58 year old male CC: Chest pain

Here’s an interesting case sent in by a faithful reader who wishes to remain anonymous.

EMS is called to the residence of a 58 year old male complaining of chest discomfort.

On arrival the patient is found sitting on the edge of the bed. He is anxious but alert and oriented to person, place, time, and event.

He was awakened from sleep by chest discomfort.

Onset: 30 minutes ago while sleeping
Provoke: Nothing makes the pain feel better or worse
Quality: Severe pressure or “ache”
Radiate: The pain does not radiate
Severity: 10/10
Time: He has had chest pain before but “not this bad”

Past medical history: HTN, dyslipidemia

Medications: Lipitor, Norvasc, ASA

Vital signs are assessed.

RR: 24
Pulse: 136
NIBP: 160/98
SpO2: 94 on RA

Breath sounds: basilar rales

The patient admits to mild dyspnea. He states that he has “gained a little weight” recently and his doctor was getting ready to put him “on a water pill.”

Temp: 99.1
BGL: 138

The cardiac monitor is attached.

A 12-lead ECG is captured.

The patient is given 324 mg of aspirin, 0.4 mg NTG SL spray and placed on CPAP.

Another 12-lead ECG is captured.

The patient is loaded for transport and another rhythm strip is captured.

What do think is going on with this patient’s heart rhythm?

What do you think is wrong with this patient?

You are 15 minutes away from the local non-PCI hospital and 60 minutes away from a STEMI receiving center.

Where would you transport this patient and why?

*** UPDATE ***

This 12-lead ECG was captured en route to the hospital.

And finally this rhythm strip.

Does this shed any light on the mechanism behind the wide complexes?


  • Bill C says:

    My impression is electrical alternans and in the context I would assume ischemia until proven otherwise and head for the PCI hospital with transmission for specialist notification/consult. The presumed fluid retention weight gain with low-grade fever also throw pericardial effusion into the possible mix.

  • Dave B says:

    ok.. trying to break this down.. rhythm is a regular sinus rhythm, regular P-P intervals, with alternating narrow and wide complexes at regular intervals. the wide complexes have a LBBB morphology, without discernible pacing spikes. seems like the impulses are originating normally in the SA node, and down through the AV node, after which, every other beat is not conducted normally through the His-Perkinje network. is it possible that due to ischemia, there is a rate related BBB, whereby every other beat is conducted normally, but the following is not due to the left bundle still being refractory due to the ischemia?
    while i am not seeing it clearly, i believe i can see some ST depression in the inferior leads, with possible ST eleavtion in aVL..also some ST depression in V5 and V6… wondering if the ischemic changes are causing the disturbances in the conduction system.

  • Christopher says:

    Woah, cool strips.

    First 3L shows a wide complex tachycardia at 130-140 with occasional wide complexes of a different morphology. The accompanying 12L shows the rate has slowed, potentially post O2. The 12L shows that the wide complexes appear to have associated P-waves with LBBB. Also present are narrow complexes, with P-waves potentially visible in V1. There is also a single PVC present. Rate dependent LBBB w/ sinus tachycardia.

    Second 12L shows roughly the same as the first 12L.

    Final 3L has 2 distinct morphologies. One is wide (A), one is narrow (B). Easily appreciable, associated P-waves before A-type complexes. Buried P-waves before B-type complexes, also associated. I believe this is sinus tachycardia with an intermittent left bundle branch block due to an increased refractory period in that bundle (rate related).

    Sick, sad heart.

  • Geoff says:

    Different morphology of the QRS complexes. It also appears in Leads I & V5 & V6, the leads that have a “typical” LBBB morphology, there is T Wave concordance. Also, in V1 & V2 it looks like the ST Elevation is right around if not slightly greater than 20% the negative deflection, or am I seeing things here or am I totally on the wrong track?

    I would lean towards the STEMI center.

  • Dooley says:

    Heterotopic transplant.

  • bigeminy is tricky.

    initial strip is almost unreadable, but R-R is consistent across the strip.

    if you look at all the strips except the first and last ones, you can see that the wider QRSs are actually part of the underlying rhythm, and the narrower QRSs arrive early. R(wide)-R(narrow) interval is consistently 0.04s less than R(narrow)-R(wide) interval. a very subtle difference.

    which makes it SR/LBBB with PAC/PJCs at a 1:1 ratio for most of these strips.

    in fact, after the final 3-lead strip, i would’ve liked to see a 12-lead without the premature complexes.

    if pt is not aware of LBBB, then this is presumed new and going to the STEMI center.

  • Tom B says:

    Thank you, burned-out medic! This is exactly the difficult I had with this case.

    Many times I have seen a narrow complex rhythm with aberrantly conducted PACs. In other words, premature beats showing RBBB or LBBB morphology. However, I don’t recall any wide complex rhythms with narrow complex PACs! That’s an oddity.

    On the other hand, I’ve seen patients with IVCD at baseline whose runs of VT were “narrower” than the underlying supraventricular rhythm! That’s pretty strange, too.

    But I agree with your most important observation, and that is the fact that the true underlying rhythm appears to show LBBB morphology. Either that or the LBBB is precarious, raising the suspicion that it could be “new” or “newish”.

    Having said that, is the mere fact that a LBBB is “new” significant? You might recall the post “New LBBB – What’s the Big Deal?” where Amal Mattu, MD (reviewing Chang et al.) argues new LBBB is not as relevant as LBBB that meets Sgarbossa’s criteria.

    Does this LBBB meet Sgarbossa’s criteria (including Dr. Smith’s modified criterion of discordant ST-elevation > 0.2 the depth of the S-wave)? It’s close! But I haven’t taken the calipers to it yet. Kudos to all who left comments!

  • Tom B says:

    I should also point out that the QTc appears to be long.

  • Dave B says:

    i will respectfully disagree, while quite possibly also being incorrect… but, if you look at the 12 lead, lead V3 shows i believe the most clear r waves, at the start of both the LBBB complex and the narrow complex. if you take calipers to the RR interval, it remains unchanged from narrow to wide complexes. the wide complexes create somewhat of an optical illusion, and depending on where you measure, could make the narrow complexes seem like they come early. but, measure the rr in V3, and please tell me what you think.

  • Tom B says:

    I thought I had seen differences in P-wave morphology, Dave B., but on closer inspection it’s possible that differences can be explained by changes in T-wave morphology.

  • because the polarity of a complex is different in different leads, it’s usually easier to choose leads that are definitely positive or definitely negative to measure R-R or S-S. (this is the same reason VT may look narrow in some leads and wide in others.)

    v3 is sort of in the transition area where the premature complexes are sort of biphasic. the question then becomes, which part of the QRS in one lead corresponds to which part of the QRS is another lead?

    instead, if you look at R-R in I, II or III, or even S-S in v1, you can see that the difference is consistently 0.04s. in these leads, you can with more certainty say that “this part of the QRS is the most positive” and “this part of the QRS is consistently the most positive across several leads.” as a result, you’re picking a solid reference point in the complex to measure intervals.

  • Dave B says:

    Tom, i also, had thought the T wave morphology was affecting those P wave morphologies..
    Burned-out medic: i was having an issue finding a good reference point that was “apples to apples”…the wide qrs was obscuring a good comparative reference point for me, which was why i chose V3… i thought the defined r waves made it a useful measurement for me… not saying i’m right, but that’s what i saw… also in leads I,II.III, i was again having a problem picking the right point to measure the wide complexes,,, however, if you measure from the start of the qrs complexes, both in the narrow and wide, you will again find that if you take calipers to those points, they are again regular with no early beats even in those leads.

  • using the beginning of QRS complexes is a little like finding j points – sometimes it’s just not that clear. also, since we’re dealing with a wide QRS and a narrow QRS, morphologies that are inherently different here, using the start of QRS complexes may not quite be comparing apples to apples.

    rather, using the tip of R waves in leads where QRS complexes are predominantly positive or negative can sometimes be clearer. if you apply that here, you can see the small difference of 0.04s consistently, which can easily be obscured by different angles of different leads if not using extreme positive or negative ends of complexes.

  • we have to be careful using R in v3 because that’s not the predominant deflection. that is akin to using Q in lead II, for instance.

  • Christopher says:

    I agree there is a variation in R-R, but it looks like it is <0.04 in all instances.

    If you look at "12-Lead 2" in V4-V6 you can see a premature beat clearly. It even has a completely different morphology from our other two beats, and almost looks like incomplete RBBB. If you march out the R-R's the LBBB beat after this premature complex arrives on time and so do the subsequent complexes. I would think the delta-RR in the underlying rhythm would be more like that premature complex if the underlying rhythm had bigeminal PAC/PVCs.

    Based on that 12L and the evolution of total LBBB at faster rates I think this is a sinus tachycardia with rate dependent BBB. I should state that I'm merely miming what I've read on rate-dependent BBB and don't have a solid understanding of why this may be.

    For this poor fella I'm likely to consider my rhythm interpretation as academic at best and he's going to get prompt transport to a facility that is PCI capable, because those facilities are likely to have stronger cardiology consults (in my patient's best interest).

    Although if he says the closer hospital has his ECG's (since I don't see anything that screams STEMI) I may defer to the closer hospital.

  • Matthew says:

    First: There is just not enough information on this patient (Thanks HIPPA), it appears this patient suffers from HTN and Hyperlipademia, plus I would think he takes the ASA for blood clot managment or more for a prophylaxis measure.

    I can see the LBB block clearly, now is that a new onset, without comparing to a old EKG who knows?

    When looking at the 12 leads, there is elvevation in the V-Leads, which lead me to a anteroseptal wall MI, but the issue that is throwing the curve ball to me is the H/R, I would do a 15 lead. Now I would be very suspicious of Cardiomyopathy and a P.E.

    Treatment: 02,IV,ASA,NTG-Only after transmission of EKG,Repeat EKG’s,Pain Managment.

    I just have one question why CPAP? Not that it is a bad thing

  • Brandon O says:

    Man, I could park my car under some of those early P waves.

    Can we talk about the evolution here? The complaint began 30 minutes ago and presumably changed little prior to arrival; yet in the ~15 minutes after EMS reaches the bedside, we’ve seen (that’s the royal “we”) a massive normalization of the rhythm. (No word on subjective improvement of the complaint, but I’d be surprised if there wasn’t.) While a spontaneous resolution is possible, this suggests to me that he improved from our treatment, which points strongly to an ischemic etiology. So, primary (perhaps MI), secondary (presumably due to the heart failure), or both (heart failure due to MI)? It does seem like an injury substantial enough to cause acute PE would be a little more evident on the monitor…

    Of course, in many systems it will be moot if you follow the AHA, because this is a presumably-new LBBB. I tend to follow Tom, and feel the literature does not support that. Either way, what’s the patient need? It may depend largely on vitals and presentation; it’s one thing to look at the rhythm, but if we agree that there was serious cardiac instability when we walked in the door, then at time of transport we may have to ask whether what the patient needs most is cardiopulmonary stabilization, or a (long trip to a) cath lab. It’s great that he appears to have made major improvements with our care, but 60 minutes is a looooong time…

  • Jonty says:

    Hard to determine any issues with an ECG with left bundle, I would say this Guy had an interior MI

  • Hillis says:

    I don’t think we are dealing with STEMI,am thinking about pericartitis with possible pericardial effusion !!
    QRS alternans, bifid large P waves and signs of heart failure.
    Why such young patient with no obvious risk factors ( exp. HTN which i suppose to be controled by medication) is decompensated ? this rise my suspicion about pericardial effusion

  • Paul says:

    I’ll put it this way… I’d be contacting the closest hospital, speaking DIRECTLY to an attending, transmit the 12 lead and EKG strips, and tell him “I am convinced this patient has a pericardial effusion until proven otherwise. If you want to run out here in the ambulance bay and do a quick ultrasound and you don’t see an effusion, I have no problem putting the truck back in gear and driving him down the road to the PCI center.”

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