STEMI best seen in PVC

See this post for a wide complex that hides ischemic findings.
See this post for a difficult diagnosis in the context of a wide complex.

Case
Here is a patient who had a cardiac arrest. Only approximately 25% of our atraumatic cardiopulmonary arrest patients have a STEMI (40% of v fib arrests) so the diagnosis of STEMI by the ECG is critical for the reperfusion decision. Here is the ECG:

The rhythm is atrial fibrillation. The QRS complex is wide, with a right bundle branch block but only subtle ST elevation in III and aVF, with very subtle reciprocal depression in lead aVL. The second complex in the ECG is a PVC, and is seen in leads I, II, and III. In leads II and III, in which the QRS of the PVC is predominantly negative (S-wave), there is marked discordant (opposite to QRS) ST elevation in leads II and III (inferior), far out of proportion to the preceding S-wave.  I believe (without proof) that appropriate discordance in a PVC should be similar to LBBB, in which the average ST/S ratio is 0.10, and excessive due to STEMI is greater than 0.20.   In lead I there is a positive QRS (R-wave) and reciprocal depression that is similarly discordant to the QRS and out of proportion.

These PVC findings confirm the diagnosis of inferior wall STEMI in this otherwise difficult ECG.

The patient had an RCA occlusion.

Probable Left Main coronary artery occlusion/obstruction, with STE in aVR, alternating BBB, and arrest

This 59 yo male had sudden chest and abdominal pain and dyspnea. He called 911. Paramedics found him in profound distress, stating "I can't breathe". He had this prehospital ECG recorded at 0953:
There is sinus tach and a wide QRS, not quite 120 ms, with wide upright R-waves in lateral leads; this is consistent with incomplete Left Bundle Branch Block. There is concordant ST depression in V2-V4, excessively discordant ST depression in I, aVL, V4-V6, and extremely excessively discordant ST elevation in aVR.

ST elevation in aVR does not make for a STEMI by itself.  When there is ST elevation elsewhere (actual coronary occlusion of a major artery), usually anterior, then ST elevation in aVR correlates with worse disease and worse outcomes.  

When there is ST depression (NonSTEMI, with subendocardial ischemia), as in this case, ST elevation in lead aVR is reciprocal to the depression found in I, II, and V4-V6.  It is not independent of these findings but is a single finding that, when greater than or equal to 1 mm, correlates well with need for bypass surgery because the left main is involved (but not occluded) or there is 3-vessel disease.  It is a good reason not to give clopidogrel, because this can cause excessive bleeding in bypass surgery.

Thus, in NonSTEMI, ST elevation in aVR is one sign of high grade Left Main obstruction or 3-vessel disease.  In any case, there is widespread subendocardial ischemia. This is not a STEMI, but can be called a STEMI-equivalent.  Cath lab activation is prudent, as these patients have very high mortality.  Thrombolytics are NOT indicated.

This ECG confirms that acute coronary syndrome is the etiology of his illness and that cath lab activation is usually indicated, and always indicated if the symptoms and ECG findings cannot be controlled with medical therapy. The cath lab was activated.

He arrived in the Emergency department at 10:13 in severe distress. He was agitated, cool, and mottled with a weak pulse and O2 saturation of 44%. The following ECG was recorded at 10:15.
There is again sinus tach, but this time with Right Bundle Branch Block and a long PR interval. Alternating Right and Left BBB is a sign of impending complete heart block below the bundle of HIS, which would lead to asystole or ventricular escape (wide and slow complex). There is persistent ST elevation in aVR and ST depression in lateral leads.

Heart rate dropped to 36 with BP 53/30. Bedside ultrasound showed a normal right ventricle but very poor LV function. After stating "I can't breathe", the patient collapsed and could not be resuscitated. No autopsy was done, so left main obstruction cannot be proven, but this is the classic clinical and ECG presentation of such pathophysiology.

Though this is STEMI, it went entirely unrecognized by the computer algorithm. The medics and physicians knew what they were dealing with but the patient died too quickly for resuscitation.

Should this patient go to the cath lab while undergoing CPR? It is the only hope for survival, and there are case reports of survival in similar situations.