Respiratory distress, chest pain, right bundle branch block, and posterior STEMI

EMS is dispatched to a 50 year old male in respiratory distress. En route, dispatch advises that the chief complaint is actually chest pain.

On arrival, the patient is found lying supine on the floor just inside the front door to his house. He is cold to the touch and pale but his skin is not diaphoretic. He denies falling and the head is atraumatic.

He appears to be mildly short of breath and admits that he is having chest pain.

  • Onset: 3-4 hours ago while walking
  • Provoke: Nothing makes the pain better or worse
  • Quality: He is unable to describe the pain (some language barrier)
  • Radiate: The pain radiates down both arms
  • Severity: The patient gives the pain a 10/10
  • Time: No prior episodes although he does state the he was recently diagnosed with anxiety and is scheduled for a “cardiac exam”

He denies nausea or vomiting.

Vital signs are assessed.

  • RR: 24
  • HR: 70
  • NIBP: 80/60
  • SpO2: 92% on room air

Auscultation of the chest reveals bilateral crackles.

A 12-lead ECG is obtained.

2010_01_08_A_wmSinus rhythm with a rate of 70. There is right bundle branch block (QRS duration ≥ 120 ms, rSR’ in lead V1, slurred S in lead I). There is an inverted T-wave in lead aVL which is nonspecific. However, the deep “down-up” ST-segment depression in leads V3 and V4 is suggestive of acute posterior STEMI.

The patient and his family request to be transported to the local (non-PCI) community hospital.

Although the 12-lead ECG does not meet the treating paramedic’s criteria for a Code STEMI he persuades the patient to be transported to the PCI-hospital which is located across town.

He intends to obtain a 12-lead ECG with posterior leads V7-V9 once the patient is loaded in back of the ambulance. He doesn’t get the opportunity because the patient goes into ventricular fibrillation. A precordial thump is not successful.

Chest compressions are initiated while defibrillation pads are placed and the monitor is charged. A shock is delivered at 150 J. After 1 minute of post-shock compressions the patient regains consciousness. He remains in sinus rhythm for the remainder of the transport.

An additional 12-lead ECG is obtained post-arrest.

2010_01_08_B_wmThere is new ST-segment elevation in lead III and reciprocal ST-segment depression in leads I and aVL. There is new “down-up” ST-segment depression in lead V2.


The patient is taken directly to the cardiac cath lab on arrival at the receiving PCI-hospital

The angiogram reveals a near-total occlusion of the left main coronary artery limiting flow to both the left anterior descending (LAD) and circumflex (LCX) arteries.

They are unable to stent the lesion. A balloon pump is placed and the patient is referred to a cardiothoracic surgeon for CABG.

Updated 03/09/2016


  • Anonymous says:

    Posterior leads? History sounds a bit AMI-ish, and localized ST-depression in anterior leads could very well be reciprocal changes.Tor

  • Tom B says:

    Tor -Great minds think alike! That's the first thing I thought of when I saw this ECG.Thanks for the comment!Tom

  • Tony D says:

    I was thinking same, perhaps the depressions are really reciprocal changes to posterior MILooks like cardiogenic shock, hold off nitro, perhaps try a fluid challenge with 250 – 5O0 ml of ns if BP does not come up, go with dopamine

  • Kevin M says:

    I want to know what med control thinks, I agree with the bolus of 200mL, but dopamine with a systolic of 80? If it gets to around 70 then heck yeah…

  • Tom B says:

    Tony D. and Kevin M. -Definitely not a decision to be taken lightly! You have to weigh the dangers of shock (poor perfusion) against the dangers of increased myocardial oxygen demand (worsening ischemia) in the presence of a possible STEMI.It's a judgment call.Tom

  • Tom B says:

    Let's talk about risk! Does this patient belong at the local non-PCI hospital? Why or why not?Tom

  • Squeezey says:

    Was wondering what the p wave like bump after the QRS in lead III is?

  • Christopher says:

    Squeezy: if you keep in mind that this guy's complexes have RBBB morphology, then it could be reasoned that the bump is part of the QRS complex (Rsr' perhaps).

  • Bob Jester says:

    8 replies and not one person answered you request for our impression with " I'm sorry my training is in medicine, I don't do impressions" I am disappointed.Back to the matter at hand. I agree with the others that this 12 lead is highly suggestive for posterior MI, I'm wondering if the hypotension isn't from RV infarct,b/c this patients RV and posterior wall are perfused (or not in this case) by the same RCA.This patient in my opinion needs a PCI capable facility in the worst way, and I would use all my powers of persuasion to get them to agree to transport to the regional PCI hospital. I would involve my base doc, any neighbors or friends I could find. I have, on one occasion, sicced a priest on a patient who was on the verge of making a bad decision.

  • Squeezey says:

    Thanks for that C. Watford. I'm still learning ecgs at uni and trying to get an understanding of all their abnormalities. Thanks for the help, I'll be sure to keep it in mind.

  • Hillis says:

    I would rather trasfer the patient to PCI.. The ECG shows RBBB with typical rSR in leads V1-2 the age determine is unkown, so it could be new right bundle branch block in the setting of acute anterior myocardial infarction. There is also very deep ST segment depression of more than 5 mm in the anterior leads which indicate critical injury or stenosis of LAD (left anterior descending coronary artery ).

  • Hillis says:

    I totally missed the diagnosis of posterior infarction !!. But we need V7, V8 and V9 to confirm the diagnosis, it is very hard to differentiate posterior infarction from anterior one in the absence of V7-9 !!. And is it possible to diagnose posterior infarction by ECG in the presence of RBBB and absence of V7,8,9 !!!!.. Am quite confused !!

  • Tom B says:

    Bob Jester – I, on the other hand, do fine impressions! One of my co-workers doesn't call me "the man of 1000 voices" for nothing! Siccing a priest on a patient is the funniest thing I've heard in a long time! :)Tom

  • Tom B says:

    Dr. Hillis – You raise an excellent point! We often think in terms of ST-elevation or new (or presumably new) LBBB.In reality, the FTT Collaborative Group found that AMI patients with new bundle branch block had the highest mortality. They did not specify right or left bundle branch block! So why the emphasis on LBBB? Probably because RBBB generally does not obscure the ST-segment the way that LBBB does.However, it's not always obvious whether a RBBB is old or new, and this case is a perfect example! We've also seen examples in previous case studies HERE and HEREPerhaps in certain circumstances (e.g., signs and symptoms of ACS and RBBB with severe T-wave abnormalities) we should treat RBBB exactly the same as presumably new LBBB!Thanks for the comment!Tom

  • Tom B says:

    Squeezey -I'm not ignoring you! It's just that C.Watford pointed you in the right direction! :)Tom

  • WindsorMedic says:

    I'm thinking the precordial lead's morphologies are more suggestive of ischemia or a possible posterior STEMI, but I wouldn't completely rule out a subendocardial NSTEMI – especially given the quality of 12-leads in the field. That being said, the pt is hypotensive, with obvious circulatory issues, and chest pain. He would definitely go to a PCI capable facility. Probably even more important with a slightly ambiguous 12-lead. This is a condition probably better diagnosed, and treated, by a cardiologist than an ED physician. No disrespect intended by saying that, it is simply a case of having the person most highly trained in the area of concern involved in the diagnosis and treatment of the pt as quickly as possible. If it turns out to be something less significant than the pt's presentation suggests, there is certainly no harm done.

  • Tom B says:

    Windsor Medic -Just out of curiosity, what do you mean by "the quality of 12-leads in the field"? Does this ECG show excellent data quality?Also, did you see the update to the case? The patient has experienced cardiac arrest.It doesn't get more significant than that, does it?Tom

  • Jesse says:

    Okay, Tom et al. Question. With an IWMI, we know that ST elevation greater in lead III than lead II is indicative of RV infarction. We also know that the RCA supplies both the inferior and posterior LV walls, and the RV, yes? So in the uncommon (but current) case of isolated posterior STEMI, how do we deduce RV involvement? Is LV inferior involvement necessary? Will there be isolated lead III ST elevation? Or is an occluded RCA that affects the LV posterior wall capable of affecting the right ventricle while bypassing the LV inferior wall entirely?

  • Tom B says:

    Jesse – The best we can say based on this 12-lead ECG is that we suspected posterior involvement, but we still have to contend with the possibility this is a "new" RBBB.Regardless, it's true that in most patients the RCA supplies the right atrium, right ventricle, and inferior wall of the left ventricle.Sometimes the RCA also supplies the posterior wall of the left ventricle. That's why you'll often see ST-depression in the right precordial leads associated with acute inferior STEMI.But the posterior wall of the left ventricle can also be supplied by the LCX, or it can have a dual blood supply. It depends on whether or not the patient is right or left dominant.So, it's true that with acute inferior STEMI, when STE in lead III > STE in lead II, it suggests a proximal RCA (right ventricular infarction) but not all patients have the same coronary anatomy.With an isolated posterior STEMI you can have a distal occlusion of the RCA (which could be the posterior descending artery which branches off the RCA) or you could have a LCX occlusion that is isolated to the posterior wall of the left ventricle.Sometimes it's hard to know for sure, and I've been very surprised by angiograms!Tom

  • SoCal Medic says:

    Jesse,You are correct that the Posterior Wall is supplied by the RCA in part, but reality is it is a branch supplied by the RCA that hits the Posterior Wall. An occlusion in that branch will cause the isolated Posterior Wall Infarction and can affect the Right Ventricle without affecting the Inferior Wall of the Left Ventricle. Tim Phalen's book published by Mosby has the artery called the Posterior Descending Artery where the Inferior Wall is supplied by the Right Marginal Artery, both branches from the RCA. Hope that helps. (sorry I could not post the pic, not quite at Tom's level of computer genius.)

  • SoCal Medic says:

    Looks like I am a day late and a dollar short, lol.

  • Tom B says:

    SoCal Medic – LOL! :) Don't worry, it's not computer genius! I just Google [blogger comment hyperlink] every time I need the code! Tom

  • Jesse says:

    "An occlusion in that branch will cause the isolated Posterior Wall Infarction and can affect the Right Ventricle without affecting the Inferior Wall of the Left Ventricle."The reciprocal changes of the PWMI are commonly visible in V1-V3 (in this case, V2-V4 ish). Is there any way that you know of to confirm RV involvement in this kind of infarction through ECG use?Thank you both kindly for your responses!

  • SoCal Medic says:

    Although the blood pressure and heart rate will make you suspect RVI, you can also take the V leads and place them on the same anatomical location except on the right chest. Typically in IWMI, you move V4 to the right chest, some people move more than just V4, really comes down to preference at that point I feel. Just remember, the 12 Lead knows not what you have done and in documentation of such a change, to write a big "R" next to any lead you move so that the Cardiologist and ED physician knows what you have done.

  • Shaggy says:

    So, are we to assume this RBBB is new based upon the evidence of the clinical picture and the Posterior MI? I am still a little groggy as to the etiology of the hypotension here, if we can in fact actually make that deduction here. Are we also looking at a generally ischemic heart, here?Our protocols would call for pressers in this case (Dopamine for us), but I do see the concern for increasing myocardial O2 demand. However, I am not sure if fluid boluses are such a great idea either in the presence of pulmonary edema. Also, would this patient be a good candidate for induced hypothermia?

  • Nick says:

    Hey Tom another great post, really interesting and I am learning alot.Just two things I want to ask about.The computer statement says LPFB however i dont see any axis deviation? I thought LPFB had RAD? (all new to me so i use the cheat way at do you think lead III looks like an osborn wave??I know it isn't with the pts story however that could make for an interesting post!!Keep up the good work! I have my 12 lead exam for STEMI recognition in two weeks and thanks to this site I should dominate it 😛

  • You just became my new best friend! 12 lead is one of my weaker points and this post has given me a little to chew on today. Not sure what PCI is, but I'm definatly calling a heart alert with this one.Glad I stumbled onto this blog.

  • Tom B says:

    Jesse – Sure! As SoCal mentioned you can do a right sided ECG and look at the RV directly.On the other hand, you would generally expect clear breath sounds with RV infarction! Hypotension and rales suggests acute left-sided heart failure! Tom

  • Tom B says:

    Shaggy – I do think we should consider this RBBB to be "new" and treat this as an acute STEMI! Even without the posterior leads showing ST-elevation and the (possibly new) RBBB, the patient is now S/P cardiac arrest and needs to be emergently cathed.I think you've answered your own question about the hypotension. If you won't give a fluid bolus because of the rales, then it's cardiogenic shock! Right?The patient is not a candidate for induced hypothermia because he regained consciousness!Tom

  • Tom B says:

    Nick – RBBB is funny when it comees to axis deviation in the frontal plane.Often RBBB shows an indeterminate axis. But a lot depends on whether or not you measure the amplitude of the QRS complex above and below the isoelectric line or you consider the area of the waves above and below the isoelectric line.For example, in this case lead I looks pretty much equiphasic. However, the R-wave is "skinny" and the S-wave is "fat". The area of the S-wave is far greater than the area of the R-wave, so some would consider this complex to be negatively deflected (electrically speaking).I would not personally consider this to be an obvious bifascicular block (RBBB/LPFB). It may be, but I wouldn't call it that based on this ECG. I've seen too many RBBBs that have a fat S-wave in lead I.As for axis, why not learn how to calculate it correctly? It's not that hard and it's strangely satisfying! You can take my tutorial on axis deviation HERE. I also include the "cheat" methods.I do see the wave at the terminal end of the QRS complex in lead III that you're talking about, but I think that's part of the QRS complex. In fact, I think it was probably part of the S-wave that was "picked up" by J-point elevation secondary to acute injury.You'll notice this "wave" is higher in the second ECG than in the first ECG.Good luck with your STEMI exam!Tom

  • Tom B says:

    The Gate Keeper – Thanks for the comment! It looks like your blog is off to a great start.PCI stands for percutaneous coronary intervention (e.g., angioplasty).Hopefully that's what happens to the patient after you call the "heart alert"! :)Tom

  • Shaggy says:

    The patient is not a candidate for induced hypothermia because he regained consciousness!Oops. I overlooked that one.My question though was if this patient had NOT gone into cardiac arrest and all we had was the initial clinical presentation and 12 lead, should we be concerned about the RBBB as considered new? Without old EKGs, I often wondered when we should be suspicious of 'new' BBBs.This is a good one by the way. This must have been a good medic crew as well.

  • Tom B says:

    Shaggy -We can use Sgarbossa's criteria for LBBB (preferably the modified form that takes into account the size of the QRS complex).RBBB typically isn't a problem because ST-elevation is not a normal finding with RBBB.This case is interesting because there's a significant ST/T wave abnormality but it's not associated with ST-elevation, at least not on the standard 12-lead ECG.With the chief complaint, the ST/T wave abnormality, changes on serially obtained ECGs, and signs of cardiogenic shock, I'd bypass the local non-PCI center for a STEMI center.The cardiac arrest removed any doubt (if there was any).I agree, this was a very interesting case! One of the coolest ECGs I've seen in a long time. The crew did a great job.Tom

  • MEDH says:

    Was the patient given aspirin and nitro?

  • aVR aVr aVR aVR. 
    Prediction of acute left main coronary artery obstruction by 12-lead electrocardiography. ST segment elevation in lead aVR with less ST segement elevation in lead V1. Yamaji et al. 

  • Justin says:

    I hope not on the nitro MEDH – too hypotensive. I think the call to go to PCI was very important for this case. We have to remember that STEMI are inclusion criterion, but are not sensitive to all AMIs. I'm not really experienced in prehospital but I think s/s cardiogenic shock and extreme chest pain should justify consult by an interventional cardiologist without the 12 lead (which is of course kindof scary looking). 
    I'd like to hear the outcome post CABG as well. While it cannot be said that the IABP is more effective than inotropic and/or vasopressor therapy ( they don't hurt either. Furthermore I think in many areas there would be huge advantage in being at a primary PCI facility (even though no intervention was performed) in transition to difinitive care (surgury) – probably less time under medical management than a non-PCI facility.

  • Kyle says:

    It appears he’s also got an osborne wave in the 2nd 12 lead… Very ominous! Good call on the medics side for PCI transport. Although thrombolysis might have been a good choice if available. It’s obvious this pt is in carcinogenic shock and the use of pressor support is warranted but like stated above it’s benefit vs risk. If there are signs of end organ perfusion than yup. If not I would be cautious. Never hurts to call and see what another brain thinks. If you carry levo might be a better option… Dopamine at moderate doses will increase 02 demand but at renal and low dosing not nearly as much so it might be a safe attempt. Could be a good discussion here

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