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 )