62 y/o M with CP radiating to the back, diaphoresis, and hypotension…

Home / Cardiology / 62 y/o M with CP radiating to the back, diaphoresis, and hypotension…

I’ve been told by one of my wise mentors that if “your patient is sweating, you should be sweating”.  Well, someone must have turned on the heater in the entire ER…

EMS called a STEMI notification for a 62 y/o M with chest pain radiating to his back.  On arrival, they hand us this EKG:

The patient’s triage vitals were BP 82/44, HR 110bpm, RR 24, SaO2 88% on 3L O2.  He complained of chest pain radiating to his back for 5 days, but now only had back pain.  His medical history was significant for AIDS and HTN.  He is diaphoretic and visibly dyspneic.  The nurse hand you this next EKG:

What do you do next?  Is this patient having a STEMI?  An aortic dissection?  Do you go to the CT scanner?  Or to the cath lab?

Leave your thoughts below, and check back in 1 week to see what happened…

By V.Nguyen @himynameisvince

For more interesting cases & all things EM, follow on twitter: @himynameisvince, @Jacobi_EM. Subscribe to new posts http://jacobiem.org/residency/interactive-classroom/


  • Eddie

    Abcs/resuscitation. Intubate the patient and call a stemi for ste in avr and st depression in anterior leads. Get the ultrasound out and look for other possibilities including tamponade and pe. This could still be a dissection, valve rupture, ruptured AAA, or sepsis. If nothing definitive on official bedside echo then consider the cath lab with ct surg on standby.

  • Chertoff

    R sided STEMI (AVR and V1 markedly elevated on 1st EKG) – given the history, probably as a result of aortic dissection into the RCA. Fastest and safest route is to stabilize best you can (ETT, CVC, pressors etc.) while cath team assembles. The cath will guide whether the case needs intervention in the lab or to go to the OR with CT surg.

  • siuf

    the ekg is the least of your problems

    this is not a stemi ekg. the patient might be having a massive mi, but this is not a stemi ekg.

    when i look at this ekg, i think hiK, medications, pre-existing cardiac disease causing a conduction defect, and less likely, new cardiac injury causing a conduction defect. this ekg is equivalent to a lbbb.

    this is unlikely to be dissection. pt with dissection have normal-ish ekgs and they’re not hypoxic.

    my first issue is to rule out hiK with an istat. renal failure can explain everything. the second issue is why the hypoxia? get a cxr. is it APE, ARDS, PE, or something else? Put some O2 on the pt. it sounds like APE for sure, except for the hypotension.

    we have c/p and a very suspicious ekg. we can debate cath v echo v nada. i would be very surprised but not shocked if the problem is below the diaphragm (aka pancreatitis).

    if the answer is methylene blue, you deserve a kick in the nads.

    how do you connect c/p, hypoxia, hypotension, and an abnormal ekg?
    the simple answer is systolic failure (?acute ?chronic ?both). an echo will answer this question. PE, dissection, tamponade, and sexy things do not explain the four major findings (alone). the underlying cardiac problem is likely ischemic (most common), v. a non-ischemic cardiomyopathy, myocarditis, dead valve, ruptured something, etc.

    so, check K, cxr, echo, asa, and a call to admit the patient.

    i don’t get diaphoretic. i’m an er doc.

  • Chauhan

    I concur with the general consensus (except Siuf, I get diaphoretic!), ABC protocols and resuscitation. Notify cardiology this pt needs the cath lab stat. I believe the initial EKG and clinical presentation is key. The initial EKG shows ST elevation in aVR and the septal leads with diffuse ST depression throughout. (Remember lead aVR is electronically opposite to the Left sided leads I,II,aVL,V4-V6, therefore depression in these leads causes reciprocal ST elevation in aVR). ST elevation in aVR > 1mm should raise suspicion for possible LMCA occlusion, LAD occlusion or triple vessel dz. (See link 1 listed below). The magnitude of ST elevation in aVR can be correlated with mortality outcomes in pts. In this case the ST elevation in aVR is > 1.5mm which according to certain studies places his mortality bw 20-75% (see link 2). It is possible to correlate the pts initial vitals (hypotension and desaturation) with occlusion of the LMCA or LAD. Knocking out the conduction system and diffuse myocardial ischemia would serve to hinder circulation and conduction. While resuscitating the pt and awaiting cardiology a bedside echo would be vital here looking for the aforementioned confounding issues valve rupture, PE, mechanical dynamics of the heart, AAA and tamponade (remember to look at your outflow tracks). It is important to note these pts tend to do poorly. There is a reason this scenario is affectionately termed the “widow maker”. Many times these pts end up on balloon pumps and undergoing both PTCA and or CABG. That’s my 2 cents. Good Case! Curious to see how he did and what he actually has.

    Link1: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2898534/
    aVR the Forgotten lead by George MD et al. Exp Clin Cardiol. 2010 Summer; 15(2): e36–e44.Clinical Cardiology: Review

    Link 2: http://lifeinthefastlane.com/ecg-library/lmca

  • West

    This is an interesting case, so I wanted to add some thoughts to keep the discussion going.

    You have an initial EKG of a patient with “chest pain radiating to the back” with the aforementioned STE in aVR and what is likely diffuse STDs in the setting of LBBB already flagged by EMS as a STEMI. Next, we see this patients EKG in house, and the STE in aVR no longer jumps out at you and looks to be of 1mm elevation. Our patient is only complaining of back pain at this time, so did he get nitro? The rate of both EKGs is about the same, so rate-related changes are out. I think we have all agreed that cath lab activation for this STEMI equivalent is appropriate, but what if we didn’t have the first EKG? What if the initial EKG and/or rhythm strip got lost, and we missed the STE in aVR? If you look at the 2013 AHA STEMI Guidelines, they have de-linked LBBB with acute MI: “New or presumably new LBBB at presentation occurs infrequently, may interfere with ST-elevation analysis, and should not be considered diagnostic of acute myocardial infarction (MI) in isolation.” If not for the EMS EKG, we are out of convicing reasons to send this patient to the cath lab ASAP.

    I think Chertoff’s idea is sexy, but those STDs everywhere don’t help us localize the lesion. What if this aortic dissection begins to involve to the left main instead of the RCA? What if there is both a left main occlusion STEMI equivalent AND a dissection? One of the IRAD studies says that there is ischemic EKG changes 15% of the time with dissection. Also, although AIDS isn’t a risk factor for acute MI, it is a risk factor for accelerated atherosclerosis, which might manifest itself as his initial EKG does.

    You need the cath to diagnose his CAD or culprit lesion, and they can diagnose a dissection there too. Even if you tube, resuscitate, sono, and start to look for causes of STEMI/ischemia mimicry in this patient, wouldn’t you be sweating if the cardiologist doesn’t want to take this patient to the cath lab and you have to call CT surgery?

  • Mar

    Just to add to everyone else’s comments, especially Chauhan’s which I think are dead-on, and to connect the dots for anyone who loathes pathophys as much as I do, LMCA and/or proximal LAD occlusion can cause cardiogenic shock by pump failure which of course leads to Siuf’s pulmonary edema. (no contraction of LV=no outflow=hypotension; similarly, no contraction=back up into pulmonary system=cardiogenic edema=hypoxia). Early PCI and reperfusion is still considered standard of care in cardiogenic shock related to myocardial ischemia

    As Chris mentioned in passing, these patients may require intraaortic balloon pumps for cardiac support and possibly CABG. This is important for us because it means we should think about whether giving plavix “per protocol” is going to help or hurt the patient in the long run (higher bleeding rates associated with patients given plavix in the 7 days prior to CABG).

    As Eddie mentioned, ABCs are always the first step. Intubation followed by pressors followed by PCI gives patients the best chance. Both norepinephrine and dopamine are considered reasonable choices for pressors in cardiogenic shock given their inotropic activity, although there is disagreement regarding which to start first . Unlike a right-sided MI, which is preload-dependant, IVF is likely to worsen this guy’s pulmonary edema.

    It’s also worth noting that a Type A dissection retrograde into the aortic valve with resultant acute aortic regurgitation could produce a similar picture, as could critical aortic stenosis (again, outflow tract obstruction)–but the EKG wouldn’t necessarily fit.

    So, I’m calling the STEMI->intubating->resuscitating with levophed->pulling out my ultrasound for a quick bedside echo, mainly to look at outflow tracts->giving CT Surg a heads up.

    This case would be extremely difficult in the ED, so kudos to those who had to navigate it.

  • Chertoff

    Sorry – point I meant to make is that V1 and aVR are contiguous leads. Proximal LAD or LMCA most likely, triple vessel next. When V1 or aVR is up, I always do right sided leads for more information.

    I agree with West – initial gut response to the case is significantly different without the first EKG. No big STs to make you go, “oooooh”. But there is a LBBB. Rather than caring about whether calling new/unknown age LBBB is same as STEMI on any given day (I think it is not unless that patient is clinically a STEMI anyway… like this one), we should make sure this is your typical LBBB. LBBB makes STEMI difficult to judge because of the already typically big (but not too big, ie. >5mm) ST elevations anteriorly on routine/asymptomatic EKGs. Like here: http://www.emedu.org/ecg/lbbb.htm. And this guy does not have that – in fact, he has ST depressions in V2-V4 (V5 and V6 too, but that is part of a typical LBBB). Ahhh, so the second EKG while not containing big ‘ol sexy ST elevations like the first, does have LBBB STEMI findings – Sgarbossa’s 2nd (http://lifeinthefastlane.com/ecg-library/basics/sgarbossa/). Plan remains activate cath lab and find lesion or dissection.

    In the case of having only the second EKG, Siuf’s fear of K+ is a good one (iSTAT is a great thing), though the persistant p waves and tachycardia would make me feel a bit better regarding that as does the presenting complaint of pain.

    My choice of pressors: dobutamine (pure pump augmentation but peripheral vasodilation) and neo (vasoconstriction). I don’t see a role for dobutamine… ever.

  • alvarez

    tough case. siuf, always the controversial, but he’s onto something.

    here’s my long winded answer simply because I’ve had a nice sleep and I’m not dealing with this patient in front of me while I’m *trying* to think.

    looking at the global picture, including my time-to-balloon metrics, the ekg in the ED is NOT a stemi. (I’d even do the ciorciarri and put a bunch of cross-outs and exclamation points in that actual EKG). At our shop now, we’d call a stemi based on the EMS ekg because they would have emailed me and fax the ED the EKG before arrival.

    Going to the cath lab or not, when I get the patient, and I see those vital signs: I’d wanna know temp (i know, who cares on this possible STEMI pt, but if he is febrile, and i’m not talking 100.1, might make me think of other diagnoses as well, especially with the hypotension, tachycardia, tachypnea, hypoxia). What’s the glucose? I know this is not a boards type scenario, but I’m assuming this is a medical alert/resusc when I’ll have all my staff for a brief time, and I have an extra hand to do a simple test while setting up for that R sided ekg. prolly not posterior, the v1 v2 morphology has more of a hyperacute T. prolly not fun for your diaphoretic patient to be tossed around anyway as you fumble for the v8 to v9.

    The STE on AVR as chris and chertoff pointed out is sexy, and I’ve had patients brought to the cath lab for that, not as a STEMI by door-to-balloon time criteria, but for concerning story/concerning ekg/doing-it-right-for the patient discussion. Not all cardiologists buy this, as amal mattu discusses on his article. http://tinyurl.com/aox5ahp

    This said, in as much as this is not a slam dunk stemi/cath activation on the EKG (unless your cardiologists at jacobi/monte still think new LBBB is considered MI), I’d want them on the phone receiving a fax of this EKG. You probably would want them anyway to approve that stat echo to be done in the ICU (the new goal is door-to-ICU/door-to-OR time in this patient =) Maybe I did learn something from siu fei.

    The cardiology call answers the debate whether cath first or CT first. If the cardiologist is willing to cath the patient, you’ll diagnose MI and dissection, and not have to botch the patient’s kidneys with a double dose of IV contrast. You can even give a heads up to the CT surgeon that there might be a dissection case going to the cath lab. (I’m sure they’ll give you the finger and tell you to call them if you confirm the diagnosis, but at least you tried (and documented in the chart).

    Remember, and I’ve seen more of this than the classic dissection. Not all will be hypertensive. Not all will have radiation to the back.

    That said, that axis change is impressive, and inferior leads look a lot different from the first EKG, and dissection is still in the differential although, agreed, hypoxia in dissection, not so much.

    Regarding the LBBB: no discussion is ever valid without a reference to wikipedia, so here it is.. if you apply sgarbossa criteria, not really STEMI-ish. http://en.ecgpedia.org/wiki/MI_Diagnosis_in_LBBB_or_paced_rhythm


    While the nurses (or residents) are drawing blood, I’d ask for a dire K (or super stat K or whatever it’s called now to get a K back ASAP). An i-stat would be sufficient. Pt with AIDS. Is he on bactrim for PCP ppx?
    here’s a nice article on hyperK mimicking our ekg. kinda. http://crashingpatient.com/medical-surgical/electrolyte-disorders/potassium-disorders.htm/
    ok, the t’s in the article are more peak-ish.

    I agree with eddie re: intubation. I’d want phenylephrine at bedside though. Simple mixture, 1ml (10mg/ml) of phenylephrine into 100ml of NS, every ml being 100mcg, and I’ll start the pt on the drip peripherally 1ml/min to titrate the BP up. http://emcrit.org/wp-content/uploads/push-dose-pressors.pdf I’ve had cases of shock, and when I intubate, decrease their preload further, and they crap out even further, including a ruptured aortic valve case presenting similar to our case (IVDA, AIDS, ruptured a valve from his endocarditis, presenting as STEMI-ish). Actually, paralyzing them cuts back on their adrenergic response, and also leads to them becoming more hypotension. again, another plug for the peripheral pressor.

    While we’re waiting for the RSI/vent/push dose pressor, I’d put an u/s probe to r/o ptx/tamponade (prolly too early for dressler if he had MI a week ago, but from AIDS?)/AAA. If you’re lucky, that aortic dissection will head south a little, and you’ll catch the aortic flap. I’m sure Kurtland would have sono’d the leg to r/o DVT, which would secondarily help to r/o PE.

    If this is behaving more like cardiogenic shock, I agree partly with Chertoff. Yes, fluid might worsen the patient, but who cares if I’m intubating him, he’ll pee it out. I’d rather get some volume in while setting up for the intubation, rather than dropping that preload further. Phenylephrine/bipap combo might tie you over while setting up for that intubation, or even better, subdissociative dose ketamine + bipap (it’s already in the RSI box, easy for nurses to get than phenylephrine). I’d also want Levo/dobutamine setup while we’re intubating if I don’t see a good squeeze on my bedside echo. When I intubate, i’d again use ketamine/roc for that extra kick in blood pressure, and roc because I have no idea what that K is and would not want to use sux.

    Why am I giving PCP to someone who’s potentially having an MI? good question. Because if he is having a STEMI, he’s heading to the cath lab. If he’s not having a stemi, and this is something else, i’m augmenting the BP. If he’s having a dissection, well then, I’ll reserve my response for the M&M.

    By now, cardiology would have called and would have said, “I want a repeat ekg,” and you would have asked, “they’re doing the ekg, front and back right now, but, if it’s not a stemi, would you still take the patient to the cath lab?” If the answer is “no” then i’d get a CT chest dissection study, hopefully, from ED to CT to ICU, one fell swoop. I’d hold off on the ASA (you have 24 hours to give by CMS criteria if not a stemi =), hold off on plavix, hold off on anticoagulation.

    Great case.

    btw. i’d cut back on the orders depending on the resources, of course, and prioritize appropriately. i’m running this scenario as if i’m working on an overnight shift at my shop now where at the very least, i’ll have 4 nurses during the initial resusc, a couple of techs, and maybe a resident.

  • Mar

    Can you use dobutamine in cardiogenic shock? I haven’t used it much, but most of the texts say that with frank hypotension you have to be careful of the vasodilator properties, although you get the inotropy. I wouldn’t use dopamine (higher risk of arrhythmia and tachycardia)…luckily, Cochran is in the middle of doing a review of the literature on pressors in cardiogenic shock.

      • alvarezzy

        right. you can’t use dobutamine on its own. it’s like beating a dead horse. in as much as dobutamine gives great inotropy, it causes vasodilation (beta 2)…

        historically, we use dopamine/dobutamine combo, but in cardiogenic shock, there’s evidence (albeit from a subgroup analysis) that dopamine has higher mortality. yes, dopamine is more arrthymogenic than levo. So. i tend to use levophed/dobutamine combo for the nontachy, or epi/dobutamine if I need an extra chronotropy.

        again. before i even use dobutamine, i put a probe to check the heart and see if there’s enough squeeze. if there is, dobutamine will just be a waste. I really mostly use dobutamine for bad cardiogenic shock. also, if pt develops hypotension despite the levo, I check the IVC. if it’s pretty collapsable, I know I need to give more volume (NS or blood). prolly should check this, too, before starting dobutamine, as part of your E-FAST or whatever it’s called now.


  • alvarezzy

    vince just pointed out that by sgarbossa criteria, pt does have >3 points.. “very +ve by criteria #2 and by the modified criteria #3 (ratio ST:T >0.20)” so by this criteria, STEMI still. i had to zoom in to v3 to give criteria #3 credit. v2, some beats had 5mm, some >5mm.

    again, a nice conversation with the cardiologist (i.e. fax the ekg… in questionable situations like this, it’s good to get backup rather than hanging your hat on, “well, maybe, i think it’s >5mm, but well, I think, maybe on that second beat, it’s not…”). I’d continue with protecting airway/etc.

    i would still withhold the ASA/heparin/plavix until clear plan for cath/CT. There’s a few boxes you can tick off during charting to get the powers-that-be off your back for delay in door-to-balloon time/aspirin, etc if this really is stemi.

    what’s the K?

  • Derreck

    Great comments, please keep it up! You can now subscribe to this page and recieve emails when new material is posted (upper right corner of this page). You can now also be notified when someone comments on a post by selecting the “notify me” box below the “leave a reply” area (you must first post a comment to recieve follow up comment notifications).

  • SteveMcG

    This is awesome, great case, great discussion…I’m learning things and how to think about things…

    Plus, now that Homeland is on hiatus, I can’t wait to find out how this turns out.

  • siuf

    When dissection dissects back into the coronaries, it usually hits the R cor and the resultant EKG is an inferior wall STEMI, not this weird crap.

    Based on the secondary analysis of one big study, the drug for cardiogenic shock may be levophed (at least it’s somewhat in vogue now).

    There was a “aortic balloons don’t work” study recently published in nejm.

    This case isn’t really all that challenging or interesting, unless it’s one of those things mentioned that will get Vince a kick in his groin.

      • siuf

        that’s funny…

        my first email (not posted) when i saw this case was to tom and vince… “this is a moderate size PE that should be thrombolyzed”. (it’s funny only if you were at the last journal club).

    • vshah

      While I agree with Siuf that most dissections directing back to the coronary arteries involve the RCA (inferior wall findings), here is an interesting discussion which sites several references (case reports, etc) indicating that — while less common — aortic dissection can involve the L-coronary as well:


      All that being said–I see from the comments above there are several issues at debate:

      1) Would this EKG be classified as a STEMI?
      1a) Based on what? LBBB & Sgarbossa’s criteria? Or based on the EMS EKG which reveals more prominent AVR/V1 STEs (LMCA infarction). Or is this just and LBBB with “borderline findings” and not a STEMI at all?

      2) Why the did the two EKGs change? Is there an underlying dissection and the ischemia pattern is changing? Or was some intervention done (Nitro, etc) that we’re unaware of?

      3) Why is the patient hypoxic? APE (ischemic or not) vs. Valvular pathology? Is there anything about this case that leads us to believe that PE ties this all together (the presentation seems a little off for PE; esp given the dynamic EKG findings).

      4) For ** sake…what’s the K+??!

      Anyways, great reading all of your thoughts. I agree with most of you– it’s hard to NOT send this patient to cath lab and also request a STAT ECHO (perform in ED as well). A root aortic dissection, cardiomyopathy, flail valve leaflet, and even a saddle embolus can all be seen on ECHO. And I agree with cath + notifying CT Surgery just in case (despite getting “the finger” as Alai mentioned).

      A few more links:

      Aortic Dissection TEE: http://www.youtube.com/watch?v=bniPm6C7UwY

      Aortic Dissection TTE: http://www.youtube.com/watch?v=L91vprk-K28

  • 1 ). So the Smith modified sgarbossa criterion from 2012 is the ST/S ratio. It was mis-typed above. The idea to improve the existing sgarbossa criteria came from its low specificity in general and low sensititivity in regards to picking up anterior STEMIs. The idea was presented as an abtract in Circulation in 2008 and as an abstract at a SAEM conference in 2010 before being published last year in annals: http://download.journals.elsevierhealth.com/pdfs/journals/0196-0644/PIIS0196064412013686.pdf .

    In this study, they determined the cutoff point of a negative ST/S ratio that was at least 90% sensitive for people in Minnesota with LBBB, presented with ACS, and were cathed with confirmation of acute coronary occlusion. Here they found it to be > -0.25 (the previous studies had used > -0.2). I tried to explain this to one of my senior residents, and we found the negative value to be somewhat confusing, but the negative comes from the downward deflection of the S wave in leads V1-4, where this rule applies.

    The ST/S is > -0.25 in V1 of the first EKG.

    2). I’m not sure what your talking about with V2 and V3. In EKG #1, there is no significant STE there; and in EKG #2, the ST segments are concordantly depressed, so the Smith Modified Sgarbossa rule nor the 5mm absolute critera apply.

    I had a patient two weeks that had small STE and had a ratio that was barely inclusive within the rule, but if you read the M&M section of their paper, they assigned any STE < 1mm a ratio score of 0.
    Basically, you need more than a 1mm of STE for this criteria to be used, and he doesn't have it in V2 or V3 of that first EKG.

    As Chertoff pointed out, EKG #2 meets criterion 2 of Sgarbossa. We had missed this before, because most of us were focusing on the first EKG. I'm still interested in why the second EKG is different from the first. Also, the sgarbossa rule may be giving us a false positive.

    3). Still rooting for this being something unusual, like a dissection into the LCA. Going along with Suif's suggestion that this is actually just a toxidrome of methylene blue in a patient with multivessel disease and a LBBB, I had thought this could be from a drug-induced methemoglobinemia from Bactrim. He's got AIDs and should be on it, right? But, I guess he'd look like a smurf before he had EKG changes though.

    Since this is on twitter now,…

  • alvarezzy

    hehe, andrew. we didn’t dismiss the patient’s pain. we intubated him so he didn’t have to feel the pain =)

    west, you’re right on the modified sgarbossa. does not fit criteria #3 on 2nd ekg. i misread/misinterpreted the criteria. i blame wiki.

    methemoglobinemia, although a fun zebra, should not give you the clinical picture of this patient.

    i take it from the name of the ekg file that this was indeed a stemi and the question really is cath vs. CTA? http://jacobiem.org/wp-content/uploads/2013/02/CP-LMCA+prox-LAD-EMS-EKG.jpg

  • mattsilver74

    Ahh siuf, always stirring up controversy just for the sake of controversy… but in this case, I am afraid you are right. Lets go back to the history: 5 days of chest pain radiating to the back, HIV, hypotension, diaphoresis? Seems strange, no? If this were a STEMI for 5 days, he would have already completed his infarct… given the LBBB and global ST segment changes, likely a large infarct… he’d be dead. Still think it is cardiovascular in nature, just not STEMI from CAD. Diaphoresis and hypoxia, speaks to heart failure. High on the differential: peri-myocarditis, endocarditis w/: 1) acute valvular insufficiency 2) papillary rupture, 3) septic emboli to coronary, or sepsis with myocardial dysfucntion, acidosis and hyperkalemia (but why the back pain?). K is a thought, but if elevated is likely secondary to another process given the presenting signs and symptoms. Large PE… nah, too easy. And as wet outside, assuming wet inside… doesnt fit PE.

    Treatment priorities: ABC’s. Can try bipap as temporizing while you scratch your head or other parts, but will likely need to intubate eventually. If too sick or not tolerating bipap, can intubate straight away, but would use DSI in this case… if you slam this guy down, he will die- already circling the drain. If so worried about K, who cares… give him an amp of Calcium to stabilize those myocytes and move on… this is not a case of isolated high K. Can temporize the BP with push dose pressors as noted above. Next steps: central line with pressors (levo +/- dobutamine, CXR, bedside echo. No cath lab unless echo reveals regional wall motion abnormality. CT? not sure if this is needed. If the question is STEMI vs dissection with coronary involvement, than the answer is cath and aortogram, not CT. And if you are going the CT route, than definitely intubate lest you be running a code on the scanner.

    And since I feel that we have beaten, kicked, stabbed and shot this dead horse… the answer please…

    • andrewchertoff

      Yeeeeaaaaaaa Silver!!!!! You can take the man out of Jacobi, but you can’t take the Jacobi out THE MAN!!!

      Loved your discussion for its simplicity (Gennis-esque, especially “If so worried about K, who cares… give him an amp of Calcium to stabilize those myocytes and move on….”), great differential and diagnostic/treatment pathway – love the myocarditis, endocarditis (even though my money isn’t on it).

      Discussions definitely need to be had about how to more safely intubate the hypotensive peri-mortem pt. and push dose pressors (though I usually just throw levo through a decent peripheral when I have one until we’re out of the woods).

      Hope all is well on the Left Coast!

      • alvarezzy

        “If so worried about K, who cares… give him an amp of Calcium to stabilize those myocytes and move on….”
        i’d like to just add, if you are giving calcium, i’d repeat the ekg. for the juniors, ca++ has nothing to do with shifting K, but you should see normalization in the ekg if the abn ekg is indeed from hyperK. in a way, ca++ here is diagnostic.

    • Eddie

      I still think this is an ischemic looking EKG and would call STEMI. Is this ischemia from acute coronary arterial blockage or from some other cause of myocardial hypoperfusion is the question. He could have been having pain for 5 days that reached a critical point on day of presentation. So LBBB (new or presumed new)with ischemic type symptoms is falling out of favor as a STEMI equivalent but some would say LBBB with hemodynamic instability should be considered for PCI (J Am Coll Cardiol. 2012 Jul 10;60(2):96-105). A bedside echo is faster than an I stat. Most of us wont be able to evaluate for valve rupture/AAD but can see a pericardial effusion/dilated RV/tell gross wall motion abnormalities while cards comes.

  • Michael Jones

    Nice stuff Silver and Alvarez — west coast representing. I’ve been quietly sulking that we can’t discharge this patient. Now, where are the rest of the alums? Anybody else want to do things differently than what’s already posted? Would love to hear from somebody out in the community who doesn’t have cardiology or CT surgery readily available.

    My take on this is keep it simple — quick echo (don’t forget to check his IVC to see if he’s volume up or down–even an US retard like me can do it in less than a minute), mix up some pressors (push dose or levo gtt–whichever you’re most comfortable with), tube him, and get this guy to the cath lab. Once he’s on the cath table, you’ll have ruled in or out most of the bad stuff on the dDx’s above.

    Silverberg — what’s the answer? How did this play out in Monte-land?

  • pik

    Wow. Lots of smart comments, so many that I lost track of the case. Perhaps you guys did too?
    Guy looks like crap and has dynamic EKG changes. EMS strip looks like STEMI. I keep reading “not a STEMI” but then STE in V1 and AVR. I would worry a lot and not give Plavix in the ED. Then it becomes a L bundle. Which is typically a bs reason to call for cath. Unless you really suspect it’s brand new. Which should present in cardiogenic shock. You know, crackles, hypoxia, hypotension. Wait a sec, that’s exactly how he’s presenting. How do we explain the dynamic ekg change here if we’re not highly considering ACS? Not impossible that it’s K but cmon, is it likely?

    Dissection? Could be. Only goes to RCA so doesn’t fit? That’s a myth. Dissections spiral around following the path of the smooth muscle fibers, that’s how they cause those asymmetric pulse and neuro deficits. Dissection causing STEMI is rare. But causes 0.3% of STEMI. So let it be dx in cath lab if pt. stable enough to get there. That may not be the case here, so intubation and stabilization could coexist with a stat chest and even a bedside echo.

    Consideration of K, repol problems, and STEMI mimics makes for a great read but in real life I’m changing my shorts, recalling that HIV is a CAD risk and grabbing for phenylephrine as others have mentioned while I rapid page for Cards. Totally agree with the “at least I tried” comment regarding a heads-up to CT Surg.

  • doctorrobert

    Vince alerted me to this (great) discussion, and I’d like to reply with my thoughts on some excellent questions he asked me over email:

    1) Looking at this EKG, do all patients presenting like this belong directly in the OR with CT Surgery – and not the cath lab?

    -An important goal of CT surgery in this case is to do bypass surgery (as well as other structural interventions as needed)–and you can’t know where to sew in the bypass grafts unless you have a coronary angiogram to show you where there are suitable targets in the coronary arteries. This patient definitely needs stat cardiac catheterization, along with an stat echocardiogram to identify other cardiac structural disease that might require treatment during bypass surgery (e.g. ventricular septal rupture, free wall rupture, mitral papillary muscle rupture, and endocarditis–which can present like this when a vegetation embolizes into a coronary artery).

    2) What is the utility of IABP in this case?
    -Intra-aortic balloon pump (IABP) or another circulatory support device should probably be put in at the end of the catheterization procedure, when you already have groin access from the arterial sheath you were using for the cath (and have ruled out absolute contraindications for IABP, including severe aortic insufficiency and aortic dissection)

    3) Our differential dx (for a short moment) included AO dissection. Is that reasonable? This looks like a Scarbossa-positive LBBB, STEMI equivalent. Is that a reasonable interpretation?

    Aortic dissection–with the dissection extending into the coronary artery and/or pericardium–is in the differential diagnosis in this case. Although it’s rare for Ao dissection to present this way, it’s crucial to prepare to diagnose it promptly in this case. The cath team should image the aorta with the catheter on their way up the aorta to the coronaries.

    Finally, I’d like to respectfully disagree with Siuf’s comment:
    “with all the talk about ABCs, the ekg is probably an “H”.”
    -IMHO, in a possibly cardiac case, the EKG is a top priority, especially in this case where a standard cardiac monitor would reveal a wide-complex tachycardia of uncertain etiology

    -Rob Siegel (a cardiologist at Jacobi) (who hopes to someday know as much cardiology at mattsilver74)

  • vshah

    I’d like to add to my comment above — that this forum is awesome. How often are we bringing new cases to the table? I could spend 10 hours reading articles and watching video lectures — but I’d rather just listen to the thoughts / opinions of those whom I’ve grown to trust / respect over the years. We should be going over interesting cases whenever possible! Glad to see everyone’s doing well…

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