12-Lead EKGs

cointosser13

cointosser13

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What are some good websites that teach a lot about 12-lead EKGs? If anybody has a good link please send them my way. I like to go more in depth at understanding EKGs, rather than just knowing that if there's ST elevation then it's a bad EKG. I don't want to miss anything.

One other question: what do people mean when they say "reciprocal changes" in 12-lead EKGs? Im still not cluing in at what they mean.
 
I couldn't tell you anything about websites but 2 books I would recommend (yeah, I'm that old) are Dubin (to learn basic EKG reading) and Garcia (to go much more in depth with 12 lead). As for reciprocal changes, remember that a 12-lead is looking at the heart from different angles. When you see ST elevation in some leads, those leads are looking at the infarct from the front (direction of current flow). The reciprocal leads are looking at the area of infarct from behind and see it differently (T wave inversion/ST depress). Dubin actually explains this really well.
 
Check out the Facebook pages pre-hospital 12 lead ecg blog, ecg medical training, ecg & cardiology.
 
 
Ha.

The comments on most of the posts are useless. Everyone seems to think of something completely different.

ImageUploadedByTapatalk1439138774.614775.jpg
 
ERDoc said:
2 books I would recommend (yeah, I'm that old) are Dubin (to learn basic EKG reading) and Garcia (to go much more in depth with 12 lead).
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Yahhhhh! I should get commissions from Garcia because I recommend it to everyone. Fantastic book. I started out with Dubin and then picked up Garcia when I was unhappy with Dubin's lack of depth and lack of practice EKG's. I feel like you could just go straight to Garcia and save yourself some trouble. The book is designed to be worked through 3 times basically, each time you add a little bit more detail/depth, so it eases you into things pretty well.
 
"The comments on most of the posts are useless. Everyone seems to think of something completely different."

This can be frustrating for people. It was true when I worked as a cardiac monitoring technician in a critical care stepdown unit. "Ask 3 different cardiologists...." Then I realized that one of them really knew because.... and this is important... he could explain why.

There's a difference between a dismissive "Baaaaaa that's just aberrancy" and "Hey, Tom! How are you? What do you have there? Aberrancy? That's not typical of aberrancy at all -- it's almost certainly polymorphic VT -- let me show you why."

BTW the ECG you posted shows RBBB and LAD occlusion. Anyone who thinks of something different is wrong.

Tom
 
Everyone wanted to call that anteroseptal because of the precordial elevation :/
 
Does it really matter if somebody says anterior, anteroseptal, or anterolateral wall MI?

I know people will call it an anterior wall MI if there is at least elevation in V3 and V4 regardless of if there is elevation in V1 and V2 or V5 and V6.

I know people might call it an anterospetal wall MI if there is elevation V1 and V2 too.

They'll call it an anteriolateral wall MI if there is elevation in V5 and V6 too.

They all represent occlusion of the left anterior descending (LAD) artery.
 
Aprz said:
Does it really matter if somebody says anterior, anteroseptal, or anterolateral wall MI?

I know people will call it an anterior wall MI if there is at least elevation in V3 and V4 regardless of if there is elevation in V1 and V2 or V5 and V6.

I know people might call it an anterospetal wall MI if there is elevation V1 and V2 too.

They'll call it an anteriolateral wall MI if there is elevation in V5 and V6 too.

They all represent occlusion of the left anterior descending (LAD) artery.
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Nope, just referring to the follow the leader style of commenting you see on the FB pages. Blanket statements and key misses.
 
teedubbyaw said:
Nope, just referring to the follow the leader style of commenting you see on the FB pages. Blanket statements and key misses.
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Yeh, I kinda dislike how those Facebook pages have turned out. They aren't bad, but they aren't as good as they used to be. I think we used to have good combination of beginners, intermediate, and advance interpreters. I feel like they are oversaturated with beginners, poor quality ECGs, or ECGs with patient information (people outside of the US post there so they don't know or care for HIPAA since it doesn't apply to them). The moderators will now delete ECGs with names and dates on them or that are poor quality. Seems like only a few people have read the rules. I am not sure what to do about all the beginners. I don't think they should be denied a learning opportunity, but it does seem like a lot of them just guess or say what they think without explanation. It is hard too with lack of vignette or follow up on the ECG too.
 
I like the 12-lead ECG for Acute and Critical Care Providers by Bob Page. I read Dubin's book before this, as well. Page's book requires a solid understanding of basic ECGs before you read it.
 
Aprz said:
Does it really matter if somebody says anterior, anteroseptal, or anterolateral wall MI?

I know people will call it an anterior wall MI if there is at least elevation in V3 and V4 regardless of if there is elevation in V1 and V2 or V5 and V6.

I know people might call it an anterospetal wall MI if there is elevation V1 and V2 too.

They'll call it an anteriolateral wall MI if there is elevation in V5 and V6 too.

They all represent occlusion of the left anterior descending (LAD) artery.
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If I'm seeing this right on my phone, I think(?) Tom might have been refering to the elevation in AvR, which can indicate proximal LAD or left main disease. One finding that might actually make a difference, because it suggests the treatment may be CABG rather than stenting.

Oh, and another vote for Garcia. And amal mattau's big 8 hour 12-lead lecture, slides and audio are free on freeemergencytalks.net
 
With widespread depression (particularly in the lateral leads & V4) and elevation in AvR that is greater than 1mm elevation in V1... You're looking at a Left Main Occlusion or significant proximal LAD occlusion. Pretty much every thing that feeds off of the LMCA is experiencing subendocardial ischemia and it has not yet become transdermal or more likely killed them.

This is a killer, that is sometimes overlooked. And since we don't see "elevation" we don't call it in. We're taught to ignore AvR... I remember bringing one in, activating the team en route (the RN was like... "sooo.. is it orrrrr not") and the ER doc called it off on arrival. We literally went into the dictation room as I was explaining it and he googled it. He was like, "Oh, ****.... You're right."

The patient was in the cath lab shortly after. I did not follow up on pt outcome.

That was the day I wanted to be a doctor. If he could do it, I could do it. Granted, he wasn't a cardiologist, but still.
 
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I just took a page out of Steve Smith's playbook and started calling anterior STEMI "LAD occlusion" which avoids the problem of having to say absurd things like "anteroseptal STEMI with lateral extension". ST-elevation in aVR with widespread ST-depression is rarely due to left main coronary occlusion (which few patients survive). It's more likely to represent subendocardial ischemia due to left main stenosis (much different from thrombotic occlusion), so-called "3 vessel disease", demand-side ischemia from tachycardia (in a patient with CAD), perhaps even anemia (which I've seen a few times). Our post-VF ROSC patients frequently have the ST-elevation in aVL (sometimes also in V1 and V2) with widespread ST-depression, and frequently they end up going for multi-vessel bypass.
 
TomB said:
...ST-elevation in aVR with widespread ST-depression is rarely due to left main coronary occlusion (which few patients survive). It's more likely to represent subendocardial ischemia due to left main stenosis (much different from thrombotic occlusion), so-called "3 vessel disease", demand-side ischemia from tachycardia (in a patient with CAD), perhaps even anemia (which I've seen a few times). Our post-VF ROSC patients frequently have the ST-elevation in aVL (sometimes also in V1 and V2) with widespread ST-depression, and frequently they end up going for multi-vessel bypass.
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Yes, it is also a reliable indicator of triple vessel disease. However, that said, it is also a very, very good indicator of LMCA occlusion. Here is a quote from a study by the Journal of American College of Cardiology to support:

"The finding of lead aVR ST segment elevation greater than or equal to lead V1 ST segment elevation distinguished the LMCA group from the LAD group, with 81% sensitivity, 80% specificity and 81% accuracy... In acute LMCA obstruction, death occurred more frequently in patients with higher ST segment elevation in lead aVR than in those with less severe elevation. CONCLUSIONS Lead aVR ST segment elevation with less ST segment elevation in lead V1 is an important predictor of acute LMCA obstruction. In acute LMCA obstruction, lead aVR ST segment elevation also contributes to predicting a patient’s clinical outcome."
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Here is the link to the source:
http://content.onlinejacc.org/article.aspx?articleid=1127535

Either way you slice it... it is really bad news, and has a very high probability of patient death.
Regardless of what you call it, those findings in EMS it should be treated as vitally as a traditional STEMI.
 
It may be bad news but I don't agree that it should be an automatic prehospital cath lab activation unless there is consensus on this point with Emergency Medicine and Cardiology.

Steve Smith, M.D. writes about this frequently and specifically mentions the Yamaji study.

http://hqmeded-ecg.blogspot.com/2014/08/the-difference-between-left-main.html

"The study by Yamaji et al. is cited as evidence that STE in aVR > STE in V1 is 81% sensitive and 80% specific for identifying the LMCA as the culprit.72 [Incidentally, this study has been cited among the general ACS literature;68 however, it applies to STEMI only, as methods required TIMI 0-1 flow.] If its conclusions are accurate, and one considers that 0.4%-3% of LMCA occlusions make it to the cath lab alive, then the positive predictive value (PPV) of STE in aVR greater than STE in V1 is only 1.6%-11%, rendering this finding useless. Furthermore, in the study by Kurisu et al. of consecutive STEMI, written as a letter, 25 (about 3% of those with anterior STE) had LMCA occlusion; they compared ECG measurements of the 25 LMCA occlusions to only 30 each of consecutive LAD, RCA, and circumflex occlusions and found sensitivity and specificity for LMCA, vs. LAD, of STE in aVR greater than STE in V1 of 40% and 93%, resulting in a PPV of only 15%.70"

Tom
 
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