I was shown this ECG. The resident asked: "Steve, what do you think of this ECG in this Cardiac Arrest Patient?"
Here is more history:
An elderly woman with h/o CAD and CABG presented after out of hospital cardiac arrest with subsequent resuscitation and return of spontaneous circulation. It was an unwitnessed arrest and down time was unknown. The initial prehospital rhythm was asystole.
Here is the initial ED ECG:
Here was my response:
"What was the potassium?"
Answer: 7.6 mEq/L
The QRS is very wide.
Case continued:
The physicians thought this was STEMI and activated the cath lab.
Cardiology opined that this was a metabolic ECG.
Later, the K returned and they treated the hyperkalemia aggressively.
There was a complex resuscitation which included, among other medications, administration of calcium and insuline.
1 hour later, this ECG was recorded:
See these other hyperK cases also:
Case 1. A Tragic Case
Case 4
Also, see this collaborative post on critical hyperkalemia written by Pendell Meyers with edits by Steve Smith and Scott Weingart:
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Here is more history:
An elderly woman with h/o CAD and CABG presented after out of hospital cardiac arrest with subsequent resuscitation and return of spontaneous circulation. It was an unwitnessed arrest and down time was unknown. The initial prehospital rhythm was asystole.
Here is the initial ED ECG:
 | |
|
Here was my response:
"What was the potassium?"
The QRS is very wide.
Case continued:
The physicians thought this was STEMI and activated the cath lab.
Cardiology opined that this was a metabolic ECG.
Later, the K returned and they treated the hyperkalemia aggressively.
There was a complex resuscitation which included, among other medications, administration of calcium and insuline.
1 hour later, this ECG was recorded:
 |
| Improved |
See these other hyperK cases also:
Case 1. A Tragic Case
This patient presented with weakness.
45 minutes later:
Case 3
 |
| PseudoSTEMI due to Hyperkalemia |
Case 4
 |
| PseudoSTEMI due to hyperkalemia |
Also, see this collaborative post on critical hyperkalemia written by Pendell Meyers with edits by Steve Smith and Scott Weingart:
Very interesting case. However, on the first ECG, I really wonder how not to call at first place an inferior MI + RV involvement, mimicking a Brugada pattern.
ReplyDeleteInsightful case. Knowing serum K+ was markedly elevated — it is easy to look back at the initial ECG in this case and see that apart from the marked Brugada-1-like pattern seen in lead V1 — all other chest leads show peaked (if not pointed) T wave peaks with narrow base. This should be a tip-off to the severe hyperkalemia. The 2nd ECG on this patient (with the notation, “improved”) is more obvious for hyperkalemia, as much of the confusing ST-T elevation and depression is now resolving. All in all, this case is a great reminder of how one needs to repeat the ECG after treatment of hyperkalemia before one can accurately comment on the presence or absence of acute ischemic changes. This case is also a reminder that Brugada-like patterns that do not constitute Brugada “Syndrome” (ie, Brugada “phenocopy”) may result secondary to either cardiac arrest or marked hyperkalemia — with these ECG changes resolving after the underlying disorder(s) are treated.
ReplyDeleteKen,
DeleteThanks.
It is very possible even before the K returns. I would say this ECG is pathognomonic for hyperkalemia.
Steve
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DeleteThis comment has been removed by the author.
DeleteAlain,
DeleteOne must see many of these, but to me it was pathognomonic for hyperkalemia.
And easy to verify with the laboratory.
The Brugada phenotype, the peaked T-waves, and the downsloping ST elevation all fit perfectly together for hyperK without any MI.
I would not activate the cath lab once my impression is verified with the laboratory K value.
Then treat it aggressively.
If after K is treated there is STEMI pattern on ECG, then of course activate cath lab.
In this case, the followup ECG showed resolution of STE, as you would expect with treatment of the hyperK.
Steve
Another question would be: where do you think end the QRS, let say in III, in the first ECG? As what I'd see like big lateral mirror image of STE in inferior change in the second corrected K ECG as a merely clear S wave, so was this STD in III was indeed a giant S have with a very large QRS?
DeleteAlain,
Deletegood question. I think the easiest lead to find the end of the QRS is V5. Then draw a line down to lead II across the bottom to find the end of QRS in II. Then go to far right, find that point again and go up to lead III. You will find that the apparent ST elevation is not due to QRS but is indeed ST elevation (you wrote STD, but you must have meant STE (?)). However, hyperkalemia can cause ST elevation not due to ischemia!
Steve
Thanks Steve.
DeleteSorry, I meant STD in derivation I. Just to continue on this point. QRS in V5 doesn't look so large, maybe 130 ms or so. Which men that STE in III / STD in I are not QRS related.
BUT, if you look in the "corrected" ECG, the QRS in I and III is indeed very large, with a deep S wave in I and ST pseudo-elevation (related to RBBB) in III (although we still don't see much S wave in V5-V6 and this QRS doesn't look much different than the previous). Which is a bit curious.
My point is really about the nature of this STE and STD in I and III. Can it be partially explained by a very wide QRS (with giant S wave in III)?
I still don't see how does post arrest STD and STE wouldn't be called inferio-RV-maybe post acute stemi. Do we have the rest of the story? Tropos? Even if I "know" this pattern, it also contain all criteria for STEMI.
Cheers.
Alain,
DeleteAll good points. And I can't prove that this patient had no ACS. Ischemic STE and STD are very common after prolonged arrest from poor perfusion during the arrest. Type II STEMI. It does remain possible that the patient had ACS with a spontaneously reperfused artery, but these kinds of STE and STD are frequently seen with severe hyperkalemia and resolve with its treatment. Did the STE/STD resolve from Rx of K? Or was there coronary occlusion that reperfused spontaneously? Peak troponin I was very high at 44.5 ng/mL, making occlusion sound likely. But prolonged down time (unwitness + 30 minutes of CPR) in cardiac arrest can do the same thing. She had brain death so no angiogram was done. However: what strongly argues against any type of ischemia causing these ECG findings, and that I did not mention, is that after resuscitation, she had an echo with hyperdynamic function with no wall motion abnormality. With type 1 or type 2 STEMI, she should have had a wall motion abnormality.
Thanks for the great comments!
Steve
Also: that echo was done near the time of the STE/STD.
DeleteInitial ECG has rightward axis..rare for STEMI... think tox think metabolic...
ReplyDeleteWhile I noticed the signs of hyperkalemia on the first ECG, I still seem to be seeing ST-elevations in leads III and aVF on the second ECG. Are there any clues as to why this patient would not need the angio suite?
ReplyDeleteAnother point is that hyperkalemia is sometimes seen after cardiac arrest due to lactic acidosis, and might not have been the precipitant of the original arrest. It still should be emergently treated of course, to prevent a second arrest.
Best regards,
Maarten Van Hemelen
IM Resident
Maarten,
DeleteGood question. If you look closely, there is no further ST elevation. It is QRS that you are seeing. The QRS is still wide, and results in a pseudo-ST-elevation.
As for lactic acidosis, you are correct, and this patient did have lactic acidosis. The combination results in many pseudo-STEMI patterns, but still is PSEUDO, not STEMI.
I would not blame you for taking such a patient to the cath lab. It may occasionally turn out to be ACS, but the primary problem is potassium!
Steve Smith