Cardiology Case 01

Here we go with what I hope will become a regular feature of the St. Emlyn’s blog – a cardiology case of the month.  This is something I’ve been running for short while in my department, so it makes great sense to start sharing the cases with a wider audience, in the interests of #FOAM.

I certainly can’t promise to live up to the genius of Amal Mattu or Steve Smith, but still I hope you’ll find this a worthwhile feature!  They’re the scribbles of a busy academic emergency physician so please bear with me if there are one or two typos.  The details will be based on real cases from my experience but, in the interests of confidentiality and after speaking with our data protection experts, key details will always be amended to ensure that no patients are identifiable. On to case 1…

A 45 year old man is brought to hospital by paramedics after being found by passers by sat on the roadside.  The paramedics can’t obtain a coherent history and score his GCS as 13/15 (E3V4 M6).  They perform an ECG and transport him to hospital.

On arrival the patient is agitated and non-compliant, has a blood pressure of 90/40, a GCS of 13 and 2mm equal and reactive pupils.  You elicit generalised abdominal tenderness with guarding.  The patient denies chest pain.  

The ECG is below…

Ambulance ECG

Case discussion

Here we have a patient with a diagnostic ECG for inferoposterior STEMI. There can be little doubt about that. We have up to 5mm ST elevation in leads III and aVF with deep reciprocal ST depression laterally and anterior ST depression with tall R waves suggesting posterior STEMI. The challenge in this case is the clinical presentation. The patient has no chest pain and there are things that we wouldn’t expect with a straightforward STEMI. On the one hand, we know that time is muscle and we don’t want to delay revascularisation, whether that be by thrombolysis or PCI. However, these treatments come with significant risks of causing major haemorrhage and that’s not something to be taken lightly when the presentation is not straightforward. We have to consider other pathology that we might be missing, including the possibility that the STEMI could even be secondary to another disease process with associated physiological stress. Indeed, plaque rupture is often secondary to an ‘acute risk factor’ causing surges in blood pressure. Perhaps that helps to explain why AMI is more common on a Monday! Due to their shape and typical position in the coronary circulation, coronary plaques may have to withstand pressures that are up to 7 times normal arterial wall stress. Add in to the mix the fact that unstable plaques will have eaten away at their own fibrous caps leaving only the single cell layer of endothelium between the lipid-rich, procoagulant core and the circulating blood, and you can see why surges in blood pressure might lead to plaque rupture. We also have to consider ‘STEMI mimics’ that could give us a false positive ECG. A number of conditions can do this, and it’s worth considering these in this patient. We may, for example, want a blood gas and a BM to exclude DKA. So, what shall we do on a practical level for the patient in this case? First, we need to explain that GCS. Before we can do that, it’s just not safe to administer powerful antiplatelets or thrombolytics. We could, for example, be seeing a subarachnoid haemorrhage complicated by STEMI here. So I think we need a cranial CT as a standard of care. That much is probably a given. What about the abdomen? There’s significant abdominal tenderness and guarding. The question is whether we need to be sufficiently worried about that to delay treatment of the STEMI. What are the primary diagnoses we need to consider? For sure, we need to exclude a AAA. Thrombolysing a patient with a leaking AAA probably isn’t going to go very well. Fortunately, in the era of ED ultrasound it’s relatively straightforward to all but exclude that diagnosis if we can visualise the whole aorta and document a diameter.


OK, so let’s say that we’ve got as far as obtaining a normal CT head, abdomen and aortogram. The blood gas shows a metabolic acidosis (base excess -6) and the patient’s condition remains unchanged. What should we do now? There are several options… (a) We could administer thrmobolysis. The patient is agitated, has a low GCS and is non-compliant with treatment. Undertaking an invasive procedure under these circumstances is not without risks. Thrombolysis is not as effective and has higher haemorrhagic risks – but perhaps the balance is tipped given the increased risks of a physical intervention in this particular situation. (b) We could treat the patient conservatively with antiplatelets and close observation in a Coronary Care Unit. (c) We could take the patient to the Cath Lab for primary PCI. This has the greatest efficacy but won’t be straightforward.


So what actually happens next? We opt for primary PCI, under benzodiazepine sedation. The RCA is occluded and therefore stented – with a door to balloon time of around 120 minutes. The peak troponin T is 2000ng/L. Our patient recovers uneventfully. This was a STEMI with no chest pain – unusual but it happens. What caused the drowsiness?  I won’t elaborate precisely, even in this essentially hypothetical case, but it could be explained by an acute psychosis, an overdose, a seizure or simply reduced cerebral perfusion.   As for the abdominal tenderness, well.. I just wanted to throw a little red herring in there for you! After all, in reality our patients don’t read the text books, do they?!

Hope you enjoyed the case.  This is the first, hopefully of many, so all feedback is very gratefully received.

Rick Body

If you liked this, you may also like the other cases in this series:

22 thoughts on “Cardiology Case 01”

  1. Nice catch! Really interesting and scary case. STE in lead III exceeding that on lead II suggests right AMI could be present as well, were right leads performed?

    1. Thanks Mattia, great point. The potential benefit of identifying the right sided infarct would be that we could more confidently challenge the patient with IV fluids to address the hypotension. In the case presented, the hypotension gradually corrected itself.

      Ordinarily, I would get RV leads though.


      1. Great post.

        A V4R lead shouldn’t have been too hard to get, but will the hypotension resolving I think you’re right that it wouldn’t have changed anything.

        If the patient had remained significantly hypotensive will altered mental state, would you have still gone to the scanner? Or go to the cath lab?
        I had a patient with a similar ECG once, GCS 10 or so after collapse with ROSC. Talked with the cardiologist who agreed to take straight to cath lab. Unfortunately the patient had a catastrophic intracerebral bleed, with no known risk factors.

        Most patients (unless they’re drug seeking perhaps) don’t read textbooks… perhaps they read blogs instead?


        PS. A patient with clozapine-induced myocarditis could potentially mimic this case I think – psychosis, small pupils, ECG changes mimicking STEMI…

      2. Great point Chris – thanks for the comment! And thanks for pointing out a great differential – clozapine-induced myocarditis. Not something I’ve ever treated but I gather it’s not so uncommon…

        The issue of CT transfers in hypotensive patients is a really important one. The textbook answer is no – hypotensive patients don’t go to CT! In practice, I’ll take hypotensive patients to CT in the right circumstances. So, if I believed that this patient’s hypotension was caused by the STEMI, I was doing all I could to address it but ultimately it wouldn’t settle without reperfusion, but I still needed to exclude important diagnoses prior to PCI, I’d go for CT – provided I judge the patient to be sufficiently stable.

        This is one big reason why the CT scanner is adjacent to Resus in the plan for our re-designed ED. If CT is an extension of Resus, it’s much less of a big deal to take sick patients there. Resuscitation continues to the point of scan – and you leave the patient for barely longer than you would for a portable x-ray.

        Thanks for visiting, Chris. We love what you do at – a seriously amazing resource.

        As for patients reading blogs, who knows – maybe that’s a new angle for #FOAM?!

    1. Hi Henry, great point. I’ve never actually seen a STEMI mimic with such focal inferior changes personally. However, the reference I linked to described a case of a patient in DKA with quite convincing inferior ST elevation and even some reciprocal ST depression – and they ruled out for AMI. Medicine never ceases to amaze, eh!

  2. Wow Rick you do know how to find them! Two thoughts…..why did you consider your pretest probability of dissecting aneurysm to be low – was it the absence of chest pain? And in terms of fluid challenging for the hypotension, what about bedside USS of IVC collapsibility?

    1. Hi Kirsty!

      I guess I got the impression of a low pre-test probability for dissection mainly from gestalt. Obviously it’s plausible that the patient could have had a dissection. But to get that he’d not only have had to dissect without pain, but dissect to include a coronary artery and also have a STEMI without pain. I felt it was unlikely clinically. What’s more, I pushed for PPCI over thrombolysis as you get an anatomical verification of the diagnosis prior to intervention.

      I guess 500ml initial challenge would have been safe, had we needed it, if we’d proven RV STEMI. USS guided fluid resuscitation is a good idea though – nice point!


  3. Don’t you just love working in Virchester! Cases like this seem to crop up all the time and I’m beginning to wonder if our patients don’t just fail to read textbooks, but rather consider it rather more sporting to write their own.

    I do like this case as the ECG is SO diagnostic that it can railroad people into thinking that only one diagnosis is possible, in this case that would have been a lucky guess, but you are absolutely right to get a full CT scan (essentially a trauma CT) to look for additional anatomical problems before embarking on thrombolysis/PCI.

    Did you consider a CT coronary angiogram as part of the work up here? I’m not sure of the technical aspects to say whether it would interfere with the other investigations but worth a thought.


    1. Hi Simon,

      The question about CT coronary angiography is a really good one – and it will make a great topic for future discussion on the St. Emlyn’s blog. There are many reasons to doubt whether CT coronary angiography would actually be useful in our population in Virchester, but that’s for another day.

      The use of multidetector CT (MDCT) has previously been described ( Essentially this is a ‘one stop shop’ designed to help rule out the big three in chest pain: ACS, PE and dissection. Forget your D-dimers, Wells scores, chest x-rays, TIMI scores… Just get an MDCT and you’re done. (?) [That’s a capital question mark, by the way]

      That means it’s entirely plausible to run both a CT aortogram and a CT coronary angiogram. I guess the question is whether it would have been useful to us given the situation. I’m not so sure. Our pre-test probability of STEMI is so high given that ECG. We just want to be as sure as possible that loading the patient with powerful antiplatelets and going for PPCI is safe. That means ruling out other things – but we’re not really looking for a test to ‘rule in’ STEMI. We can be confident enough to treat that without further investigation, provided that we can establish the safety of doing so.

      Under those circumstances, the coronary CT would probably be surplus to requirements. You could argue that a normal coronary CT would get us to a post-test probability where we would no longer push the issue of PPCI. But that seems unlikely. More likely, we’d get a positive scan but need to wait for the report, increasing door to balloon time. Or, we’d get an inconclusive scan and be no better off. Here’s a link to a nice vignette of coronary CT to diagnose stent thrombosis…

      Coronary CT is quite a hot topic in Virchester. It deserves a separate post at some stage, I’m sure!


  4. Dear Rick, Great case.

    Above all it is this type of case that illustrates the power of PPCI (regardless of the limitations that you mention) over thrombolysis. I agree that in this case a CT head would be appropriate – blood in the head would be about the only thing that would preclude PCI and the attendant need for anticoagulation/antiplatelet therapy. I’m interested in your comment about cranial CT being a ‘standard of care’ – perhaps you could qualify that? You’re not suggesting for all STEMI surely?

    The way you describe the case I would also have been extremely concerned re aortic dissection which is not uncommonly complicated by RCA involvement – could also, through, carotid/vertebral involvement explain the GCS. So given the need to go to CT the aortogram is reasonable too – although it wouldn’t be the first time that aortic dissection has been diagnosed in the cath lab (not recommended, but not as much of a disaster as you might imagine).

    CTCA??? Don’t get me started but hey guys this is a STEMI! A STEMI!!! If this patient needs an angiogram they need to go to the lab…end of story. I think you would have a lot of trouble finding a cardiologist or even radiologist happy to put this pt on for a CTCA.

    Finally, Clozapine? I don’t think so – see this we wrote a few years ago . Since then I’ve been involved with a Phase IV program and receive about 70-100 queries/yr about cardiac safety of clozapine and never seen or heard about anything vaguely like this case. Certainly wouldn’t want people to start worrying about that in this clinical context.

    1. Agree about CTCA, a question for academic interest only really.

      If it looks like a duck, quacks like a duck etc.

      Thanks for the comment.


  5. The question about CT coronary angiography is a really good one – and it will make a great topic for future discussion on the St. Emlyn’s blog. There are many reasons to doubt whether CT coronary angiography would actually be useful in our population in Virchester, but that’s for another day.

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  11. Andy Blackmore

    Very late to this particular party, I linked through from the latest Cardiology Case post.

    Do you know of any evidence (anything stronger than anecdote) for inferior STEMIs being harder for the patient to localise pain?

    I’ve seen three inferior STEMIs this year where the patient was either “pain free” (but sweating buckets) or else had vague abdominal pain and a complaint of being “just not right” or “can’t get comfy”.

Thanks so much for following. Viva la #FOAMed

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