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Thursday, November 10, 2011

Why paramedics need to read EKGs, and not just read interpretations.

Two patients, 2 EKGs, and 2 very different stories! Both these patients came into the Bridgeport ED, 1 of them by EMS. One of them went to the cath lab, while the other got some tests and a sandwich.

So, here's the EKG for pt #1, a 40 y.o. male who was complaining of some brief, transient, and sharp chest pains:


And for Pt #2, a 60 y.o. male who had drank a 12-pack by himself, vomited, and now complained of chest pain:
So, who got the expensive metal in their coronary artery, and who got the expensive sandwich? Which one would you have called in as a PAMI?


One of the prominent roles for EMS is in identifying the ST-elevation myocardial infarction. The basic idea is simple ("time is myocardium"), but trying to decrease the time from symptom onset to balloon inflation is pretty complex, and involves multiple decisions, actions, and environments.

Now, the role for EMS is seemingly straightforward - give the aspirin, get an EKG, and call up the ED early if you have a potential cath lab activation. Heck, the protocol seems fairly black and white.


But our patients were not put on Earth to follow the protocol, were they?

Now, pt #1 would seem like an easy cath lab activation, but a close look at the ECG suggest benign early repolarization, or perhaps pericarditis, as the most likely culprit. He had a mess o' ECGs and troponins over the next few hours, and nothing came up funky. He appreciated the sandwich!

Pt #2 had the not-so-helpful computer interpretation; "Cannot rule out Anterior infarct." Logically, you can put that on every ECG you record, since you rule out an MI with sequential troponins, over many hours! But despite the patient's intoxication, this ECG is actually classic for a bad problem, an occlusion in the proximal LAD. When we got this ECG right after he rolled into room 5, I immediately activated the cath lab. The interventionalist found a complete occlusion of the LAD just proximal to the first diagonal.
D1 = First diagonal. Lotta real estate downstream from there!
If you take another look at EKG #2, there are impressive ST-segment depressions in multiple leads, and multiple regions. Up until now, the conventional wisdom had been that this was an NSTEMI, and did not require emergent intervention.

Research over the past 10 years has changed our perspective, however. The key is in aVR, the "forgotten lead." The definite ST-segment elevation in that lead suggests an occlusion of the proximal LAD, perhaps even the left main coronary artery. If you look at the picture above, you see that the Left Main segment is responsible for >75% of the blood supply to the left ventricle. Widow-maker, indeed.

This isn't in the guidelines - yet. In one recent article, a group of cardiologists and emergency physicians suggested additions to the currently accepted cath-lab activation criteria.

Let's focus in on that last one...
So, this is all proposed stuff for now - what do you do tomorrow when you're bringing in a guy with this EKG?
Hint: Not just drunk.
Well, follow the rest of the SHCGB guidelines - ASA, IV, O2, monitor, and grab some more ECGs during transport, especially if the symptoms change. Talk to triage about bring this this patient to room 5; they may not end up going to the cath lab, but I would prefer to see that patient sooner than later!

13 comments:

  1. I'd add that in your last ECG a posterior look should be made as well, but I'm sold on LMCA-STEMI-equivalent.

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  2. Agree about getting the posterior leads - it would be nice to have some *real* ST segment elevation to show the cardiologist!

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  3. Im a paramedic student... i completely understand now why Pt 2 need emergent care, but im still lost on how Pt 1 wasn't also an emergent Pt... SOMEONE HELP MEEEEE...

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  4. http://ems12lead.com/tag/benign-early-repolarization/ shows some good examples to help you out
    To be specific though - no reciprocal changes in the limb leads. The Rr' in v4 is a benign sign. The T waves are all asymmetrical - a good sign of non-ischaemic heart. There is sign of LVH due to the height of the QRS in V2+V4 (>35mm) and probably in aVF (20mm) which could explain the st depression in the III and aVF

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  5. I can honestly say that 1 year ago prior to becoming infatuated with "EMS 12 Lead ECG blog" I would have called the first ecg a STEMI but now I can catch BER and pericarditis right off the bat. Nothing better than that feeling of reading the conclusion to the case study and realizing you would have done the right thing. Our cath lab here is 18-20 minutes away from the local hospital and I absolutley would have contacted my med control to bypass the local, I wouldn't activate cath lab for #2 because it's technicaly NSTEMI with our current protocols but I would call the Doc at the PCI facility and give him a heads up so this guy gets seen asap.

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  6. Christopher, i am not sure if you are familiar with this... but according to the teachings of Dr. Amal Mattu, ST elevation in aVR plus ST elevation in aVL (which the second ECG has) is 90% specific for an LMCA occlusion.

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  7. alcohol always distracts providers...

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  8. True. They are not "just drunk" until they've had a head-to-toe, EKG, troponin, ammonia, CT head, FAST exam, UA...

    And THEN they're just a drunk. With a big bill.

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  9. To be fair Dave, I agree but take it with a grain of salt, as there's a fair amount of debate over exactly how predictive the aVR concept can be. Dr. Mattu -- whom I love -- is the main proponent of its usage. IMO the patient's clinical presentation may often be the best additional element for the differentiation, which means that that our drunk here (didn't look too bad) was a toughie for sure. Serial tracings may help.

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  10. Brandon,
    while there may be a fair amount of debate, there are many highly regarded studies now out there speaking to the validity of this. Dr. Mattu is no longer the main proponent, but one of many.. I heard him speak of it last, and i probably should not have attributed it mainly to him lol. If you like, i can forward you the links to much research on this, although i suspect you can find it yourself as well.

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  11. More links for aVR stuff, all free full-text. I haven't actually read these, but take a look! Mattu isn't an author in any of these.
    http://www.ncbi.nlm.nih.gov/pubmed/18297153
    http://www.ncbi.nlm.nih.gov/pubmed/19346660
    http://www.ncbi.nlm.nih.gov/pubmed/16444621
    http://www.ncbi.nlm.nih.gov/pubmed/16479036

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  12. Brandon sums it up nicely.
    I've said this elsewhere, and I too love Dr. Mattu, but I think as part of being such an engaging speaker, he tends to overstate things a bit. His appearance on EMRAP.tv actually introduced me to the idea of aVR elevation a couple of years ago, and for a while I was really big into the concept and would mention it whenever given the chance, but over time I've become increasingly disappointed in how it's used (and not used).
    On one hand, I've seen a case where I whined and complained as the sign wasn't recognized and cath was delayed until a second trop came back (extremely) positive. Looking back, I mostly think I was lucky, but the patient's condition was the major clue he was very sick. I've also seen several less impressive candidates where they just ended up admitted for UA/STEMI, however I don't have further follow-up on them or any cath results.
    On the other hand, the problem with increasing awareness of this sign is that I've seen it being increasingly misused to over-call proximal lesions, usually in case discussions with (some rather bright) EMS folks. Just as in STEMI, there's a whole lot of nuance to the ECG findings of proximal lesions, and they have to be fit to the clinical picture.
    Having read the papers you posted a couple of years ago, but being a bit rusty on them, I'll buy a specificity of 90%, however only in selected patients (good stories) with useful tracings (not complicated by tachycardia/arrhythmia/conduction disturbances). Anything that causes depression in leads I and II concurrently will result in elevation in aVR, so it's not like aVR has some unique and special insight into the pathology of the LMCA. Elevation in aVR is the same exact thing as depression in (-)aVR.
    Dr. Mattu like to say that it's the kind of finding that should drag in the cardiologist at 3am, but in my very limited experience (and the few others who've shared theirs), it's mostly the patient's condition that's going to dictate whether the cardiologist is coming in anyway.

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  13. All that being said, it's still something I actively look for and believe has a role in patient care, I just don't know if it's proper utility has been realized yet.

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