complex that is a mirror image of RBBB morphology in lead V1!With bifascicular morphology (RBBB/LAFB) it's impossible to tell differentiate LAFB from Q-waves from previous inferior MI.I see the tiny terminal R-wave in lead III, but remember, you should be measuring the ST-segment against the TP-segment, not the PR-segment! False positives are more common in the presence of a tachcyardia! What if I told you serial ECGs were performed with no changes in QRS/ST/T morphology?Tom

  • Tom B says:

    RobertB -Let's call it a ST-T wave abnormality, and not an ST-T wave change, unless we observe the change ourselves or have an old ECG for comparison! Tom

  • Christopher says:

    I see the mirror image now, and will keep in mind how LAFB can confound things. My STE measurements were lazily done on a small screen, which apparently is fraught with error! When the TP is as scrunched up as it is, where is the appropriate "line" to measure from?Clinically I should have been sensitive to IWMI + tachycardia being fairly rare. Another thing I just saw, PRi is slightly prolonged 0.22, "trifasicular"?

  • Tom B says:

    Christopher – When the TP-segment is "scrunched" up like it is, it's not always possible to tell where the baseline is! That's why you have to be careful and use things like changes on serially obtained ECGs to make the STEMI determination! Good catch with the 1AVB making this a so-called "trifascicular block".Now, one last point, what do you think about the computerized measurement of the QTc?Tom

  • Christopher says:

    I calculated 0.38-0.4 as the QT interval. RR I have at 0.68, so QTc is QT/Sqrt(RR) = 0.46.Poor man's guide for HR's greater than 70 says QT UL is: 0.4 – (((HR – 70) / 10) * 0.02) or in this case 0.34.QT of 0.38-0.4 is prolonged for 100bpm. QTc of 0.46 is prolonged for males (but right at the upper limit for females). Also marching out the QT, it definitely looks longer than half the RR.

  • Tom B says:

    Christopher -For some reason when I wrote that question I thought the P-wave was mistaken as part of the T-wave by the computer, but on closer inspection I no longer think that's true! Thanks for the refresher on the QTc! Overachieving as usual! :)Tom

  • Brian B says:

    I agree that this EKG looks ugly and there is some elevations and inverted T waves. I would activate the cath lab and drive fast to the hospital. There is no question the patient needs hospital care. The elevations could be a result of the previous MIs. With no EKG to compare it to, there is no way to determine this. One differential diagnosis… See More to rule out in the hospital setting would be that of a possible PE. EKGs in general are not very good diagnostic tool for PEs. The patient had a sudden onset of dyspnea, low O2 sat, tachycardia, is bed confined in a nursing home, and has slightly diminished lung sounds/rales. These are all symptoms that point toward a possible PE. Sudden shortness of breath without exertion is often a tell-tell sign of a PE. I would like to see some lab work such as a D-Dimer and some imaging like a V/Q scan or a CTPA.On a side note, I think it should be stressed to treat the patient and not the monitor. The patient is responding to the oxygen therapy and all the vitals seem to be ok for the high anxiety situation. The patient isn't reporting chest pain or showing diaphoresis. The only thing that is pointing to MI is the pt's history and the ugly EKG. I guess my point is to not get tunnel vision on a certain diagnosis. Driving fast and calling for help is always a good idea!

  • Geoff says:

    I'm cheating here a little bit after reading the other comments. I too was keying in on the ST segments in the inferior leads. Leads III & aVF still look a bit elevated to me though, ST in aVL looks a little depressed/flat. The elevations in lateral leads though still look a bit elevated. I see the tri-fascicular block as well.I was also looking at the ectopic beats in V1-3. Can you apply Sgarbossa Rule to those ectopic beats? V2 & 3 look depressed and V1 looks elevated a bit above the 25% guideline. Am I reaching too far here?To be honest, I think if I saw this in real life I would call a STEMI.If the QTc is on the upper edge of prolonged, are you worried about a dysrhythmia starting? Does the trifascular block and Prolonged QT together mean anything?

  • Christopher says:

    I agree with you that their QTc seems a bit odd, but their QT is right on target. I wonder what formula they use for their QTc, or why my RR is different from theirs, because I can't explain why my calculator comes up with a different value 🙂

  • Hillis says:

    And why not ? The patient is a good no excellent candidate for PCI.. The past medical histroy of NIDDM ,HTN previous MI with the same presentation all suggestive of silent MI .The ECG also doesn't look good .. There is RBBB the onset is undetermined, so it could be acute due to extensive anterior MI or acute MI in the setting of old RBBB . There is also STE in the inferior leads II,III ,aVF and lateral leads V4,5,6 .. Think about right ventricular involvement ( the STE in III> II) .The definitive location of MI by is difficult to make by ECG alone .The patient in this case could have multiple silent MI, so the PCI is necessary for diagnostic and treatment proposes

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  • Anonymous says:

    HIIn this ECG, there is RBBB with left axis deviation which is due to left anterior hemiblockSo, this patient has bifascicular bloch which will lead to complete heart block

  • Bren says:

    Hi all,I agree with1st degree AV block + RBBB + LAHB. But I can't see that anyone has commented on the potential for Right Ventricular hypertrophy. IE R V2 + S V5 >1.05mV (Using Sokolow index.) I realise that should shift the axis right, but it would/could be masked by the LAHB? This might be relevant in the Shortness of breath/failure setting in this patient.. although he doesn't seem in too much respiratory distress (speaking freely0 and sats come up nicely on oxygen.I wouldn't call STEMI and activate cath lab on this patient until further diagnostic criteria obtained (Old ECG, etc).Also, since there is pretty much rSR or RsR or qSR etc in every lead, would that lean towards possible IVCD? Lead 1 doesn't look like a classic RBBB, but neither does it look like a LBBB. How would that effect ST segments?I think there is too much going on to just activate a Cath lab based on this ECG alone…..My $0.02 anyway.. anychance of a solution soon?Cheers,Brendan

  • Tom B says:

    Brendan -The cardiologist was not impressed with the ECG and the patient did not go to the cath lab (at least not emergently).Tom

  • Mark P says:

    Suggests a large area of previous infarction – apico-lateral (Qs in V3-V6), and inferior (II, III, aVF). LAHB sometimes masks inferior infarcts as it produces a rS pattern in the inferior leads (due to endocardial -> epicardial activation of the inferior wall, without the opposing force of endocardial -> epicardial activation of the anterior wall), but not in this case as the infarct is large and complete. The computer has called acute infarction because it is having difficulty determining the T-P segment, and therefore can’t measure the degree of ST elevation accurately.

  • Tom B says:

    Interesting! Thanks, Mark P.!

    Tom

  • john says:

    sinus rhythm with 1st degree AV block, RBBB, acute ANTERO-LATERAL AND INFERIOR WALL MI. definitely an occlusion of the LAD

  • john says:

    MAKE THAT .sinus tachycardia.

  • Ryan says:

    Simple answer for me. No. Without an old comparison EKG, I’m not calling that a STEMI. Yes, there is elevation, but, without something to compare it to, how much of that is normal? He can’t have much working heart tissue left, and constant failure is probably normal, not to mention strain. So, it’s possible that some level of elevation is always present. I’m going to treat him so he is comfortable, obtain a right sided EKG, and transport. I will forward the right sided EKG, and normal 12 lead on. Otherwise, I’m not overly concerned. Im leaning more twoards an exacerbation of CHF….not to say there isn’t cardiac involvement, but, not enough to activate a STEMI.

  • Dave G says:

    Appears to be a inferiolateral wall mi. His previous mi's presented the same Brian B. lets not put too much thought into it and let the physicians decide. 
    My gut is go with that. 30 years it hasn't done me wrong

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