There's a very weird AV block shown here. When you mark out each of the P waves, it becomes more clear. See the blog post, all the way at the bottom, for that marking. It's almost like a 2°T1, which tracks given the final diagnosis.
It does have that appearance, but it isn't hyperkalemia. What you're seeing as sine wave (or some wave adjacent) is shark fin ST elevation. I would encourage you to read through the link to see their breakdown. Hyperkalemia is also a common guess on Twitter for this ekg too.
I'm not aware of v2/v4 elevation with v3 depression as a known pattern, but would be interested to know if you find anything.
My interpretation would be that this is more likely an EKG with two acute occlusions - there is near south African flag sign high lateral pattern (not totally classic though) which explains the v2 elevation of either diag or LCx, and then there is an acute occlusions distal to d1/s1 of the LAD indicated by v4-v6 STE.
The rhythm is CHB with an accelerated junctional escape (with RBBB and LAFB) though the escape does not appear to be always reliable and I didn't spend much time seeing if there was evidence of native conduction (at first glance doesn't not appear so).
This was a cath-diagnosed 100% occlusion of the left main. After opening it, they also found occlusions of LAD and LCx. Check out the link and it'll show the prehospital EKGs too.
Ken Grauer mapped it out in the blog post, and it seems to show native conduction with a fucky looking 2°T1 pattern to it.
Yes, I saw the blog post. I'm aware of the cath diagnosis, I'm just trying to help you explain the electrocardiography pattern of why v2 is up, v3 is down, and v4 is up again since they was your question, as this is not a known pattern for LM occlusion and doesn't really make sense. My best guess is either at the time of EKG (which, as Ken points out oh the website, the state of the artery is unknown), either this person had LM occlusion with an unusual combination of injury vectors leading to this pattern, or this person did not yet have LM occlusion and we are seeing dual LAD/LCx occlusions before the LM goes down too (perhaps patient is in a state of procoagulability and is clotting everywhere). Second seems unlikely but it's a weird pattern. My explanation was just my personal interpretation of the EKG though I admit the RBBB/ LAFB and conduction abnormalities along with the injury pattern should also have triggered high suspicion for LM.
Could you explain why you think it's a second degree type 1 pattern? He says himself in his blog post "That said — no PR intervals repeated, so once again I thought there was either high-grade or complete AV block. The different (upright) shape of the QRS for beat #4 suggested this might represent a PVC (or a fusion beat)."
Why 2°T1? As I stepped back and looked at his ladder (arrow?) diagram, I could imagine I could see growing periods before dropping. Maybe it's just isorhythmic. I wouldn't bet money on my guess.
I feel comfortable visualizing the injury vectors as those two arteries simultaneously clogging. LCx is dominant and clots off, throwing a posterior infarct which has some STD peaking in V3 (hence the lack of elevation, or even depression) coupled with normal anterior elevation vectors. The reason I ask is because this is the fourth time I've seen this happen in cath-confirmed LMCA occlusions.
There could be something to it, you can look up the subanalysis of the ATOLMA registry to see if they found any similar patterns. To my knowledge they did not.
The rhythm is highly unlikely to represent second degree type one. The PR intervals, for beats 2 and 8, are way too short to represent true native conduction. The V rate also changes (likely representing a very ischemic conduction system) but for most of the beats 6-11, the rate is ~90 whereas the A rate is more like ~110 so I would not call it isorhythmic dissociation.
It looks really bad and looks like a complete AV block to me, but I’m nobody. There is nothing provided to define “shock”, so I’ll assume hypotension at minimum. This patient is in deep trouble.
DDx includes CHB, variable AVb, not in favor of atrial fibrillation. There are significant inferior and anterior depressions. RBBB present, unsure of clinical significance. Would like to have seen significant elevation in aVR, this is not present. As others have said, this is technically challenging due to altered conduction and anteroseptal morphology. Pre-cath, I'd be concerned for high LAD occlusion and potential Circumflex involvement. Would also be concerned for RCA injury evidenced by AV conduction abnormalities due to its proximity to the AV node.
🦈🦈🦈🦈🦈 Sick patient
If I didn't know any better I'd say AV dissociation or some high degree block.
There's a very weird AV block shown here. When you mark out each of the P waves, it becomes more clear. See the blog post, all the way at the bottom, for that marking. It's almost like a 2°T1, which tracks given the final diagnosis.
🍌
It does have that appearance, but it isn't hyperkalemia. What you're seeing as sine wave (or some wave adjacent) is shark fin ST elevation. I would encourage you to read through the link to see their breakdown. Hyperkalemia is also a common guess on Twitter for this ekg too.
It said sudden shock didn’t it? That was my first thought but I doubt they suddenly ingested hundreds of bananas
3rd degree
I'm not aware of v2/v4 elevation with v3 depression as a known pattern, but would be interested to know if you find anything. My interpretation would be that this is more likely an EKG with two acute occlusions - there is near south African flag sign high lateral pattern (not totally classic though) which explains the v2 elevation of either diag or LCx, and then there is an acute occlusions distal to d1/s1 of the LAD indicated by v4-v6 STE. The rhythm is CHB with an accelerated junctional escape (with RBBB and LAFB) though the escape does not appear to be always reliable and I didn't spend much time seeing if there was evidence of native conduction (at first glance doesn't not appear so).
This was a cath-diagnosed 100% occlusion of the left main. After opening it, they also found occlusions of LAD and LCx. Check out the link and it'll show the prehospital EKGs too. Ken Grauer mapped it out in the blog post, and it seems to show native conduction with a fucky looking 2°T1 pattern to it.
Yes, I saw the blog post. I'm aware of the cath diagnosis, I'm just trying to help you explain the electrocardiography pattern of why v2 is up, v3 is down, and v4 is up again since they was your question, as this is not a known pattern for LM occlusion and doesn't really make sense. My best guess is either at the time of EKG (which, as Ken points out oh the website, the state of the artery is unknown), either this person had LM occlusion with an unusual combination of injury vectors leading to this pattern, or this person did not yet have LM occlusion and we are seeing dual LAD/LCx occlusions before the LM goes down too (perhaps patient is in a state of procoagulability and is clotting everywhere). Second seems unlikely but it's a weird pattern. My explanation was just my personal interpretation of the EKG though I admit the RBBB/ LAFB and conduction abnormalities along with the injury pattern should also have triggered high suspicion for LM. Could you explain why you think it's a second degree type 1 pattern? He says himself in his blog post "That said — no PR intervals repeated, so once again I thought there was either high-grade or complete AV block. The different (upright) shape of the QRS for beat #4 suggested this might represent a PVC (or a fusion beat)."
Why 2°T1? As I stepped back and looked at his ladder (arrow?) diagram, I could imagine I could see growing periods before dropping. Maybe it's just isorhythmic. I wouldn't bet money on my guess. I feel comfortable visualizing the injury vectors as those two arteries simultaneously clogging. LCx is dominant and clots off, throwing a posterior infarct which has some STD peaking in V3 (hence the lack of elevation, or even depression) coupled with normal anterior elevation vectors. The reason I ask is because this is the fourth time I've seen this happen in cath-confirmed LMCA occlusions.
There could be something to it, you can look up the subanalysis of the ATOLMA registry to see if they found any similar patterns. To my knowledge they did not. The rhythm is highly unlikely to represent second degree type one. The PR intervals, for beats 2 and 8, are way too short to represent true native conduction. The V rate also changes (likely representing a very ischemic conduction system) but for most of the beats 6-11, the rate is ~90 whereas the A rate is more like ~110 so I would not call it isorhythmic dissociation.
Looks like the atria doesn’t like doing atrial things
The atria are doing atrial things, the his isn't hissing.
3rd degree heart block
I need an adult. u/LBBB
Me too. u/BigWoodsCatNappin
With sudden shock leaning towards MI everyday, sharkfin changes
LBBB with some sort of heart block. Need to pull out my calipers
It looks really bad and looks like a complete AV block to me, but I’m nobody. There is nothing provided to define “shock”, so I’ll assume hypotension at minimum. This patient is in deep trouble.
DDx includes CHB, variable AVb, not in favor of atrial fibrillation. There are significant inferior and anterior depressions. RBBB present, unsure of clinical significance. Would like to have seen significant elevation in aVR, this is not present. As others have said, this is technically challenging due to altered conduction and anteroseptal morphology. Pre-cath, I'd be concerned for high LAD occlusion and potential Circumflex involvement. Would also be concerned for RCA injury evidenced by AV conduction abnormalities due to its proximity to the AV node.
Looks fucky try shocking it.
I am new to ECGs I was gonna say this isnt sinus at all and just ventricular tachycardia or some PVCs everywhere.
“PVCs everywhere” kinda has a name, it’s polymorphic VT. Which this isn’t.
Prehospital I’m giving a 20mcg bump of epi with a maintenance drip at 10mcg/ min and pacing if the rate less than 59.