What Happened?

A 68 year old male, with no significant medical history, presents to the local ED (non-PCI) with chest pain. He had been doing some gardening, when he suddenly felt chest discomfort (8/10), non-radiating with diaphoresis. His wife drove him to the ED. Once there, he was given ASA and NTG, and the following ECG was acquired:

His vitals were as follows:

  • HR:    104 and regular
  • BP:     118/68
  • RR:     20 and regular
  • Skin:   cool, pale and clammy
  • Lungs: clear bilaterally
  • SpO2:  99% on O2

After a short time, the patient was given another treatment and entered the following rhythm:


  • What do you think happened?
  • What is the rhythm?
  • What do you think they did next?


  • Brad J says:

    First rhythm looks to be sinus tach w/ 1st degree AV block and periods of a sinus pause/arrest. Inferior MI w/ posterior involvement.

    Second rhythm looks to be a repolarzation rhythm given the recent history. It looks like the ASA and nitro are starting to resolve the clot.

  • Brad J. says:

    I forgot to add, I’m pretty confident that he went to the cath lab after receiving heparin therapy.

  • Brad J. says:

    Doh! I meant reperfusion, not repolarzation. 

  • Crystal says:

    I’m gonna say accelerated junctional in the second as there are no p waves unless they are hidden still showing inferior mi it this was around here life flight would be called ASAP for this patient to get to a cath lab

  • Chee Yong Chuan says:

    Interesting tracings! Was cracking my head to figure out what had happened, not easy indeed. 
    68 year old male with acute onset chest pain, diaphoretic, given the standard treatment for suspected acute coronary syndrome. ECG shows:
    1) ? sinus rhythm, QRS complexes are not seen to be preceded by upright P waves. In leads where P waves are supposed to be clear and well defined(II,V1), they are no where to be seen
    2) Axis normal
    3) Narrow QRS complexes with regular R-R intercal at a rate of about 100bpm (not sure why  the machine states A.Fib. Looks quite regular to me
    Rythm: ? Accelerated junctional rhythm?
    4) Significant concave ST elevation seen over inferior leads(II,III,aVF) resembling tomb stone morphology with reciprocal changes over lead I and aVL.(3-4mm horizontal ST depression in lead aVL with T wave inversion. Subtle ST depression in lead I can also be appreciated
    5) Small Q waves over lead III and aVF if interpreted together, likely to be pathological
    6) There is also subtle ST elevation over in lead V5 and V6. ST segment looked steep in V5 while a convex STE is seen in V6. ST depression in aVR likely to be reciprocal changes of lateral leads
    7) 4-5mm horizontal ST depression over V1-V3 with poor R wave progression. Although R/S ratio<1, it is still highly suggestive of posterior MI
    8)QTc borderline prolonged favours ischemia/infarction
    In conclusion the first ECG likely to show: accelerated junctional rhythm with possible infero-latero-posterior MI, culprit artery wraparound LAD?
    ECG 2 on the other hand shows a few oddities 
    1) Dominant R wave in aVR. Can it be limb lead reversal? This feature is not seen in the first ECG
    2) No prominent P waves seen but QRS complexes exhibited R-R variation. Heart rate has slown down a little and I think I saw what likely to be fibrillatory waves in lead V1, II,aVF. New onset atrial fibrillation?
    3) If lead placement was not altered. Deep pathological Q waves are now seen more clearly over inferior leads(II,III,aVF).
    4) T waves are now tall and broad, suggestive of hyperactue T waves
    5) QTc now more prolonged as compared to ECG 1 (507ms)
    Impression: Progressive elovution of infarction as Q waves and hyperactue T wave are more prominent. New onset A.Fib?

    Please enlighten

  • adam says:

    First is inferior mi with 1st deg av block along with LBBB.
    Second is still showing the infarct but it is being resolved by collateral circulation and nitro

  • DW says:

    Inferior STEMI with likely concomitant RV involvement (tread VERY with Nitro, if at all here). Second rhythm is a reperfusion rhythm likely obtained after the administration of lyrics, and for which nothing should be done provided the patient remains stable.

  • Mel says:

    1.) Looks like sinus with a pause and a PJC toward the end, and 1st degree avb. RBBB. The ST seg and tachy rate are hiding the p waves. Id say pericarditis but the lateral leads (V5& V6) dont seem to be showing anything. At least from my cell phone. Its hard to rule out a higher heart block rather than a first degree (2nd type I). Inferior/posterior. Septal and Anterior reciprocal changes for sure.

    2.) That is a big difference than the first ecg. Im going to prob go with pericarditis. Just my 2 cents.

  • Paul says:

    Sinus rhythm with some dropped complexes (call it sinus arrhythmia if you want, either way…) presenting with inferior wall injury, and a 2nd EKG demonstrating AIVR as an apparent reperfusion rhythm. Continue treatment and get this patient into the cath lab for appropriate intervention/stabilization to include placement of transvenous pacing wire(s) until this rhythm corrects.

  • Mr T says:

    Ok. I have some concerns. First, why would you all be so quick to give nitro. If you give normal doses of nitro, you are likely to make things significantly worse. This pt is pre load dependent, nitro will decrease pre load!

    Also, there have been comments about nitro and ASA resolving clots. This doesn’t happen. Please re-read your pharmacology texts. Thank you, that is all.

  • Brooks Walsh says:

    I think Brad is saying that it's a reperfusion arrhythmia, and I agree. If you look at the second ECG, you can see that the last QRS in aVF and the first complex in V3 are almost identical to those in the first tracing.
    Nice case!

  • Joshua Barber says:

    Where is the right sides ECG? Who give nitro to someone with inferior wall MI, and a pressure of 118, without obtaining information about the right ventricle…. Thoughts?

  • Alina says:

    Inferior STEMI, thrombolysis (eg. tenecteplase), reperfusion rhythm.

  • Danny says:

    I was not aware that ASA and Nitro resolve clots. I would be hesitant to give Nitro to this patient without first obtaining at least an RV4.  Nothing should be done providing the patient remain stable? This patient is having what looks to be a large Inferoposterior MI, possibly with RVI as well. They need to transported to a facility with PCI capabilities.  I see many different opinions on the rhythms that are presented in both of the EKGs. I am honestly not sure what the actual rhythm is or what would cause such a drastic change.  I do not see any obvious P waves, so I would hesitate to call it sinus. Educate me?!  Great post as usual.

  • Arnel C. says:

    ECG #1 – AF, STE III>II, STD aVL >I, STD V1-V4, STD V3/STE III( ~1), prominent S than R aVL
    Inferior wall MI, RCA culprit artery.
    ECG #2 – Regularized AF, complete heart block with ventricular escape rhythm vs AIVR due to AVN involvement of the RCA. Pace

  • Arnel C. says:

    ECG 1 correction (rhythm)- SR, 1st degree HB, atypical wenckebach or long cycle wenckebach

  • Eric says:

    How are any of you diagnosing posterior involvement without a 15 lead? It cant be done, yet people are doing it…

  • adam says:

    Noone said nitro resolves clots, it causes vaso dilation allowing circulation to pass clots. As for ASA I have no idea as we don’t use it in the UK. Posterior mi cannot be diagnosed by a 12 lead only posterior leads can accurately diagnose posterior mi. Reperfusion w.ould only occur if thrombolytics were administered or ppci.

  • Robert says:

    AFibb w/ RVR (irregular w/ hr > 100)
    Inferior Wall MI, Probable RVI (ST Elevations in inferior leads w/ st elevation in lead III exceeding that of lead II)
    Posterior Wall MI (Net positive R waves in lead V2, V3 w/ st depression)

  • Robert says:

    2nd 12 lead:

    AIVR (A common rhythm after reperfusion therapy) 
    Side note: AIVR should never coincide w/ ventricular tachycardia. Whenever a heart rate is less than 120 that is wide, regular, with absent p waves, always assume it's not VTach. Differential diagnosis for HR < 120 include AIVR and Hyperkalemia.

  • Kit says:

    Clear inferior MI and possibly posterior involvement. You mention that this is not a facility with the ability to cath, I suspect the patient was thrombolysed and the second ECG is post thrombolytic. Could this be a reperfusion arrhythmia?

  • Kit says:

    Also, Adam ASA is the abbreviation used for aspirin.

  • Danny says:

    While I agree that you truly cannot diagnose posterior involvement without a 15 lead, there are certainly clues that would make one HIGHLY suspicious. Depression in V1-V3 is much more likely to be posterior STEMI vs. ischemia. Also, there have been studies that show that subendocardial ischemia will not localize on an ekg. Either way, we are nitpicking here. It wouldn’t be that difficult to do a 15 lead to confirm.

  • Nick Adams says:

    First one shows a junctional tachycardia with 2 pauses noted with a sinus escape and prolonged PRI of 280ms.
    ST elevation in leads II, III, and aVF. Reciprocal ST depression in leads aVL, V1 – V3. The ST depression is reciprocal to Posterior wall involment from a right dominant patient. Meaning his RCA is what supplies the PDA. A right sided ECG is in order prior to NTG administration. Pt’s B/P is ok at the moment, but may drop agressively if this is a RVMI. The evidence is there that indicates the pt’s SA node is affected (Junctional rhythm), and the pt is cool, pale and clammy. All of which is indicative of a proximal RCA occlusion. This patient needs at least 2 IV’s with 18g ir better and 2 1,000 mL’s NS bags hung and ready to preload this patient again.

    Second 12 lead shows AIVR diagnosed the same as you would with VT. ERAD with a positive complex in V1 is 99% specific for VT. Being that the rate is below 100 bpm, I would therefore call this AIVR. V1 also has a positive morphology and a Fireman’s hat appearence, and an absense of PW’s. This could be due to reperfusion, but doubtful being that the patient did not receive Thrombolytics. Coronary vasodilation is minimal at best with NTG alone. As long as the pt is tolerating this rhythm, I would hold off on antidysrhythmics and transport the pt to a PCI center. Aintidysrhythmic’s are contraindicated in a patient that is displaying a bifascicular block or greater. EKG #1 shows a normal axis and the QRS duration is less then 120ms, so a bifasicular block is not suspected. The patient’s sinus rhythm did become bradycardic enough to cause the junction to take over as the primary pacemaker @ just over 100 bpm, and then the junction failed which caused the ventricles to take over in the 90’s. Reguardless, I would be very causcious in taking away what he still has. If I did decided to give an antidysrhythmic, I’d have the Defib/Pacer pads in place and at the ready, and probably not give the bolus, but start the drip. You don’t always have to give the bolus whether it be Lidocaine or Amiodarone. Reguardless, this patient needs reperfusion at a PCI center……..that’s the treatment.

  • Nick Adams says:

    @ ERIC – – People are diagnosing a posterior MI based on the fact that there is ST depression in the AnteroSeptal leads, which is caused by of 2 things.  #1 – AnteroSeptal ischemia, or #2 Receprocal ST depression of posterior elevation.  Given that the posterior wall is fed by the RCA in the majority of the population, the LCX in others with very few being fed by both.  It is safe to assume that the posterior wall is being fed by the RCA in this patient.  The patient either has a mid RCA occlusion that is effecting the inferior and posterior walls, or less likely the patient may be having multiple occlusions.  To really get the whole picture of what is going on and narrow down where the block is, a 15 lead ekg should be done.
    Someone also mentioned that lead III's ST elevation is greater then lead II's.  While that is an indication that this may be a proximal RCA occlusion, I wouldn't bet my license on that fact.  Instead, I would verify with a 15 lead EKG or at least a V4R.
    Oh, and BTW, I did see someone diagnose A-fib.  This pt is not in A-fib.  It's a junctional rhythm with 2 pauses which escaped with a sinus beat.  The PRI is prolonged, so I'm not 100% sure these sinuse beats actually caused a reaction.  The rhythm did return to an accelerated junctional rhythm though.
    My analysis of the AIVR is only to prove that the second 12-Lead is ventricular in nature.  I used the rules of "calling VT" from other VT mimicers to prove that this is ventricular in nature, and not a RBBB junctional type aberrantly conducted rhythm.  Because the rate is below 100 bpm, or in ost cases below 120, this cannot be VT………..so it's AIVR.  Either way, it does originat in the ventricles, and is not using the normal electrical pathways.  Did the junction finally crap the bed?…….maybe.  It is not because of reperfusion…..ASA will not do that because it's an antiplatelet, not a thrombolytic.  Just as NTG does not throbolyse clot formation, and has minimal coronary dilatory effects.  I think the second strip is purely a worsening of the pt's condition.

  • Mel says:

    Nick I agree that the 2nd strip is a worsening rhythm… however I am not convinced this is junctional in nature.

  • Billy Bob says:

    First is a fib, IWMI STE >3 than 2 suggestive for RVI and ST depression in V1-3 suggestive of posterior wall involvement; given RCA supplies both in most people Id say thats what it is (confirm with 15 lead/V4R if we have time). Also notice a p wave at the end 1st degree block. And Ive never heard of nitro and ASA dissolving a clot let alone in that time frame (anythings possible but HIGHLY UNLIKELY). As mentioned before we don't want to kill his preload with nitro so bolus bolus bolus or be CAREFUL. 2nd rhythm appears to an accelerated junctional however with the same in it except now we have an upright V1 and AVR with ERAD and prolonged QT I think V tach is following very closely. Be ready to code him and get him to PCI!!!

  • Billy Bob says:

    Correction I think that 2nd rhythm is an accelerated IVR

  • Billy Bob says:

    And my answer is (sorry for making 3 posts about this) I think that the nitro in conjunction with the huge multi area MI may have decreased his preload to the point of making the AV node ischemic and knocking it out giving us the resulting rhythm/situation.

  • Billy Bob says:

    LOL one more! I noticed above it says the pt received "another treatment," so it is possible that this is a reperfusion rhythm but only if he did in fact receive thrombolytics!!

  • h dawg says:

    He got
    A: thrombolytics
    B: NTG bolus followed by a NTG drip
    C: holy water
    and the rhythm is indeed AIVR.

  • h dawg says:

    He could have coded too, went into v-tach or something and this is s/p cardioversion.

  • Prehospital RN says:

    I would say the second EKG shows an accelerated idioventricular rhythm … likely due to reperfusion (were thrombolytics the “additional treatment?”) … if this is the case it requires close monitoring, but if hemodynamically stable no specific treatment is necessary and will probably resolve on its own.

  • Dustin says:

    1st 12-lead is A-fib with a tachycardic rhythm.  With the ST elevation in II,III and AVF along with depression in the anterior leads this is an acute inferior and posterior MI.  15 lead would be nice and minimum of a right sided 12 lead.  NTG should be used with caution.  The QRS is not long enough to be a bundle branch block.  
    The 2nd 12 lead is a reprofusion rhythm after the administration of a thrombolytic.  It is a slow VT with a negative QRS in V6 and ERAD.  Also notched downstroke on QRS in V1.  I wouldn't initially treat the rhythm if  the condition allowed.  Patient still needs to be transported to a PCI.

  • Danny says:

    So some people do not believe that this patient needs a PCI? I do not believe that this will resolve on its own… Scary.

  • Jason says:

    1st ECG:  Sinus tachycardia (rate about 115/min) with acute inferior infarction complicated by Type I A-V block manifest in the form of a prolonged 13:12 Wenckebach period; one ventricular premature beat (18th beat) presumably originating from the left ventricle (LV).
    2nd ECG:  Accelerated idioventricular rhythm (rate about 91/min) presumably originating from the LV.  The AIVR is probably dissociated from a sinus mechanism (unknown rate).  The 8th and 10th beats are probably ventricular captures.

  • Nick Adams says:

    OK ….OK  JASON, You got me….lol.  Good job Brother.  After a closer look in V2 and V3, the is what appears to be a very flattened upward concaved sinuse beat before every QRS complex.  This, I believe, is a preceding PW in front of every QRS.  So the first strip may very well be a ST with a 1st degree AVB.  If you look at the V1 at the bottom of the strip and really look at the ST segments and the inverted TW's, you can see a subtle change in the morphology of the TW's and the last ST-TW is more prominent like this may have been caused by a PW that could not conduct.  End result:  ST with a 1st degree AVB with intermittent episodes of Wenkiebach.
    The second strip is AIVR still…..lol

  • Sammy says:

    First is Wenkebach with very long PQ (buried in previous depol/repol somewhere), it's not sinus and it's not AVB 1, you won't get dropped beats and sudden obvious p-waves post-drop with these. And inferior/posterior STEMI of course.
    Second is AIRV (don't have to be but this is ad typical reperfusion arythmia and this guy/gal should've been in the cathlab by now).
    Keep it brief guys, long interpretations aren't always better!

  • Dustin says:

    Don't really see the Wenkebach in the first 12 lead…  

  • Robert says:

    Nick/Jason, nice eyes on the 1st 12 lead.
    Interested to see what the rhythm is. It would be nice to have a long rhythm strip of leads v2/v3. Hard to tell if it's just a U wave after the T wave, or a subtle P wave. Definately different morphology than the P wave in the dropped beats/escape beat, so I'd be hard pressed to think it's a heart block, and i've never heard of wenkeback at 13:12.
    Differential Diagnosis? Well, it's regular, narrow complex, > 100/min, presence of p waves in the dropped/escape beat, possible p wave vs u wave in lead v2/v3. I'm gonna go w/ Nicks answer, Junctional Tach w/ sinus escape beats.

  • downward displacement of pacemaker

  • Christopher says:

    I think the first ECG is subtly Wenckebach, only due to the P-wave seen towards the right end of the strip and the slight shortening of the R-R between the first three complexes of the long run.
    A much longer strip is needed to confirm that this is 2AVB Type I versus SA Block considering the gap at the end of the strip is 2X the preceeding R-R.
    Regardless: ischemia in an inferior pattern with gaps in the strip? SA or AV node impairment!

  • Mel says:

    1. Sinus Tach with occasional exit block… Major elevation in II III aVF with reciprical changes in septal leads = 15 lead should have been done…. to double check before giving nitro… Anterior leads are good so start him on 2 to 4 lpm O2, start NS and give 324mg ASA orally. (nitro dependent on 15 lead in this case) If V4R had shown depression or elevation I'm gonna bolus 500ml NS before starting Nitro therapy. Im already headed to a cath lab facility
    2. Extreme Right Axis deviation (ventricular origin) but the rhythm looks like multifocal PVCs to me and I believe the BBB is a Left BBB kinda hard for me to make it out becuase I am not seeing any dicernable p waves on the second one at all (which also means I have no idea where you guys are seeing 1 or secound degree blocks because I just dont see those there at all)
    IMO they made this guy worst by giving NITRO because of the Inferior wall MI without confirming the aVR (as you can see with the ERAD that the nitro made it worst PLUS Nitro is contraindicated in patients who are tachycardic)
    Priority would have been O2, fluids, ASA, rapid xport to cath lab… but a 15 lead should have been done prior to Nitor in in this case

  • forsythfd922 says:

    Mainly like reading all of these comments/opinions on here, but have a few questions regarding terminology and such….
    1)  What is an "AIVR"?  Is it just as plain as it sounds, an accelerated version of an idioventricular rhythm?  I either never heard this term, or have forgotten it, lol.
    2)  Have never seen a tachycardia contraindication for NTG, although it does seem common sense if the patient is preload dependent on a profound tachy rhythm.  I personally wouldn't call 104 preload dependent…..I would probably withhold it if the rhythm was greater than or equal 120-ish, though.  Since, in my mind, you drop the preload here, the rhythm increases
    3)  Even with RVI, isn't this a relative contraindication to NTG?  You should still give it, permitting the BP is in the >110-100 systolic, from what I understand.  Reason being is that I have mainly seen for is that the 1st NTG typically drops the SBP up to 30 points, the subsequent doses not as much.  This drop is the reason I like the paste better than the tablets….you can take some of the paste back…
    4) Whoever identified ASA as a PAI (Platelet Aggregation Inhibitor; also anti-platelet) was correct, it doesn't  "-lyse" anything.  Neither does NTG.  They don't necessarily fix the clot, just help to prevent it from getting worse.

  • Christopher says:

    You're correct, AIVR is "accelerated idioventricular rhythm". This is any ventricular rhythm faster than 40 but slower than ~120. VT is 120-130+ ish… 🙂

  • Danny says:

    Forsythfd922… Interesting that you mention a contraindication for nitro with Tachycardia.. I have seen it published in one place.. The 2010 ECC Guidelines book. It states that nitro is contraindicated for bradycardia under 50, tachycardia without presence of heart failure, and RVI. I would also like to see some clarification and reasoning behind this! : )

  • james says:

    This really looks like junctional tach w/ complete block and the noted elevation in INF leads and reciprocal depression.Need a longer strip.
    The second has such marked elevation that I would be hard pressed to call AIVR or accellerated junctional.I would also not bet the farm against it being a progression of the infarction vs. reperfusion.Cathlab's job to determine that.

  • Dan says:

    i cant see any p waves preceding QRS complexes in the first ecg so i dont see how there is a first degree AV block. anyway, inferoposterior infarct with AV dissociation, possibly third degree av block. The pwaves are contracting during ventricular contracting hence the notching on the qrs complexes. The AV dissociation is likely to have been caused by infarction, and based on the size of elevation i would say that the pt has been ischemic for over 2 hours and infarction is well and truly occuring. The second rhythm is your AIVR caused by thrombolysis (tenectaplase, enoxaparin and clopidogrel) which is a completely normal response. i certainly would not be giving this guy nitrates, maybe some morphine at best. i would want a V4R to confirm right sided involvement, id say this guy has an occlusion mid to proximal RCA…. @Danny, nitrates are contraindicated where im from for rates over 150 as rates this high are not getting effective strokevolume/Cardiac output, giving GTN will only reduce it further. 

  • ScottT says:

    Possibly right ventricular involvement. Good idea to get a right sided ECG or atleast V4R. Hold on nitro and morphine until confirmed that it isn't preload dependent. But we all know, ASA and cath lab are about all that matters.

  • Hilary says:

    Inferior STEMI with reciprocal changes. Also appears there is an AV block. Possible right ventricular involvement but would need a V4R tracing to support that theory! I'd be interested to hear the outcome of this patient!

  • Dan says:

    To me the second 12 lead does not show improvement but worsening. The nitro probably decreased cardiac output causing increased work for the alreadydy injured heart causing a worsening of the infarct and creating a bundle branch block. Id like to see a second set of vitals that go with the second 12 lead.

  • GeorgN says:

    The first ECG is an abvious inferoposterior STEMI. I guess the treatment was some kind of fibrinolytic therapy. The second ECG shows AIVR as a sign of reperfusion.

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