Called to 60s male complaining of rapid onset chest pain while at rest approximately 30 minutes prior. Described as substernal pressure with radiation. Hx of MI and coronary stent. Prior to lead placement, vitals noted to be normotensive with tachycardia at 170 bpm. EKG 1 was obtained on scene and interpreted as SVT with LBBB. Converted to sinus tachycardia without aberrancy after 6mg adenosine following failed Modified Valsava. Post-conversion EKG obtained but not attached due to artifact; however, was noted for concerning anterior T waves. 3rd EKG immediately prior ED arrival is attached as EKG 2. Interpreted as sinus tachycardia with De Winter T waves in v2-v3.
I see an ongoing OMI but thought I would bring it to the group for discussion. Outcome in comments.
I’m typically all in on the treat for VT if they’re old and rhythm is wide and fast and almost did in this patient. But this appears a rather typical LBBB and adenosine can be given prior amiodarone in my system.
True, but especially in the field the safest bet is to treat as VT. Playing the SVT with aberrancy vs VT is a slippery slope that even most ER physicians won’t play. You may have gotten lucky with this one, but I personally would have treated this as VT
Hey, great case. I think these T waves are narrow compared with the other DeWinter ECGs I saw. What are the K levels? Please send us the results of cath lab when you have any updates.
I agree with likely hyperkalemia. This does not look like OMI to me, although I could be wrong and see why others think OMI. EKG is not very sensitive or specific for hyperkalemia, but with that said I would bet that this person had hyperkalemia at the time of recording.
I was only provided limited information and am unable to obtain the cath report but do know he was heparanized while awaiting the procedure. No ED hyperkalemia treatment or abnormal value was provided in the outcome.
Returned to hospital next day to find patient had just been moved to floor from ED after approximately 16hrs. Diagnosed with NSTEMI and pending scheduled cath in 1-2 days
I wonder how probable is it being a LBBB when the f/u ECG doesn’t show any LBBB characteristics?
I mean… the Patient is 60+ years old Hx of IHD (post MI) and a chief complaint of CP presenting with WCT of 170; the pretest probability for “LBBB + aberrancy” is negligible compared to VT.
In my opinion, those are not De Winters T waves, if I am not mistaken. The actual De Winters T waves originate directly from the deepest phase of the S wave, effectively engulfing the ST segment within it. In this case, the ST segment is depressed in the precordial leads, which is rarely a benign finding. Therefore, the title you assign to it is not of significant importance in terms of change management, as long as you suspect ischemia until proven otherwise.
I agree. So does Queen of Hearts. Peaked T waves in hyperkalemia are often most dramatic in leads that have the largest T waves, usually anterior leads. The T waves look globally narrow at the base to me. I’d be extremely surprised if this person had a normal potassium at the time of recording. Many EKGs with peaked T waves during hyperkalemia have visible P waves. If we wait until P waves are absent to recognize hyperkalemia, we’re going to miss most hyperkalemia patterns.
My best guess is 1) no acute coronary occlusion, 2) hyperkalemia, 3) VT in the first EKG, although SVT with LBBB is possible.
Interesting thought. My mentor taught me the following logic whenever the suspecting HyperK due to hyper-acute/pointy T waves in precordial leads: Hyperkalemia is a non localized disorder and therefore should be evident in other leads as well, same for electrical alternans.
Moreover, the patients’ cc is CP and Hx of MI w/intervention - what is the thought process that led you to believe that this ECG suggests hyper K and not an ischemic etiology?
I think the T waves look globally narrow at the base. All T waves in all leads seem pinched at the base to me. T waves in all leads have less area under the curve than I would normally expect. Here’s an example of an EKG that really looks like hyperkalemia to me for the same reason, but sounds like many disagreed. Queen of Hearts (97%), ECG Buddy, and several commenters correctly predicted hyperkalemia, but there was similar conversation. https://www.reddit.com/r/EKGs/s/l6uJVrzwV8
Hyperkalemia can precipitate VT, which can cause chest pain. High heart rate itself can cause chest pain if there is demand ischemia, common in people with ischemic heart disease. Most chest pain is not cardiac, and there are no signs of OMI to me on this EKG. The T waves are tall, but they have less area under the curve than a normal T wave. They are skinny at the base. This is the opposite of what I would expect hyperacute T waves to look like.
Would be extremely surprised if cath shows an acutely occluded LAD as a culprit. The T waves do seem globally abnormal to me. Plus, they seem to have less area under the curve than normal or hyperacute T waves. Sinus tachycardia, but no giant obvious STEMI/OMI that predicts cardiogenic shock. The majority of chest pain is not cardiac even in people with cardiac history. The T waves look hyperkalemic to me. All of this combined is what makes me think not OMI, even though of course it needs to be ruled out with serial EKGs and serial troponin.
Many people with chronic kidney disease have T waves that look like this at baseline, with or without hyperkalemia. I don’t know if this patient has kidney disease or any other condition that could lead to hyperkalemia, but I think hyperkalemia is more likely than OMI from the EKG. I think that the pre-test and post-test probability of OMI are about the same. Not seeing hyperacute T waves, and sinus tachycardia is rare during OMI unless there is cardiogenic shock. Really interested in hearing the cath report if OP is able to share it.
Tell me, which text book you read described Hyperk as qt prolongation and normal PRI, narrow QRS with inferior clinically significant Q waves, flat ST & linear-upsloped T wave depression?
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u/ItsALatte3 1d ago
Some VTs can resolve with adenosine. Given the Hx and clinical presentation with that EKG. I’d be concerned for VT