An elderly male with history of MI 10 years prior called 911 for chest pain.
Here is the prehospital ECG:
|What do you think?
Computer only noted RBBB.
There is sinus rhythm with RBBB. There is a bit of ST elevation in III and aVF, with reciprocal ST depression in aVL. This is a subtle inferior MI.
Is there more?
In RBBB, there should be some ST depression in V1-V3, discordant to (in the opposite direction of) the R’-wave. But unless there is a huge R’-wave (as in RVH), this ST depression should not exceed 1 mm. And the inverted T-wave should be proportional.
Here there is more than 1 mm of ST depression in lead V2, and the inverted T-wave in V3 is hyperacute. This is posterior STEMI.
Moreover, look at V6. There is ST elevation with a hyperacute T-wave (there should never be STE in RBBB!). This is lateral STEMI, which supports the diagnosis of posterior STEMI.
Frequently, in posterior STEMI, one can see subtle STE in lead V6.
I knew this was an inferior posterior MI, so I activated the cath lab.
We recorded an ED ECG:
|There is now more STE in inferior leads.
The inverted hyperacute T-wave in V3 is more pronounced.
The ST depression in V2 and V3 is more profound.
Interestingly, the STE and hyperacute T-wave in V6 are not evident.
Just for my own interest, I recorded posterior leads. Unfortunately, that ECG was lost.
But what I want to share with you is that there was no ST elevation in posterior leads! And this cannot be blamed on reperfusion, because leads V1-V3 were recorded simultaneously with V7-V9, and they were identical to the above ECG.
Once you have made the diagnosis of posterior MI (with or without associated inferior or lateral MI), you should not believe negative posterior leads. They are often falsely negative!
Posterior leads are recorded through a lot of impedance of the intervening lungs, and the voltage simply many not be adequate. It is true that the QRS is also very small in posterior leads, so (as always), proportion is the most important element. That is why the “criteria” for posterior leads is only 0.5 mm. However, in this case, there was not even 0.5 mm of STE.
Another ECG was recorded:
|It is looking somewhat better.
The T-waves are not as deep in V2 and V3
There is some terminal upright of the T-waves in V2 and V3, typical of reperfusion.
Culprit Lesion (s):
99% thrombotic occlusion of the mid-circumflex, which is the culprit lesion for the patient’s acute chest pain syndrome
70% in-stent restenosis of the pRCA
Severe disease of the distal/apical LAD
The estimated left ventricular ejection fraction is 40-45 %.
Regional wall motion abnormality – inferior.
Regional wall motion abnormality – lateral. (remember that posterior (inferobasal) is now called “lateral” in echocardiography)
Post reperfusion ECG:
|This is a normal RBBB.