In the post-STEMI world, we talk about “occlusions.” So rather than argue about how many mm of STE there are, we say there are signs of ischemia suggestive of occlusion. Instead of having the troponin turn positive, shrugging and calling it an “NSTEMI,” we’d rather go look at the EKG for signs of the occlusion we missed.
I’ll be posting some of the EKGs we reviewed in conference with the cliff notes and teaching points here.
Point 1: ST depressions don’t localize. This means that seeing these in one anatomical area of the EKG does not mean that the heart has a problem in that area. Seeing them in nearly all leads is even less likely to be actionable- Cards wants evidence of a “culprit” lesion. So why should we care about them? We should only care about them when they are actually reciprocal changes of STE (possibly subtle/early) in other areas. When you see impressive ST depressions, you should be looking carefully at the OTHER leads.
Have a look at the EKG below, then come back to the text
Your eyes likely go right to the anterior leads, but then you should notice the not-so-subtle abnormalities in the others. In this case 77% of you chose to activate cath. There is STE both inferiorly and laterally, although not as impressive as the reciprocal depression. You could make a case for right-sided leads here. Posterior MI is possible but less likely without the tall R wave anteriorly (the mirror image of a posterior Q). The changes in I, L, and inf. leads is one that other EKGs from these cases mirror- the changing shape of the ST to T wave during occlusion. The ST straightens, the T becomes taller and wider.
Point 2: Proportionality– the mm of STE are proportional to the total voltage. When the R wave is tiny, a tiny STE is enough to make me concerned. This concept is echoed in Dr. Steven Smith’s “Is it repol. or is it occlusion” formula, as well as in the modified Sgarbossa rules for anterior STE. The proportion rules apply to the T waves, too. A dynamic change will cause a hyperacute T, being taller and wider compared to the QRS complex. The more it looms over the R wave, the more we should worry.
Take a look at this EKG.
There are inferior ST depressions, with scooped, abnormal segments. These are reciprocal to the anterior occlusion. There is loss of the anterior R waves (look at the change between V3 and V4- that is not normal progression). There are hyperacute T waves anteriorly. They tower over the R voltage. The T wave in V1 is abnormal (larger than in V6, in absence of a bundle or LVH). This is an early occlusion. Only 46% of respondents voted to cath that.
Here is another example of proportionality and reciprocal change:
Here there are again ST depressions inferiorly. So we should look at the other leads. Anteriorly the R wave progression and T waves seem normal. Laterally, nothing jumps out at first. But the R wave voltage in L is poor. The ST/T wave in L is small but potentially concerning in view of proportionality. Coupled with the ST depressions, this is high-lateral MI. An old EKG was procured, showing a tall R wave in L, with a baseline inverted T. A mere 8% of the group voted to cath that. This case was a delay to cath in real life as well, and only aggressively treated after the troponin turned positive. (I know, I know, EM is hard.)
Point 3: “Area under the curve.” A unifying theory of T wave evolution is that all changes bring in more area under the curve. As the ST segment changes from concave to convex? Captures more area. As the T wave gets taller and wider? More area. As the “deWinter’s T” starts below the isoelectric point? More. Can you fit the QRS inside the T? That’s bad. Here is another example of anterior occlusion with flat ST segments and very tall and towering T waves anteriorly with proportionally large and wide inferior T’s as well.
68% of you voted to cath that- there is ALSO notable STE anteriorly with poor R wave progression.
Point 4: The widowmaker. The particular scenario of diffuse ST depression EXCEPT for in V1 and avR must be mentioned as a “high risk but lots of caveats” pattern. The EM doc is on the lookout for a left main lesion. Here’s an example.
This EKG scared the providers, as it did our Cards consultant at conference. There is STE in avR that is larger than that in V1, which is concerning for L main disease. There IS a misconception that ALL patterns like this represent imminent death. Since a L main or very proximal LAD lesion can cause a diffuse ischemic insult, this pattern can be mimicked by the so-called Type II MI or demand ischemia. If you see this pattern with a HR of 220? Fix that. If the pt. has a massive GI bleed? Fix that. If the clinical context is an MI? Cath that!
Again, the EM doc is sensitivity, the Cards consult is specificity. I’d have a low threshold to make the call with this EKG.
