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.
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.