Sometimes activating a “Code” type process can be a judgment call that not’s so straightforward because of the presence of features outside of the standard activation criteria. What call would you have made with this patient?
A 70 year old man is brought to the ED by ambulance at 0500 with one hour of non-radiating “heavy” central chest pain. His past history comprises IHD (graft to LAD 5 years earlier) and cerebrovascular disease (TIAs) He is anticoagulated with Warfarin for the latter, and is otherwise well and independent for ADLS. En route he has received oxygen via Hudson mask, sublingual nitrates and intranasal Fentanyl, but despite this has unrelieved chest pain. His vital signs are normal on arrival and there are no previous ECGs immediately to hand.
Describe and interpret his ECG, then outline the actions you would take thereafter.In particular, would you activate a “Code STEMI” call to bring in your interventional cardiologist and catheterisation laboratory staff at 0500 for this patient?
The ECG shows sinus bradycardia at 60/min, with significant widespread ST depression anteriorly (V2-6), laterally (I and aVL) and inferiorly (II), with ST elevation in aVR. There is RBBB and LAD (c/w LAFB), constituting bifascicular block. (PR interval is borderline normal at 200 msec) Pathological Q waves in I and aVL, and poor R wave progression laterally may represent previous infarction in this vascular territory. There is a single atrial ectopic, and the QT is normal at 440 msec.
In this context of previous revascularisation, typical cardiac pain, and the ECG findings above, the provisional diagnosis is acute coronary syndrome. The widespread ST depression and ST elevation in aVR may signal proximal left coronary artery occlusion. There are important differentials to consider of course (aortic dissection, PE, other cardiac, amongst many others) but further history, examination and investigation will help to rule these out.
My actions now
- Gather further history/previous ECG/ complete general examination
- Control pain with titrated IV opioid and GTN infusion
- Continue O2 administration (yes I know there are questions about this)
- Maintain monitoring and good supportive care
- Reassure and explain the situation to the patient
- Send routine blood tests (FBE, U+E, Trop, INR, Gp+hold)
- Order bedside portable CXR
- Hold off anti-platelet agents pending further data and cardiology consultation
- Keep nursing staff aware of plan, and prepared for urgent transfer
- Documentation of above
- Contact on call interventional cardiologist
The question of whether or not to immediately activate a cardiac interventional protocol is tricky here. Catheter lab activation criteria are divided into two broad streams – firstly where typical STEMI features are present and no contraindications exist, ED doctors or pre-hospital paramedics should initiate the process directly without seeking approval first, ensuring notification of relevant staff and administration of protocol based therapy. (“Code STEMI”) There are many systems/hospitals which use a process like this and significant reductions in time to reperfusion have been demonstrated. Here’s an example:
The alternative approach occurs in situations where there are atypical or complicating features necessitating a discretionary judgment call by consultation between the ED doctor and the interventional cardiologist.This took place with our patient and these are the factors that were weighed up in making the decision
- Good premorbid health status
- Clinical features most consistent with ACS, and ongoing pain
- Absence of typical STEMI criteria, but concerning widespread ST depression and ST elevation in aVR
- Pre-existing anticoagulation with Warfarin
- Difficult time of day (especially for staff on call who are to work that day)
The decision in this patient was to activate the lab immediately, so the patient was consented, Clopidogrel administered, and transfer occurred on arrival of lab staff. His study revealed 20% occlusion of left main, 50% occlusion of LAD, and widely patent circumflex and RCA vessels. His LIMA graft was patent, and there was only mild left ventricular dysfunction, so a medical approach to therapy was pursued. The initial arrival Troponin level was 55 (normal < 15) and peaked at 155 the following day, confirming a small ACS.
Lessons from this patient:
1. Many “protocols” are in fact guidelines that require significant, high level interpretation and decision making to optimise outcomes from their use. Remember when contacting on call staff during the night to be concise and focussed in describing abnormal data and its clinical context – there’s a lot going on in this ECG which isn’t easy to summarise, but still of high importance.
2. ST elevation in aVR may signify proximal left coronary artery occlusion and should prompt assertive investigation and management ( LITFL )
I would have still activated a Code STEMI in this case. The selling points for me are, 1) ongoing pain, 2) the widespread ST depression with elevation in aVR (prox LAD or LMCA disease worries me), 3) 5am doesn’t bother me -- if the service is available and its use is warranted then time of day should not play a role.
Go Ian!
Agreed, even if avr didn’t catch your eye, the general ugliness of the ekg plus sx would make you suspicious. How to avoid the pitfalls of “not STEMI, just depressions?” Remember that depressions don’t localize- but reciprocal changes tell you where the bad heart wall is- so look for the hidden STEMI in the leads that DON’T attract your eye. See ugly depressions? Start looking at other leads for frowny face curves and STE in leads with low voltage R waves (where it will be <2mm STE and not slap you in the face.)
Thanks ++ for your input Pik
Not sure I agree with you that “depressions don’t localise” in assessing ECG in ? ACS.
What do others readers think?
I believe what Pik is referring to is that ischemia itself does not produce localized ST-depressions, but rather a diffuse pattern. Localized patterns of ST-depression should have you looking for reciprocal ST-elevation (possibly subtle).
I agree with Pik though it would be best said that ST depression doesn’t localize subendocardial ischemia. ST depression should always prompt you to inspect reciprocal areas that might present even subtle ST elevation. Reciprocal changes do localize.
ST axis evaulation may represent the best way to approach the problem. Finding an ST axis that is directed anteriorly (STE in V1-V4), posteriorly (deepest STE depression in V1-V4 or STE V7-V9), inferiorly (STE I, III, aVF) or high laterally (often subtle STE aL) is suggestive of coronary occlusion. On the other hand, when STE axis is pointing superiorly (STE aVR) or rightward (isolated STE depression V3-V6) you are confronting with subendocardial ischemia. Not certain though how this works with bundle branch blocks.
Tough case, excellent managment. Yet I’m wondering does aVR STE and diffuse ST depression apply to a RBBB when suspecting a proximal coronary involvement?
There are 2 main points that I would consider:
1) We should expect an appropriate discordant repolarization.
2) Has anyone shown that aVR STE in the context of RBBB has the same prognostic value as with normal conduction? I recall Cheut-Kit Wong and colleagues failing to show an association between aVR STE and worse outcomes when considering patients with RBBB. Do you have any other references?
No, not aware of any further references on this
You’ve got two major players here: acute posterior infarction or, as others have said, left-main occlusion. Each has findings matching and conflicting with their classical presentations.
Leaning towards posterior infarct, you have a tall R-wave in the right precordials (in excess of that seen even in a typical RBBB) with maximal ST-depression in V2-V4 and upright T-waves. You also have ST-depression in aVL and a bit of elevation in III (but there’s a lot of artifact), where-as in LMCA occlusion you’ll usually see the opposite, but I also haven’t seen many of those tracings with concomitant RBBB. Posterior leads V7-9 should be performed, especially since a positive result should pretty much guarantee a timely cath.
In favor of LMCA occlusion, the ST-depression is not confined to just the right precordials, but rather spread across the majority of the ECG except for V1, III, and aVR. Well-developed Q-waves in I and aVL, along with tall R-waves in the right precordials and poor R-wave progression, make me think that perhaps this patient had an old postero-lateral MI. Without an old ECG or cath report this is just conjecture, however.
Here’s what I’d want to see. First, posterior leads. If they showed even 0.5mm of elevation then they would be confirmatory of posterior STEMI and the patient is indicated for immediate reperfusion. Still, because of the amount of ST-depression I’m seeing and the clear elevation in aVR, it would probably be prudent to hold clopidogrel because it doesn’t offer too much but will likely delay CABG should an LMCA lesion or multiple diseased vessels happen to be found on cath.
If posterior leads are negative, and I have a feeling they would be, it’s gotta be LMCA or proximal LAD disease until proven otherwise in cath. If you get any resistance from cards, this patient has chest pain refractory to medical management and an ischemic ECG, which is something that requires intervention last I checked. Unless the patient is clearly going to cath when they hit the door, I’m of the type that would prefer to hold opiates if possible (or at least minimize their dose) until they are accepted by cardiology so that ischemic pain is not masked and the accepting physician recognizes that there is still ongoing ischemia -- but this is a whole essay unto itself and not the focus of this comment.
162mg ASA, nitro drip titrated to BP or pain, [insert whatever meds cardiology would like, with the note above concerning clopidogrel in mind], and off to cath this patient should go.
So that’s my view of things, take it with a grain of salt as I’m the EMT bringing in the patients and not the one actually consulting cardiology and arranging for further care.
Fascinating case with a great lesson, and I’m still shocked he didn’t have an acute lesion. By the way, what kind of concentrations are your troponin levels reported in? ng/dL? In my part of the States they’re usually in mg/L, so seeing numbers like 55 and 155 thrown around as minor ACS gives ME chest pains.Thanks a ton for sharing.
Thanks for your thoughts Vince -- well considered. The units are ng/L here
There is an ST elevation in avr and widespread ST depressions, its possibly subendocardial ischemia in a guy with a tight left main. However the first thing that came to mind when i saw the ECG is that this is a posterior wall stemi. But even this diagnosis is complicated by the presence of an rbbb. All considered this man given his age and co morbidities and history needs to be cathed. I would not hesitate to wake up the cardiologist!
If in doubt call. My motto. At the very least you have a grumpy cardiologist, but ease of mind that you did the best thing for your patient.
Interesting case. Overall -- I agree with Vince D’s excellent commentary. I offer the following:
i) The CORRECT action was taken in this case -- even though no acute occlusion was found. In a patient with known coronary disease who presents with 1 hour of “heavy” chest pain and an ECG like this -- he NEEDS to be taken to the cath lab -- period -- end of story in my book (regardless of the hour of the night, and regardless of whatever the cath may show).
ii) As Vince states -- there are very deep Q waves in leads I,aVL -- which strongly suggests prior infarction. And -- we do NOT have a prior tracing. And -- the nature of the RBBB pattern that I see in lead V1 (with minimal ST change) -- and then that overly tall R wave in lead V2 just looks funny for something that is entirely acute …. That said -- one sees diffuse “ugly” ST depressions on this tracing with ST elevation in aVR and RBBB/LAHB -- all of which suggest the possibility of acute very proximal LAD occlusion.
iii) Diffuse ST depression DOES “localize” the lesion -- esp. in the context of ST elevation in aVR -- to the left main and/or very proximal LAD. In that context -- seeing RBBB (and also in this case LAHB) supports that anatomic location.
iv) I’ve developed a free on-line resource to assist in localization of the infarction (which also reviews likely conduction system damage to be seen). Please CHECK OUT at: https://www.kg-ekgpress.com/ecg_-_coronary_anatomy-mi_localization/
If in doubt I would call (everytime)