50 year old male CC: Chest pain

Here’s a really interesting case submitted by “Anonymous from Ann Arbor, Michigan.” Wolverines! πŸ™‚ Sorry, Buckeyes.

EMS is called to the residence of a 59 year old male with a chief complaint of chest pain.

Past medical history: Dyslipidemia
Meds: Zocor

The patient was given 600 mg ASA by the spouse prior to EMS arrival.

Onset: Fairly rapid during sexual intercourse
Provoke: Nothing makes the pain better or worse, not reproducible on palpation
Quality: Described as pressure
Radiate: Right arm
Severity: 5/10
Time: 30 minutes prior to EMS arrival, no previous episodes

Patient is alert and oriented to person, place, time and event.

Skin is pink, warm and moist.

Breath sounds: clear bilaterally

No JVD or pitting edema.

Vital signs are assessed.

RR: 22
Pulse: 80
BP: 124/84
SpO2: 99 on RA

BGL: 134

The patient was placed on the cardiac monitor and a 12-lead ECG was captured.

What is going on with the patient?

How would you treat the patient and why?

See also:

50 year old male CC: Chest pain – Discussion

43 Comments

  • Chris T says:

    wonder if the patient has been near an digitalis?

  • DaveOC says:

    A. fib with LBBB and ST depression in v1-v3 and STE in lateral leads v5 and v6. Sgarbossa’s criteria for concordant STE > 1mm is met in v5 and v6.
    Posterior EKG, IV, NTG and transport.
    Advise the wife to dial down the bedroom gymnastics….the old guy can’t take it !

  • Chris T says:

    Well im not sold on a-fib. Looks very regular and what i think the machine sees as fib waves might just be artifact. Im at junctional tach.
    There is some kind of repolarization problem I think. Im not 100% why. Looks like a digitalis effect but no Hx. I do see possible lateral MI. excessive elevation. And concordant STE and STD that have reciprical in II,III,aVF
    STEMI protocol after consult with Medical control.
    Standard AMI Tx.

  • Chris T says:

    oh yeah, make sure he aint doped on viagra.

  • Rm says:

    Concordant ste in I avl v5 v6 … STD in v1-v3. Posterior leads, the usual tx, and cath lab!

  • Phill Giggleman says:

    DAVE OC…excellent pt. education!!! CLASSIC!!!

  • RayG says:

    People joke about wanting to go this way. I’m sure you would feel differently if it were to happen to you. If sildenafil was taken would be what I would be thinking. Give O2 and consider further treatment in route to ER.

  • 12leadekg says:

    I too see concordant ST elevation in leads 1, AVL, V5 and V6 along with ST depression in V1-v3. Positive Sgarbossa Criteria. Posterior Lateral MI. 02, IV, NTG and transport to PCI Center.

  • Robert F. (Las Vegas) says:

    Oo funky monkey! I aint sold on afibb as well.

    Interpretation: Regular rhythm, wide, appears to be retrograde p waves proceding the qrs complexs (v1 & v2).
    Accelerated junctional rhythm @ 92 with LBBB (QRS>0.12,LAD, & broad monophasic R waves I,V6)Concordant segments in I, AVL & ST depression in leads v1, v2.

    Treatment: Call the cath lab
    O2, IV’s, ASA (although I won’t be giving any more if she gave him 600 mg!), and I want a Right Sided 12 lead before I start loading him up w/ NTG & Morphine. Make sure viagra, etc. isn’t on board.
    Cheers!

  • kiersten says:

    i’m just an EMT student, but I think I would leave the 12-lead on, put him on a nasal cannula, and transport in a position of comfort.

  • Xina says:

    As an EMT-Basic, I’m pretty new to this, so please tell me if you think what I would do would be appropriate.

    A-fib. No need for o2 because he has 99% sats on Room Air.
    I’d then give NTG and Aspirin (I’m sure you can give both?) as preventative measures, keep hooked to the ECG, get o2 ready just in case, defib ready just in case and transport.

    This is what I would do if no ALS were available and I’d call control for any guidance.

    What do you think?

  • Echacon says:

    Totally agree with the LBBB and lateral elevation. O2, 2 large bore IVs, NTG, ASA, vitals, Rapid transport. Call to activate cath lab if you can do that. Get a good history. With is recent activities he may be on some ED drugs. Always put on O2 in an MI or Stroke. No matter what the sats show.

  • Will Roberts says:

    I would agree on the afib only cuz Im white and nerdy and got out my trusty calipers. There are no distinct p waves with a widened QRS >.10ms. The rhythm is irregular although I will say upon first look I thought it was. 12 lead confirms LBBB which explains the widened QRS. Now the question you have to ask yourself is this. Is this a new onset LBBB? You might (although unlikely) get this from your history. As one of the docs I work with says treat them logically for what will kill them faster. I would treat this as an active AMI and treat per protocol. (O2, IV with NS, ASA, NGT, Morphine if there is no contraindications)

  • Mark says:

    After seeing 12 lead, call in findings, the history of onset during sex is important and i would find out if any sildenafil type drugs were used, that would contraindicate for nitrate use as may cause BP to fall…..iv access, o2 and defib at ready, continuous monitor and reassess en route, can consider morphine for pain relief.

  • KO says:

    Path. left axis deviation + Anterior hemiblock
    QRS > 120 > BBB ( in this case Left)
    no nitro at this time, place quick pads on, be ready to pace or defibrillate. Is he a candidate for fibrinolytics, get him to the cath lab!!

  • Aaron says:

    Sinus with LBBB, one big question for the history? is the pt on any meds such as Viagra, or any sexual enhancements drugs? very important, treat pt with 02, WATCH BP if the answer to my question is Yes, They get hypotensive, Nitro, morphine if no relief, Transmit 12 lead, Transport. A good history is the secret to this pt. Aaron Emt-P.

  • Christopher says:

    I’m not sold on the LBBB as the qR in I/aVL and the Rs in V6 is very uncharacteristic of LBBB. What I do have though is elevation in I/aVL/V5/V6 with clear depression in V1-V3 and maybe some in III/aVF. Posteriolateral MI is highly likely, and I’d call a STEMI alert on this one.

    No fixed R-R, so I’m leaning to a-fib (given the absence of P-waves). Seems like an odd new-onset at 50 years old, but maybe he wasn’t aware this was in his history. Other option is prolonged 1AVB and PACs causing the irregularity.

    Either way, atrial activity and ventricular response are not problems for this fella πŸ™‚

  • Dan says:

    I have to agree with KO here. That QRS really stood out right away.

    Xina, Do not remove the O2. Give O2 to this PT. Treat your PT not your equipment. Remember that rule forever.

  • Baker says:

    Xina your aggresion as an EMT-Basic is awesome you will make a great Medic someday, learning a little ahead of your scope of practice is a great thing and will help you a great deal as you progress through ur carrer. As far as your treatment goes its pretty good, i dont completely agree with the A-Fib it looks to regular and i believe the 12-lead is picking up artifact although the p-waves arent really detectable, i would go ahead with the nitro as u said as long as the pt. has not taken any ED meds, i would probably withhold the ASA due to the large amount the pt.s wife has already given him, but to answer your question yes you can certainly give both ASA and NTG. Dont let the fact that the pt.s 02 sats are good detour you from giving supplemental 02, remember anytime the heart muscle strains its generally due to a lack of 02 secondary to a lack of blood flow due to a probable blockage so anytime you expect a cardiac event always give some form of supplemental 02 to help reduce any uneeded strain on the heart. All in all you would have done a great job so keep it up, i hope to see more of your posts on here. I personally believe due to the lack of prior cardiac hx that this is probably a new onset LBBB that is masking the true severity of an underlying MI, pt. needs all possible ALS care and rapid transport to a Cath facility.

  • Aaron says:

    Its also very hard to see ST elevation in a bundle branch block guys, need enzymes to confirm,

  • Chris T says:

    AAron have you read DR Smiths post on concordans and excessive discordance to determine STEMI in presents of LBBB? This EKG meets his criteria for STEMI alert. I highly recommend it. I was once educated that it was very “hard to tell” cause LBBB can mimic a STEMI. From this site I have learned better!

  • AxelF says:

    Hi everyone.
    I’m a student paramedic from germany and some statements concerning O2 as standard treatment for MI-patients leave me a little confused…
    Echacon wrote: “Always put on O2 in an MI or stroke”
    According to what I’ve learned from the 2010 ERC Guidelines not every MI-patient needs O2, in fact there is data to support that it may be harmful to some. (I’m sure most of you have heard about the hyperoxemia concerns)
    My point is: This patient doesn’t meet the criteria for O2 as long as he maintains his SpO2 level and doesn’t show other signs of hypoxia. So I would agree with Xina on this point.

    Or am I completely off the track?

  • Robert F. (Las Vegas) says:

    What a great case!

    I’m still looking at this rhythm and it appears very regular, I think the reason the LBBB looks abnormal is due to retrograde p waves in numerous leads. I’m still going with accelerated junctional w/ LBBB!!

    Side note: Inferior wall MI’s are very consistent w/ lateral-posterior wall mi’s, there appears to be slight st depression in lead II as well, i’d be very very cautious w/ the NTG, and make sure to get that Rv4/right sided 12 lead as well as an IV access ready for some fluid boluses. Jnctional rhythms are common with inferior wall mis as well as RVI’s.

    Cheers!

  • Baron says:

    I’m not sold on the fib either, guys.
    I’m going SR, with RSA the likely culprit of the irregularities.

    Well.. with the caveat that when Chris says there’s no fixed RR and he’s leaning toward fib, I tend to want to agree. His ladder diagrams are quite impressive!

    I’m also thinking LBBB. While I agree with 6 letters that it looks a little odd, I think the STEMI is to blame for that.

    The q’s in I and aVL could be caused by necrosis from the high lateral infarction.

    And as for laterally, I believe the AMI lowered the LBBB R wave voltage (as is seen in LVH with STEMI) and may have somehow altered the R progression pushing S waves into V5.

    While the s in V6 could also possibly be from altered progression, I think its just as likely that there is no s wave at all. What looks like an s wave may just be an almost vertical ST segment.

    My final thought is of possible ST elevation in II with the minor depression in III and aVF. Given that III is the most reciprocal lead, and aVF the next over anatomically (and showing slightly less depression than III), I’m considering a left dominant LCX and concomitant inferior injury.

    The left dominant thought is admittedly more of a long shot, but I’m fairly confident in the LCX being the culprit coronary.

    I look forward to learning of the results! I wonder if he finished before calling 911…lol!

  • Mark L says:

    AxelF, isn’t it funny how quickly guidelines change? πŸ™‚ The current 2010 AHA guidelines state for Acute Coronary Syndromes to titrate oxygen to maintain a SPO2 of 94% or higher. The guidelines don’t ban the use of oxygen (it does actually suggest starting a 4 lpm nasal cannula then titrate), but I think the point here is that you don’t need to blast 15 lpm by NRB on them in this particular case.

    I seriously doubt this is A-Fib (looks like motion artifact that is throwing off the MRx interpretation), but wouldn’t it be awesome if it was so that the guy could tell his wife, “Baby…you make my heart skip beats?”

    Although I think most clinicials seeing this LBBB would probably be pretty agressive, looking at Sgarbossa’s, this is how I would rate it (I could totally be wrong though)…

    1. ST elevation β‰₯ 1 mm concordant with QRS complex – PRESENT (V5, kind of V6 but I think there is some wandering baseline)

    2. ST depression β‰₯ 1 mm in lead V1, V2, or V3 – PRESENT (V1, V2)

    3. ST elevation β‰₯ 5 mm where discordant with QRS complex – Not present

    Aside from Viagra…levitra? Cialis? Herbal supplements?

  • Michael M says:

    I do not think this is a left bundle: Q wave in lead 1, part of LBBB criteria is monomorphic R wave in 1 without q waves. I contend there is a q wave in lead 1 and avl. Also LBBB should have monomorphic R in v6. V6 shows more of a RBBB morphology with a slurred s wave. I do not know even I would even call that a monomorphic S wave in v1, looks more like a Q wave. With that said It seems to not meet either criteria for LBBB or RBBB. With a QRSD >120 ms, QRS of -47degrees with a qR in lead 1 and a rS lead three we have LAH also we have a really long QTc of 498ms. So we have a wide qrs that to me does not seem to meet either LBBB or RBBB seems like it could be intraventricular conduction delay. Time to start diff dx for wide qrs>120 ms with a long QTc 498ms,for this which I have not done yet.

  • g kliniewski says:

    my thoughts , bifasicular block with lateral wall ischemia the block rbbb, left anterior fasicular blockage

  • Robert F. (Las Vegas) says:

    Michael, looking at this 12 lead again, i think you’re right!

    I think that there is a RBBB pattern going on there. I think lead V1 would have a positive R complex if it wern’t for the significant depression, v2 looks like it has similar rsr’ pattern as well. Can i change my answer from a LBBB to a RBBB!

  • eff dog says:

    with regards to sat of 99% on RA. I really don’t care how much o2 is in his finger tip. I know to suspect that his heart muscle isn’t getting enough so i will give him a little extra. i would suspect viagra-type drugs even though he denies it so prepare with large bore and fluid bolus prior to NTG. Also a concern with the ED, is alpha “stimulant” type erectile stimulants (eg. cocaine). ask him in private from the wife might give more honest answers? maybe ask the wife- I had a pt deny ED drugs – and the wife shouted “tell them what you took, honey!”. He’s not explicitly tachycardic or hypertensive but it could be on board. cardiac Enzymes are normal for 6 hours so I would not withold treatment for results. Love the use of Scarbossa’s guide πŸ™‚ even though the pt’s morphology isn’t textbook! Thanks.
    E.

  • ARSHAD HASAN says:

    HR-100.
    BBB.
    ST Elevation-V4,5,6(ANTERO LAT MI)
    Fibrilatory Wave-positive
    Rx.
    Along d line of MI
    1.ASA
    2.STATIN
    3.NTG
    4.Enoxaparin(s/c)
    5.diethyle morphine

  • Christopher says:

    Taking a really close look at the R-R, I’m going to amend my previous statement about “A-fib”. I think instead this is 1AVB with sinus arrhythmia (the R-R gets progressively smaller during the strip, then lengthens at the end).

    Otherwise the R-R during the middle of the strip is pretty consistent (standard deviation of only 25ms) and represents a gradual increase in heart rate from 80 to 110.

    I wonder if the patient was asked to slow his breathing down or to take a deep breath in order to get a clean strip?

  • NYCMedic says:

    eff dog, so basically what you’re saying is, you want to treat with your “gut” feeling, rather than using evidence based medicine? Latest guidelines DO state that for a person that is not hypoxic, supplemental O2 can actually be harmful. (http://www.americanheart.org/downloadable/heart/1256243465576ACS-015A%2014-Aug-2009.pdf)

    Seems like an IVCD to me. Possible posterolateral STEMI. Also, seems like a machine misinterpretation for a-fib, I think I see P waves in V4-6 albiet with a short PR, so I’m saying sinus or accelerated junctional. I’d activate the cath lab, and do MONA. If he’s not dyspneic and maintains his SpO2 I personally would withhold the “O”, but according to my protocols I cannot.

  • Chris Bishop says:

    INT: AJR c LBBB. ST Elevation in Leads V-5 and V-6. Possible depression in V-1, V-2, V-3.

    TX: High-flow O2 via NRB Mask, position of comfort, SAMPLE Hx (no erectile meds.), IV TKO NS, NTG, Transport,call a STEMI Alert, consider morphine sulfate if pain gets worse.Ongoing Assesment and Check interventions.

  • Medic-Shmedic says:

    Appears junc, regular occurring QRS. But with LBBB, I’m not 100% sold that the ST elevation is true STEMI. BUT…tx as cardiac chest pain. Run a couple more EKGs enroute. Ask about boner juice hx. Thats it in a nutshell.

  • ZTM says:

    With the discordant T-wave, wide QRS, predominantly negative QRS, left axis deviation in V1, would that not help confirm LBBB?

    ZTM

  • JOSH says:

    IV, 02 ASA, NIRTO. IN THE PRESENCE OF A LBBB YOU CAN NOT RULE OUT AN MI. I WOULD WANT TO SEE AN OLD EKG TO SEE IF IT IS A NEW ONSET. DIG TOXCITY IS A POSSIBALLITY, BUT UNLIKELY. HE IS DISPLAYING NO SIGNS OR SYMPTOMS. PT NEEDS A CATH LAB.

  • Renee says:

    Pt has chest pain during “exercise” (really doesn’t matter what exercise), which is highly suspicious of ACS right off the bat, even before the ECG. Vitals are pretty good. BG is a bit high. I agree with the masses that A-fib is not the culprit here. I also have questions if this pt is taking Viagra or another analog, even without a prescription. Junctional rhythm. STEMI is not huge, but enough to activate a STEMI call. O2, ASA, Nitro, IV, and Cath lab time…

  • Slayer says:

    Well now… the reason why most STEMI programs have a LBBB excluder for activation of emergent cath is evident here. Slow down on the diagnosis folks. QRS is what it is. Measure it out and mark the beginning and end on paper. Take those marks and travel around to each lead. The second mark is where your J point is. You may be surprised to see there is not ST elevation where you once thought. HR is elevated…. rare that we have STEMI with that on short onset time. T waves are asymmetrical (less for patho in origin). Q waves are not at least a third of R waves directly related (also less likely patho in origin). Last but not least, it’s pressure and not pain. Yes, he needs a cardiac work up but an emergent procedure? Nope.

    Peace!

  • VinceD says:

    Gah I had a nice explanation typed out but lost it. Here I go again, slightly more rushed…
    Definitive lateral STEMI (STE I, aVL, V5, V6), most likely with posterior involvement as well (STD V1-V4), which is enough to activate the cath lab and treat. There may also be anterior involvement (Q-waves V1-V2, poor r-wave progression), which I’ll get into later, but this is not likely. Understanding the rest of the tracing is where things get a bit dicey for me.

    Rhythm is most likely normal sinus with sinus arrhythmia (see Christopher’s comment), but finding p-waves is a bit tricky. I’m somewhat comfortable with calling the PRi 110ms based off of what appear to be p-waves corresponding to the adjacent QRS complexes in V4-V6. A little short for a PR-interval, but it’s the best explanation I can work out.

    The wide QRS is the other aspect of this tracing that causes me some angst. It is very atypical for a LBBB with the morphology of the precordial leads. Some folks were put off of LBBB by the q-waves in I and aVL, but since there’s a very likely lateral MI, these q’s would not be unexpected. LAFB with secondary QRS widening (tall R’s in I and aVL, LAD) is a possibility I suppose and fits nicely, but I’ve never seen one with such a wide QRS, so I’m equally as likely to just call it a non-specific intraventricular conduction delay (IVCD).
    The final option is a RBBB+LAFB masked by anterior involvement of the MI. This would nicely explain the tall R’s in I and aVL and the left axis deviation. If the anterior myocardium were involved, Q-waves could mask the typical RSR’ patter in V1 and V2 and cause poor r-wave progression across the precordials, although I have never seen one do so to the extent seen here. RBBB could also account for the s-waves in V5 and V6, although the morphology isn’t quite what I would expect (initial r is a little too wide). Although this final explanation would be very elegant if it were the case, I’m just not convinced enough to make such a call and without prior/later ECG’s to compare with would just call it a non-specific IVCD.

  • David says:

    treat the patient not the monitor… MONA and transport to an intreventional cath lab for sure. Really a bad tracing as well. Possibly poor application by medic or en route 12-lead. Pull over… this alows the little man in the box to work better. : )

  • eff dog says:

    @nycmedic- quite often actually. and in response to the link provided, thank you, and I enjoyed and learned from. But I did note that the overwhelming majority of the studies presented said things like, “suggests…sugestive…may be a clinical corelation…p score=not convincing…study population size of 14 patients =too small…some of the evidence suggests”. For everyone that said O2 is bad for you, another said it is good for you. This does not proove “evidence based medicine”. Until it does, I will give pt’s with signs of hypoxia (cardiac or otherwise) O2. Respectfully,
    E.

  • NYCMedic says:

    The link I provided didn’t appear to show any strong evidence of benefit, and at the same time showed evidence against. As you said, we have not found undeniable evidence either way, so wouldn’t it be best to meet in the middle and treat a patient that appears clinically hypoxic until their SpO2 is adequate, but not make them hyperoxemic? Seems the safest bet…

  • eff dog says:

    nyc- that’s what I am doing. since I don’t have a finger probe in his myocardium, I am using my 12 lead to evaluate his O2 levels. I am making him systemically hyperoxemic in order to treat him until his “spo2 is adequate” and he no longer appears clinically hypoxic (in his myocardium). We have all seen the MI pt with EKG changes improve with O2- chest pain resolved, ST segment normalised. associated symptoms resolved. All before you could reach for the M,N, or A πŸ™‚
    E.

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