The first post in our “360 Degree Heart” series attempted to visualize how the different frontal plane (limb) leads relate to one another. We also introduced the concept of “negative leads,” which are just the standard leads flipped upside down. If you didn’t read that post it would probably be helpful to start there.
This week we’re going to review another cases that emphasize howÂ the simple concepts behind the “360 Degree Heart” can improve your EKG reading.
As luck would have it, I stumbled upon the perfect addition to this series soon after writing up Part I. Many thanks to Rom Duckworth for letting me use this EKG in our little educational endeavor. He’s the editorial director at Rescue Digest, plus he’s got some great slide-sets up for browsing on SlideShare (which is where this particular tracing caught my eye).
One glance at this ECG tells me that this patient has an acute obstruction of their left circumflex coronary artery (LCx). Though this does not meet the formal, oft-maligned “millimeter criteria” of 1 mm or more in two contiguous leads, this is a legitimate STEMI-equivalent. There is acute occlusion or near-occlusion of a major coronary artery and this patient requires immediate intervention for the best chance at an optimal outcome.
How can I say this with such confidence? Perhaps you noticed the ST-depression from V2-V4, in this setting diagnostic of posterior MI. That’s great (and one of my favorite ECG findings), but we can further seal the diagnosisÂ and show a greater region of myocardium is at-risk by examining the limb leads closely.
There is significant ST-elevation in only one lead, aVL, with ST-depression in II, III, and aVF. This exposes one of the reasons why “high lateral” MI due to LCx lesions are the most “electrocardiographically silent” infarctions: Unlike the inferior and lateral walls, the EKG does not directly examine the high lateral wall. Most “high lateral” MI’s show their maximal ST-elevation in the -45 to -90 degree range, but aVL, residing at -30 degrees, is the only standard lead that comes close.
Instead, let’s consider this tracing in the “360 degree” format.
It is now evident that there is indeed ST-elevation “contiguous” to what we originally noted in aVL, we just weren’t set up to see it! The ST-elevation is actually maximal in leads (-)III and (-)aVF, extending a bit into (-)II.
Now, any time you have ST-depression on the ECG there is going to be ST-elevation in the opposite direction, it’s just that this particular pattern of ST-elevation is highly correlated with occlusion of the LCx. If the ST-elevation was more evident further “rightward,” towards aVR, then we would be dealing with a pattern of subendocardial ischemia (NSTEMI).
Which brings up one last topic I would like to touch upon: the ST-vector.
It is clear from these demonstrations that the ST-segment, when it is deviated, has a particular “direction.” It is angled towards some leads and away from others. In inferior STEMI it is directed towards leads III and aVF. In anterior STEMI it is directed towards V2-V4. These are the very basic concepts we use to “localize” a STEMI.
In this case the ST-segments are deviated towards (-)III and (-)aVF and away from (+)III and (+)aVF.
We can simplify this phenomenon and represent the general distribution of the ST-deviation as a single arrow, representing the “ST-vector,” shown below.
The arrow points towards the point of maximal ST-elevation and away from the point of maximal ST-depression.
I don’t want you to dwell on this idea or worry if it’s not immediately clear, I just want you to be aware that the concept of the ST-vector exists. I will be introducing it much more thoroughly in the future.