This case was written by Sam Ghali: (@EM_RESUS). Thanks, Sam!
Case
A 42-year-old lady presented to the ED with complaints of intermittent episodes of chest pain associated with shortness of breath for the last 2 days. This was her ECG (it is unclear if this was with or without pain):
Computerized ECG Read: “Normal sinus rhythm. Normal ECG.”
What do you think? |
Unknown Algorithm
Sam's analysis
"There is sinus rhythm with a normal rate. QRS axis is shifted somewhat to the left. Intervals are normal. Overall this is a very quiet ECG.
But if you look closely at the precordial T-waves you see a hint of terminal T-wave inversion in V2, and biphasic T-waves in Leads V3 and V4."
As above, it is unclear from the history whether the patient was experiencing chest pain at the time of this ECG, but these right precordial t-wave findings were appreciated and the patient was treated with medical therapy and admitted to the hospital.
Troponin T returned at less than 0.010 ng/L (normal)
I sent this to the Queen years later:
Version 1 of the Queen does not distinguish betwee ACTIVE and REPERFUSED OMI. She knows this is Wellen's, but only gives output of "OMI"
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YOU HAVE THE OPPORTUNITY TO GET EARLY ACCESS TO THE PM Cardio AI BOT!! (THE PM CARDIO OMI AI APP)
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A repeat ECG was performed 1.5 hours after the first (without pain):
The precordial T-wave inversions appear to be resolving. A biphasic T-wave is only really well-appreciated in V3 now. |
2 hours later (3.5 hrs after the initial ECG) she develops severe, crushing chest pain. Another ECG is obtained:
She suddenly occluded her LAD with a very large territory of viable myocardium at risk!
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Shortly after this ECG she suddenly went unresponsive and into V-Fib. CPR was initiated and she subsequently entered into V-Fib storm. After multiple shocks, 300 mg of Amiodarone, and 100 mg of Lidocaine she stabilized and was taken emergently to the cath lab. She was found to have a 100% occlusion of her Mid LAD just after the takeoff of D1 - which was reperfused and stented. Her 2nd troponin (drawn before her reocclusion/arrest) ended up coming back barely elevated at 0.015 ng/mL! (normal, less than 0.010 ng/mL)<0 .010="" font="" ml="" nbsp="" ng="">0>
She ended up doing fine and in the next few days was discharged home in good condition.
Smith comment:
T-wave inversion such as seen in the first ECG can be seen with active non-transmural ischemia. We usually see this sort of T-wave inversion AFTER chest pain has resolved and, in that case, it is called "Wellens' syndrome," and implies that when the patient had pain the LAD was occluded, but that it spontaneously reperfused and resulted in "reperfusion" T-wave inversion. In such a case, the T-wave inversion would evolve into deeper and more symmetric (pattern B) T-wave inversion and troponins would be positive.
But in this case, it is due to active ischemia, resolves with resolution of ischemia, and has little if any troponin elevation.
Here is another similar case:
Dynamic T-wave inversion (apparent Wellens' waves), all troponins negative: Unstable Angina
Sam's Learning Points:
1. Don’t trust the computerized ECG reading. The computer is not designed to pick up such subtle ECG findings as seen in this case . If this patient was discharged from the ED she very likely would have died. We must be the experts and pick up these life-saving ECG findings!
2. ACS can be a very dynamic process. For example, a coronary plaque ruptures: the vessel can undergo occlusion, spontaneous reperfusion, maybe reocclusion, again reperfusion, etc. At the time we are seeing the patient and reading their ECG remember that we are only seeing a snapshot of this process in time.
3. Unstable Angina still exists. There are some that overestimate the sensitivity of contemporary troponin assays and have come to believe that unstable angina no longer exists. This is very dangerous thinking. It is unclear whether high-sensitivity troponins will ultimately do away with unstable angina, but we are certainly not there yet. This lady nearly “ruled out with 2 sets” as her 3-hour troponin barely made the lab cut-off by 0.005 ng/mL and could have just as easily returned negative.
Smith comment
Had she not re-occluded and arrested, her troponin would not have gone above 0.010 ng/mL. She would have been discharged. Then re-occlusion and arrest might have happened at home. Thus, unstable angina exists and can be deadly.
The ECG is still important, regardless of negative troponins.
Smith comment
Had she not re-occluded and arrested, her troponin would not have gone above 0.010 ng/mL. She would have been discharged. Then re-occlusion and arrest might have happened at home. Thus, unstable angina exists and can be deadly.
The ECG is still important, regardless of negative troponins.
the second ECG was recorded after 1.5 hrs
ReplyDeleteIsn't a long time ?
Or this is justified in the patient without pain ?
A new one should be recorded when pain is persistent or when status changes. Or when status has only changed minutes ago. So, since the patient had only just become pain free, it would be better to get one 20 minutes later to see how the ECG changes.
DeleteThanks
DeleteAlthough subtle — the history and clearly biphasic T waves in V2-thru-V4 of the initial ECG in this case should strongly suggest Wellens’ Syndrome until proven otherwise. The clinical importance of Wellens’ Syndrome is the very high correlation this type of ECG finding has with a tight LAD lesion. As emphasized by Dr. Smith — specific conditions should be established before concluding that the T wave appearance seen here is consistent with Wellens’ Syndrome (ie, prior chest pain that has now resolved in a patient who has not yet infarcted — ideally with a prior ECG available to confirm that T wave changes are new …). Given lack of any prior ECG in this case — the onus falls on the treating clinician to rule out LAD stenosis, rather than the other way around … This case provides a superb example of the importance of assessing the history in context with subtle ECG changes — regardless of serum troponin values. Fortunately, the outcome in this case was ultimately good. Learning Point #4 — The original ECG was not “normal” — especially given the clinical context. THANKS to Drs. Ghali and Smith for presenting!
ReplyDeleteThanks, Ken!
DeleteGreat post! Thank you very much!
ReplyDeleteGood case, always enjoy reading these whenever you post a new one. Being a Paramedic this is invaluable for me as I'm given the responsibility of whether or not to call a stemi alert, or communicating subtle changes like this.
ReplyDelete