Acute Anterior and Posterior wall MI at the same time ! Answer to an interesting case Challenge !

Here just we want to discuss about diagnostic aspects ...
#1- This ECG shows Diffuse ST-Segment Depression ( V2-v6 with upright T waves ) . Left Axis deviation . Normal Sinus Rhythm . Tall R wave in V1=RBBB with is new too .R>S in V1-v4 and ST-Depression with upright Ts. No considerable ST changes in II, III and VF. Troponin Elevated 4+. Echo= Inferior-Mid anterior.septal RWMA. 

#2- These changes are favoring Acute True Posterior Wall ST-elevation MI . but in True Posterior the changes just only confined to the v1-v3, and we have RBBB which is fresh onset and inferior leads ( II, III and VF) are about normal then what should be suspected?
#3- Now we are suspecting RCA±LCx mostly but there are also some feature of Left Main and LAD in our suspicion ? Now how to reach the Dx.?
#4- The accurate characteristics of Left Main involvements are : Lead aVR ST elevation and infero-lateral ST depression, the presence of ST depression >0.1mV in eight or more leads , couple with ST elevation in aVR and/or V1 .HERE WE HAVE NOT ANY AS SUCH CRITERIA TO MATCH WITH THIS ,THEREFORE, THE LEFT MAIN RULES OUT.
#5- We have here the exact criteria for true Posterior wall MI , but initial Q waves and recent onset RBBB makes the case tough . so we can say there is True posterior ! but something especial is also there , and what is this ?
#6- Pericardial Q waves favoring Ant-septal MI ! So once we can say there are anterior and Posterior MI . Recent onset RBBB favors anterior wall MI on other hand Tall R in V1 shows Q wave in posterior which we have both anterior and posterior changes at the same time and echo adding to this suspicion . so but why inferior leads are spared , in Posterior wall MI there must be Inferior leads changes. next step is angiography ?

#7- Angiography shows Small Non-dominant RCA ! and it is 100% CTO, so when there is non-dominant it has no value ! and we see Left posterior descending artery arising from LCx showing left dominant then LPDA is also 100% acutely occluded , and LAD Mid is 95% occluded and D1 is 100% ostial occlusion ! 
#8- Result- Echo+ECG shown Anterior and Posterior wall MI . Angiography did show that this patient have acute Posterior and Anterior wall simultaneously but this True posterior is the result of LPDA not RCA , and anterior is due to LAD and D1.

Atrial Flutter vs. Atrial Fibrillation !

There are many similarities between atrial fibrillation and atrial flutter, there are also significant differences.Atrial flutter is an abnormality of conduction within the atria and, as with AF, the ventricles work normally.The causes and symptoms are also very similar to AF, as is the treatment, although the symptoms tend to be less severe and there is less risk of embolisation (clot formation). Atrial Flutter also tends to revert back to sinus rhythm spontaneously in some cases.

Unlike AF, atrial flutter emanates from a small group of ectopics, or a single ectopic focus within the atria. The sequence of electrical impulses tends to be more regular than in AF. The AV node, (as in AF), still acts as a "gatekeeper" and only conducts every second or third impulse due to the refractory period.

If you have difficulty understanding the refractory period, think of the AV node as the barrier at the entrance to a car park. Every time a car enters the car park, the barrier falls for a brief period before allowing the next car through. Therefore, any car that arrives at the barrier whilst it is down is blocked from entering.

The heart tends to flutter at around 300 per minute. Like AF, these flutter waves bombard the AV node but in a much more organised and regular fashion.

The flutter waves are also more well defined than fibrillatory waves and tend to look like the teeth of a saw (for cutting wood). Often referred to as a "saw-tooth" pattern.

Answer to the Case Challenge! Where is the Culprit artery ? What is your mind just Through this ECG and Clinical Scenario?

A 50 years man who is known patient of DM and HTN with family history of CAD.
Brought to the emergency department by complaints of retrosternal chest pain since 2 hours intermittently . Troponin is not increased ! BP- 140/90, HR-112 , RR- 20 .

Answer to the Yesterday Case Challenge !

#1 -The Extent of ST-elevation is from V1 up to V6 + II, III and AVF. 
Once when you want to interpret the the numbers of same territory leads such as pericordial , in fact, you are localizing the LAD. as we are seeing in this angiogram , LAD is occluded from the proximal upto Mid segment , then this should elevate the ST from V1-v4 or 5- 6. Therefore when we see as such ECG , then we should suspect either Proximal LAD occlusion or diffuse Proximal-Mid to Distal . Here we have Proximal to Mid as well as distal LAD too. 
#2- There is ST elevation in II, III and AVF (inferior Leads) . So we should suspect the inferior Wall and as a general concept inferior means RCA but here our Angiogram shown LCx both large branches of Major OM(diffusely Occluded ) and OM2 occlusion . It is in-contrast to text books which Most elevation is in lead III>II and ST depression is mostly in AVL>I then , it should be RCA , here it is not , because all of patients not matching to our pocket text book , here RCA is patent with some Plaquing but the Culprit is LCx and it is also due to being large LCx branching . 
#3- R-R regular , V1 grossly shown coarse "F" waves > in favor of AFL.
and Finally we have a strip from post PCI which is shown ST resolution favorably after Primary PCI.