Robbie

And just like ACS, these are complicated decisions that shouldn't fall on one person.

It should be a multidisciplinary tier.

In our VA, it's IR, pulmonary, and hematology anticoagulation that could convene to talk about this and what to do next.

And then Reza proceeded to give him all our books.

You know, Prof Reza, I have so many reflections, but I talk way too much.

I'll tell you that if you guys look at that EKG, there's essentially two really powerful clues that suggest PE.

The first is you just have to anchor yourself in what Wellens is.

Wellens are anterior T wave inversions or sort of T wave inversions in V2 and V3.

There are two separate clues that reinforce the possibility of PE.

First is that Wellens, when it represents ACS, very rarely extends to V1, extremely rarely.

And so V1 is also affected by this, and so that should be a trigger to the possibility of PE.

And then I think the most alarming is the inferior leads, 3 and AVF, very, very suggestive of the possibility of PE.

Then if you look more closely, you'll see...

that the patient is tachycardic.

I mean, this is sinus tachycardia.

And yeah, 300, 150, like basically borderline tachycardic.

And sinus tachycardia plus these changes is another clue for PE because patients as Proferes has told us many, many times, patients with ACS rarely have sinus tachycardia.

And then the underwhelming troponin.

a troponin in patients with ACS is proportionally high, and here a troponin that is barely twice the upper limit of normal should not, what happens with an underwhelming troponin is we worry less, but we should worry about different things, I think is the ultimate takeaway.

But Proferes, you know, I think,