This is the discussion for Elderly Female: Chest Pain. You may wish to review the case.
Ok, this was not an obvious case, at least, not until the end. As far as the patient goes, I think we all agree about the differentials: ACS vs. possible aortic dissection (due to the pain radiating to her back).
The patient had no history of problems with aneurisms, but no history of CAD either. Pain starting while under exertion, with substernal chest pain, and diaphoresis sure sounds like ACS. You could check for differences in BP in each arm, which the crew did, but this finding in a dissecting aortic aneurism is often absent. But, never bad to keep in mind other possibilities of what's going on. Now, let's review the initial ECG:
The patient had a hard time sitting still due to her discomfort, and the resulting wandering baseline and irregular rhythm present challenges to interpretation. We have a rhythm that is A-Fib. We have slight ST elevation in V1-V3 (possibly slight in V4), and ST depression in V5 and V6. Anterior MI? Maybe, but maybe not.
Several of you astutely noted that the morphology appeared to resemble LVH with secondary reploarizaion abnormalities, the so called "Strain Pattern". One addition challenge here, is that this printout does not appear to let the QRS complexes run into eachother, rather it cuts them off at the level of the overlying or underlying QRS complex. This makes it difficult to measure.
The monitor interpretation did indeed say that voltage criteria for LVH was met. However, as Tom B has mentioned so many times on this site, it is more important to recognize the morphology of Strain Pattern, than actually know the voltage criteria. Here is a snapshot of Strain morphology typical in the lateral precordial leads:
Here are leads V5 and V6 from our patient:
Similar morphology? Looks like it… we would like to see the degree of depression proportional to the height of the R wave, but unfortunatlely the complexes are chopped by the machine, adding another challenge to the interpretation. No history of MI, and the "QS" looking complexes of the right precordials sure add to the look of Strain pattern. For more on LVH and Strain pattern, check out this previous case from ems12lead.com.
What about the ST depression in the inferior leads? Let's take a look:
Could this be attributed to Strain pattern? Strain pattern can manifest itself in the inferior leads, but according to Dr, Smith of Dr. Smith's ECG Blog, "usually you can tell because the voltage will be high in the limb leads, as usually measured in aVL". That was not the case here, so I think the ST depression in the inferior leads looks to be very suspicious.
Another thought proposed about this was the possibility of "Dig Effect". Here is an example of what Dig effect looks like (note the "scooped" appearance of the ST segment):
In our patient, I see flatter, downward sloping ST depression, but the baseline is wandering somewhat and it's not an easy call. It's hard to argue if you had it on your list of differentials though, especially with the history of AF.
So what do we have? A patient who seems to have ACS with an ECG that looks like Strain pattern, but also has concerning ST depression in the inferior leads. In the comments section of this case, I think VinceD summed it up best when he said: "We'd have to watch her like a hawk and worry about worst first with this clinical picture. She doesn't qualify for urgent PCI (at the moment)…" At the moment is the key.
That is precisely the same take the crew had, and they decided to watch her like a hawk and do serial ECG's… Once again, here was the clinching ECG acquired moments from the community hospital:
In less than twenty minutes, you can see the side by side changes here:
We can see the ST elevation increased in V2 and V3 from approximately 1mm to approximately 3mm, and in V4 the increase was from about isolectric to an astounding 5mm! In addition, the ST depression in the inferior leads increased by about 1mm. Indeed, they were born out to be reciprocal changes. Keep in mind it took less than 20 minutes for these changes to be recorded on the 12 leads.
The key to this case was the serial 12 leads done by the crew. While I don't think anyone could find fault with the cath lab not being activated after the first 12 lead, it was too late to send her directly to the cath lab by the time the last one, which revealed the STEMI, was acquired. The cath lab was activated as soon as possible, and ground transportation to it was dispatched immediately. Unfortunately an unavoidable delay still occured. A D2B time of <90 minutes could not be achieved.
Although the STEMI was recognized, this case does not have a happy ending. The bloodwork showed a highly elevated Troponins (exact value unknown), but upon arrival at the cath lab, for reasons unknown, she refused all treatments.
Key Learning Points:
1- Know your morphologies and differentials. It helps you get a better patient history, and helps you figure out what's going on with the ECG.
2- In the words of Dr. Corey Slovis: "One ECG begets another"… DO SERIAL ECG'S! And, espcially if the patient's presentation changes, get another 12 lead. Many STEMI's are missed because serial 12 leads are not done. One ECG is a snapshot in time. Like one set of vitals. But they are also dynamic, and as we've seen in this case and others on this blog, they can change dramatically in very short periods of time.