I can't do anything more than guess, but as you touch on in your discussion, I believe the last two ECG's show spontaneous reperfusion as opposed to evolving or "completed" infarction. My reasoning has almost entirely to do with the T-waves and ST-segments.

1 - The resolution of the patient's symptoms corresponds roughly with the appearance of T-wave inversions (ECG 5) and directly with loss of the ST-elevation (ECG 8).
2 - This case evolved way too fast to progress from the injury pattern of STEMI to the inverted T-waves and isoelectric J-point of a completed infarct. Even if the coved ST-segments in ECG 5 were due to evolving STEMI, the J-point should remain elevated for several hours to days as opposed to minutes before returning to baseline (if ever). Such a rapid return of the J-point is much more suggestive of a reperfusion patten.
3 - The tall T-waves in V2 and V3 of ECG 5 are likely posterior reperfusion T-waves, as often described by Dr. Smith.
4 - Compared to ECG 5, ECG 8 is already starting to show rapid resolution of what I claim are reperfusion waves, with significantly less T-wave inversion in the inferior leads, shorter T-waves in the right precordials, and upright T-waves in V5/V6. Again, this is all happening way too fast for a true MI.

I can't account for the well-formed Q-waves in the inferior leads of the later ECG's except to point out that there was already what I believe to be an abnormal Q-wave in lead III of ECG 3. I might guess that the patient had Q-waves in aVF and III at baseline but the acute injury (STEMI) pattern of the first two ECG's also brought out some R-wave in those leads. Classically we think that STEMI diminishes or extinguishes R-wave height (especially anterior STEMI), but, and don't quote me on this, I think I've seen cases where the injury phase of inferior STEMI has resulted in increased amplitude of the R-wave in those leads, especially III. I'll see what I can drag up, but I'm pretty sure I'm not making up the phenomenon.

Very nice series of tracings - with excellent points made by Dawn. In particular I’d reemphasize the following:

• Rapid transition of changes from the 1st ECG at 12:39am - until the 4th ECG (labeled ECG #8) in this sequence at 1:01 am (or just 22 minutes later! ). During that time we see evolution from hyperacute ST elevation - to formation of much deeper Q waves with near resolution of ST-T wave changes. This emphasizes the importance of frequent serial ECGs in selected patient for whom the “story” appears to be evolving before your eyes.
• NOTE change to low atrial rhythm in ECG #2. An uncommon but potentially important complication is atrial infarction. Given distribution of SA nodal circulation - atrial infarction is most often seen when there is proximal RCA occlusion (less often with circumflex lesions) - so I looked carefully for PTa deviations (elevation or depression of the T wave component of the preceding P wave, during which time atrial depolarization takes place = “TPa wave” ). That said - I don’t see significant TPa depression or elevation (aVR being a common lead to show TPa elevation when atrial infarction is occurring). Atrial infarction is rare - and is usually overlooked - but neat to see, and may explain sudden onset of atrial arrhythmias (including AFib) during acute stemi (esp. when there is RCA occlusion).
• Reasons to suspect proximal acute RCA occlusion are: i) ST elevation in the 1st ECG (from 12:39) that is greater in III than in lead II; ii) Marked ST dep in aVL that is more than ST dep in lead I; iii) Although there is ST elevation in lead V6 (probably due to large posterolateral branches from the PDA) - the amount of ST elevation in V6 is less than it is in lead III; and iv) We suspect acute RV involvement because the ST segment is relatively flat in V1 - whereas with pure post MI is should be more depressed.
• As per Dawn - there is VT on the 2nd ECG (at 12:41am) - including interpolated PVCs (seen in V4,V5,V6) - which suggests high risk of impending VFib if there is not prompt reperfusion.
• Alas, the patient improves and ST segments in large part resolve - strongly suggesting spontaneous reperfusion! Note that the ventricular arrhythmia resolves. Note that sinus rhythm has resumed with the 3rd ECG (at 12:49 am).
• Doing a “mirror test” on leads V2,V3 would be highly insightful for ECG #1 (12:39am) - to ECG #3 (12:49am) - to ECG #4 (1:01am). In ECG #1 - in the “mirror test” (inverting the ECG and holding it up to the light - to get a mirror image that corresponds to what is being perceived in the posterior wall) - the T wave in V2 in ECG #1 would look hyperacute. By the “mirror test” in V2,V3 in ECG #3 - there is straighter ST elevation, now with deep T wave inversion (seen as peaked T waves in upright V2,V3). Finally in ECG #4 the “mirror test” shows virtual resolution of ST elevation with the T wave being slightly less deep. This is all consistent with spontaneous reperfusion.
• For those wanting more on the "mirror test" - See Figures 1 & 2 in my ECG Blog #80 -
• As per Dawn - there is confirmation of acute RV MI in ECG #3 (at 12:49am) - albeit ST coving and elevation in V4R is subtle indeed.
• I don’t understand why this patient was not catheterized during this admission given obvious acute occlusion (more than likely of the proximal RCA).

HIGHLY insightful to have a sequential series of tracings like this!

P.S. As to VinceD’s excellent point about why a Q wave only in lead III - this could be the result of axis shift - or even of a CHANGE in the elevation of the bed! Slight change in angle of the bed can cause Q waves to come and go in a way that is hard to predict. Have you EVER seen ANYONE record the amount of degrees that a patient’s bed may have been elevated at the time the ECG is done? Some patients just can’t lie flat when acutely ill (esp. if a component of heart failure is present). Otherwise - it is possible that the Q in lead III does reflect some necrosis from this event ...