"Shark fin" ECG in I, aVL, V4 and V5. Which artery? Hint: patient is in shock and was put on ECMO

This was contributed by Rohin Francis (Twitter: @MedCrisis), a cardiologist from England and FOAM enthusiast.

Case

A 55 year old lady initially presented to hospital with an acutely ischaemic arm. An embolic occlusion of her brachial artery was diagnosed by CT and treated with anticoagulation. The following day she developed sudden severe chest pain. This ECG was obtained:

Sinus rhythm.
The rather alarming appearance of the QRST may be mistaken for a broad complex QRS but,  in fact, her QRS complex can be clearly seen in V2, V3 and II and is narrow. What has manifested as triangular complexes is actually huge ST segment elevation seen in V2-5 and laterally in I and aVL. There is also ST segment depression inferiorly.  A proximal LAD occlusion can produce anterolateral ST elevation, but if the circumflex is also occluded, it is possible the anterior ST elevation might be attenuated and indeed here the ST elevation is less pronounced in V2 and V3.

Smith comment: Note there is ST depression in aVR, a true sign of Left Main occlusion.  Many authors state that ST elevation in aVR is a good ECG sign of left main occlusion.  This is erroneous.  (See this post for more explanation).

ST elevation in aVR is a sign of left main or 3 vessel insufficiency (not occlusion), due to diffuse subendocardial ischemia, which results in leftward and anterior ST depression (towards lead II and V5) and reciprocal ST elevation in aVR.
Left main occlusion is identical to simultaneous occlusion of the Proximal LAD (anterolateral STE: STE in V2-V6, I, aVL) and circumflex (posterolateral STE: STE in aVL, STD in V1-V4).  The opposing ST vectors of anterior and posterior can (at least partly) cancel each other out in V1-V4, so that the lateral has the most obvious STE, as in this case.  
Lead aVR is opposite an imaginary lead between leads I and II, often called (-aVR).  You can see that left main occlusion causes high lateral STE (aVL) with reciprocal STD (leads II and III); since aVR is reciprocal to this ST elevation, there is ST depression in lead aVR.

Case continued

She was immediately transferred to the primary PCI centre. On arrival she was in cardiogenic shock and haemodynamically unstable. Her BP was 80 systolic, GCS 13 and she had a grey appearance.

An intra-aortic balloon pump was inserted first and the cardiac arrest and ECMO teams were alerted. This was the initial shot of her angiogram:

The guide catheter was deliberately not engaged with the left main artery, as an occlusion was suspected. Here one can see contrast being injected towards the left main and a large thrombus sitting at the ostium. A small amount of flow is passing but not reaching further than proximal circumflex nor LAD. There is sluggish clearance of contrast from the aortic root indicative of poor cardiac output. An intra-aortic balloon pump can be seen inflating and deflating in the descending aorta.Smith comment: There is near total obstruction of the Left Main.  I am no angiographer, but I believe that this is TIMI-1 flow, which results in ST elevation.  It is not TIMI-0 flow (total obstruction/occlusion), as some minimal contrast gets through.   All thrombi are dynamic, however, and the only certainty one can have about the condition of the artery 45 minutes earlier, during recording of the ECG, comes from ECG analysis.

Passing angioplasty wires into her coronary arteries restored flow to the circumflex but not LAD. Her left main and LAD were opened using very careful aspiration and she received a drug eluting stent to her proximal left main.

Here is the aspirated thrombus:

Large red thrombus aspirated

Despite revascularisation and inotropic support, she remained in cardiogenic shock. An on-table echocardiogram revealed severe global impairment of her left ventricle. She was shocked out of VF on several occasions but continued to arrest so was placed onto femoral VA ECMO.

Peripheral ECMO increases afterload by introducing blood into the aorta and if there is no cardiac ejection, it can cause dilatation of the LV. Unfortunately despite maximal therapy in ICU, she continued to deteriorate. 

A trans-oesophageal echocardiogram revealed extensive thrombus in the aortic root and left ventricle. She died later that day. A post mortem was not performed but disparate embolic events in her arm and coronary circulation might point to an intra-cardiac source of thrombus. Thrombi tend to form in impaired ventricles, but it is unclear if the severe left failure seen on echo was pre-existing or simply a result of a catastrophic acute coronary syndrome.