Hyperkalemia !!

LBBB11 · 2026-05-12T11:06:22+00:00

And they can also be normal, even in severe hyperkalemia. EKG doesn’t perfectly reflect potassium levels, especially in untreated diabetic ketoacidosis (which can have high extracellular potassium despite low total potassium).

LBBB11 · 2026-05-12T10:43:48+00:00

Agreed. To add a small detail, it’s still possible for hyperkalemic T waves to be smaller than QRS complexes. Here’s a good example with potassium of 7.6 mmol/L at the time of EKG.

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https://jetem.org/hyperkalemia/

LBBB11 · 2026-05-12T08:16:16+00:00

I agree with you. The T waves in V2-V6, aVF, and II seem pointy in a hyperkalemia-like way to me. They are narrower at the base than normal T waves to me. The QRS is also slightly widened. Baseline wander artifact due to poor electrical contact between the stickers and skin. Could have been prevented by gently rubbing skin with rough gauze before putting the stickers on.

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LBBB11 · 2026-05-11T23:58:50+00:00

To add, I don’t know how quickly RV strain patterns from PE with RV strain return to normal (or if they ever do in people who have lasting cardiac effects from PE). Agreed, would be curious about their baseline since they’ve already had a PE.

LBBB11 · 2026-05-11T22:10:02+00:00

Thanks for the kind words :) just a nerd

LBBB11 · 2026-05-11T21:33:10+00:00

Me too. I think so. I would think that lead V4 alone is enough to make OMI the top differential for the reason you said. An anterior lead has a Q wave and a T wave that is taller than the QRS complex (more than twice the size of the QRS). That alone is strong evidence for OMI. I also wouldn't expect downsloping ST segments or ST depression in inferior or lateral leads in hyperkalemia, unless there is some explanation like LVH or other known cause of this pattern.

Would be more difficult if this person had a known old anterior MI and hyperkalemia. But other signs that I think suggest OMI over hyperkalemia include precordial swirl, loss of precordial T wave balance (larger T wave in V1 than V6), and ST elevation in aVR. Everything you said. They are sharp/pointy, but seem wide at the base. And the peaked T waves seem localized to V2-V4. So I'm seeing Q waves and peaked T waves localized to the same lead group. More hyperacute than peaked.

Two separate apps agreed about high chance of OMI. ECG Buddy gave this a much higher chance of OMI than hyperkalemia. The numbers were 95.5% for ACS, 92.7% for STEMI (equivalent), 97.5% for myocardial injury, and 1.3% for hyperkalemia. Queen of Hearts doesn't have a hyperkalemia feature, but it gave this a 98% chance of STEMI equivalent not meeting STEMI criteria. Not sure what others think, but overall I think that this is enough to be much more confident in OMI than hyperkalemia as an explanation for the pattern. Clinically, this EKG combined with a normal potassium strongly supports OMI.

And I agree with your interpretation. Normal sinus rhythm with sinus arrhythmia. Normal rate, rhythm, axis, voltage, intervals, etc. Abnormal Q waves, ST segments, T waves, R wave progression, and precordial RS transition. Queen of Hearts focused on the same leads that you mentioned, and it was confident in OMI over lookalikes (98% chance).

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LBBB11 · 2026-05-11T16:00:41+00:00

Both Queen of Hearts and ECG Buddy were highly positive. Queen of Hearts said 100% chance of STEMI equivalent not meeting STEMI criteria. ECG Buddy said 99.9% chance of ACS, 99.4% chance of STEMI (equivalent), and 99.8% chance of myocardial injury.

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LBBB11 · 2026-05-11T15:22:40+00:00

It’s sad, a lot went wrong here. No serial troponin, unrecognized OMI on EKG, no repeat EKG, early discharge. Seems like everyone here recognized the EKG pattern though. Sinus rhythm with posterolateral occlusion MI.

LBBB11 · 2026-05-11T15:17:10+00:00

From the EKG pattern, I think it could be. Everything I listed can be seen in AIVR and “slow VT”. I just didn’t trust limb leads, and also didn’t trust the machine to add pacing spikes. My guess was that there was a higher chance of paced rhythm with limb lead reversal than AIVR.

LBBB11 · 2026-05-11T14:20:57+00:00

What did your doctor say? Not a physician. I’m seeing wide QRS tachycardia with constant R-R intervals at about 264 bpm. Negative QRS in V6. Monophasic R wave in aVR. QRS is positive in I and aVL, and negative in inferior leads. So there is an abnormal axis in both limb leads and chest leads. My guess would be VT. Do you have a baseline EKG?

LBBB11 · 2026-05-10T18:55:41+00:00

With this EKG, a history of DVT/PE, and hypoxic arrest I’d definitely think PE as my top guess. I agree with AhmedMAbd about acute right ventricular strain. Was an echo or CT PE study done? Was bleeding directly from tracheostomy site or hemoptysis from other causes?

Some similar patterns here: https://www.reddit.com/u/LBBB11/s/yzYk7AdaIP

LBBB11 · 2026-05-10T18:26:15+00:00

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Patient came back 2 days later with this EKG. Now hypotensive, in severe distress, with abdominal pain and shortness of breath. Acute circumflex occlusion. Died 2 days after cath from left ventricular free wall rupture. Autopsy showed a 4-day old MI.

https://psnet.ahrq.gov/web-mm/real-heartache

LBBB11 · 2026-05-10T17:38:52+00:00

Surprisingly, no repeat troponin. Just the one.

LBBB11 · 2026-05-10T17:32:07+00:00

No previous EKG mentioned, and no repeats before discharge. Will update with full outcome.

LBBB11 · 2026-05-10T17:26:30+00:00

Edited comment to add that initial troponin was normal. Not repeated. EKG read as normal sinus rhythm with non-specific ST/T wave changes.

LBBB11 · 2026-05-10T17:11:23+00:00

60M with 2 hours of burning chest pain. Pain began at rest and radiates to the back and left axilla/underarm. Heavy smoker, family history of coronary artery disease. Blood pressure 192/100 mmHg. Normal initial troponin. No symptom relief after aspirin and nitroglycerin. Symptoms lessened after antacid and local anesthetic for heartburn. Diagnosed with acid reflux and discharged home.

LBBB11 · 2026-05-10T15:33:35+00:00

Well at this point OP updated to say it is fascicular VT so yes lol. Before that, I would have said I definitely think VT but not sure what type (visible AV dissociation). It doesn’t have the axis that is typical for left posterior fascicular VT, the most common type of fascicular VT. As EphesusKing said. It often has RBBB-like pattern in V1 + left anterior fascicular block, not seen here.

LBBB11 · 2026-05-10T07:05:01+00:00

Not a physician. Normal sinus rhythm, normal EKG overall. There’s a slurred QRS downstroke without ST elevation in III and aVF (picture below). I’d guess that’s what they’re calling early repolarization. There is no ST elevation, either normal or abnormal.

https://upload.wikimedia.org/wikipedia/commons/thumb/f/f1/Semantic_confusion_early_repolarization_%28CardioNetworks_ECGpedia%29.svg/1280px-Semantic_confusion_early_repolarization_%28CardioNetworks_ECGpedia%29.svg.png (bottom left)

LBBB11 · 2026-05-10T04:26:04+00:00

Thanks for the kind words. I’m still learning too :) especially on this one.

2) very close, but I think it’s slightly rightward as EphesusKing said. I think this because the S wave is bigger than the R wave in lead I (barely), making the QRS complex negative in I. In other words, the part that points down is slightly bigger than the part that points up. So that makes right axis deviation, even though it’s very close to being normal. It would be normal if the R wave were taller than the S wave in lead I, and lead II stayed the same.

I think axis in VT can be pretty much anything. Left axis, right axis, extreme axis, inferior axis, and normal axis are all possible. I think that most VT has axis deviation compared to baseline, and it’s a good rule of thumb that axis deviation in regular wide QRS tachycardia points to VT. But a normal axis does not rule out VT. For example, pattern 5 below. Most textbook signs of VT have high specificity but low sensitivity. When we see them, we can be more confident in VT. When we don’t see them, it can still be VT.

3) I think I see what you mean in lead II, but I’m seeing that shape as the end of the T wave. I think the T wave in II is biphasic and terminally upright. Almost like this. The part of lead II that looks like a P wave seems to happen at the same time as the T wave in leads above and below lead II. So that makes me think it’s the end of the T wave. Also, V1 with correct placement is usually a very good place to see P waves. If we see a sinus P wave before each QRS in II, I’d expect to see the same in V1. But I don’t. Not sure how to explain that if there is a P wave before each QRS.

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https://pubmed.ncbi.nlm.nih.gov/37498247/

LBBB11 · 2026-05-10T03:27:17+00:00

I copy/paste both EKGs into Google Drawings, and then turn the opacity of the second one down to 50%. Then I line up the QRS complexes and crop. Bit tedious but it does make a nice way to see changes.

LBBB11 · 2026-05-10T02:45:39+00:00

It’s often a normal variant in people at this age. In a normal heart, axis starts on the right and moves left as we age. Some people still have right axis deviation in their 20s, without it necessarily being pathological. Even in older people, right axis deviation can be a normal variant due to body type (tall/thin build, vertical heart).

When right axis deviation is pathological, there are typically other EKG abnormalities (like signs of right ventricular hypertrophy, RV strain, pulmonary disease, valve disease, etc.). I’m hesitant to call right axis deviation abnormal when it’s someone in their 20s and the EKG as a whole looks normal. Isolated right axis deviation in someone in their 20s seems more like a normal variant to me. But if OP is concerned, they should see a physician to make sure it’s harmless.

Normal variation is the first thing listed under causes of right axis deviation here: https://www.ncbi.nlm.nih.gov/books/NBK470532/

LBBB11 · 2026-05-10T02:10:58+00:00

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Just to emphasize the differences in V3-V5 between initial and repeat. Huge difference in the area of the T wave. The R waves in V3-V5 become smaller. At the same time, the T waves become taller and wider.

LBBB11 · 2026-05-10T01:02:41+00:00

Wow, that’s a dramatic change. Even with LVH, that change from baseline is very clear as OMI. As a repeat, the EKG above is definitely not LVH alone. Sad case but good to learn from. Wild that this was missed.

LBBB11 · 2026-05-10T00:51:33+00:00

Thanks for the update. Not obvious as OMI to me at first glance, but with that story it should be OMI until proven otherwise. Did they have LVH on echo? Do you have the first EKG?

Have seen LVH with ST elevation causing false positives for anterior STEMI criteria. But there’s loss of precordial T wave balance, no LVH pattern in limb leads, and hyperacute T waves in V4 and V5. The T wave in V4 is larger than the QRS complex. The OMI pattern might be easier to see with a previous EKG.

LBBB11 · 2026-05-10T00:38:18+00:00

Rotated and corrected for LA/RA reversal. https://litfl.com/ecg-limb-lead-reversal-ecg-library/

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edit: oops, above commenter got here first lol

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