Posterior MI Part I – The Abnormal V6 Sign

So here’s the case: You’ve just run an 12-lead on a patient experiencing chest pain and recognized ST-depression in leads V2-V4. Being some manner of an astute provider, your next move is to set up posterior electrodes for leads V7-V9 to confirm the hidden STEMI. You’re about to press the print button, but suddenly your monitor dies. How can you confirm that this patient is experiencing an isolated posterior STEMI and would benefit from immediate PCI as opposed to medical management?

Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

Hopefully you surmised from that title that I think you should look at V6. And not just look at it; really scrutinize it.

It’s a simple enough idea, but I don’t see it get a lot of discussion. Aside from doing the flipped-and-backwards trick when looking at V2-V4, V6 is the closest thing we have to a true posterior lead on the standard 12-lead. It makes sense that if you’re placing V6 correctly, it should be awfully close to where V7 would end up. It’s also uniquely positioned halfway between V2-V4 and V8-V9, the leads that exhibit the greatest magnitude of ST-depression and ST-elevation respectively during an isolated posterior STEMI.

Because of these two attributes, there’s actually two “V6 signs” that I’ve picked up on:

  1. The abnormal V6 sign – a result of changes in V7 affecting V6 next door
  2. The normal V6 sign – a result of the ST-deviations in V2-V4 and V8-V9 cancelling each-other out.

So let’s start with the less nuanced and controversial of the two.

The abnormal V6 sign

The “abnormal V6 sign” is any finding of ST-elevation, hyperacute T-waves, or loss of T-wave concavity in V6 when you suspect posterior wall MI because the ECG exhibits ST-depression in the right-precordial leads.

The 12-lead above is a subtle example. Yes, there are changes in the inferior leads as well, but let’s ignore those for now and zoom in on V6…

V6 from the above tracing cropped and zoomed.
Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

There is a very small amount of abnormal ST-elevation (0.5mm 60ms after the J-point). There is also worrying straightening of the upslope of the T-wave, where it has started to lose its upward concavity and “smile.” I actually find it easier to appreciate these changes zoomed-out and looking at the full 12-lead.

It’s tempting to dismiss these minor abnormalities, but let’s see what V7-V9 would show…

The posterior leads exhibit clear ST-elevation, clinching the diagnosis of posterior STEMI.
Click image to enlarge. Click here for source. Courtesy of LifeintheFastLane.com.

Here’s a similar tracing from the posterior MI section of an EMJ review article looking at the ECG in myocardial infarction:

Again there is very minor ST-elevation and straightening of the initial portion of the T-wave in V6, extending to V5.
Click image to enlarge. Click here for source.

More tracings? I’m always glad to oblige…

The T-waves in V6 feature a hyperacute morphology.
Click image to enlarge. Click here for source.

Here’s a tracing from my last post that partially inspired this one…

Leads V2-V6, zoomed and cropped. Note the abnormal morphology of the T-wave in V6.
Click image to enlarge. Click here for source.

Here’s the tracing that first piqued my interest in V6. In this case the lead labelled V6 was actually located at V7 because of the presence of a defibrillator pad, but that slight position change resulting in drastic ST-elevation really got me thinking about how close V6 is to the posterior leads.

V6 is actually located at the position of V7. Click image to enlarge.

And another…

V6 is again abnormal, with loss of concavity and slight ST-elevation
Click image to enlarge. Click here for source.

Here’s one with clear inferior STEMI. There is ST-depression from V1-V4, but elevation in V6 confirms this is secondary to posterior STEMI and not the common misdiagnosis of “anterior ischemia.”

Click image to enlarge.

Another clear inferior STEMI, but V6 clinches posterior extension…

Click image to enlarge. Click here for source.

An extremely subtle infero-posterior STEMI, but V6 is definitely abnormal in the presence of ST-depression from V1-V6.

Click image to enlarge. Click here for source.

Are you noticing a pattern yet?

This is the most subtle V6 of the bunch, but there’s definite straightening of the up-slope of the T-wave, especially in comparison to V5.
Click image to enlarge. Click here for source. Courtesy of EMS12Lead.com

As evidenced in the last tracing, there’s a very fine line between normal and abnormal when you’re looking at V6 during a posterior wall myocardial infarction. In fact, in part II of this discussion I’m going to look much more into the idea of a normal V6 being a significant finding when you suspect posterior STEMI, so look forward to that post soon.

With all the pretty pictures out of the way, let’s get something on the table. This trick isn’t really going to save lives or expose some previously unrecognized secret of electrocardiography, but let me know if it does. It’s just a shortcut I use on suspicious tracings when I don’t have the posterior leads. It’s rather unlikely that your ECG machine is going to kick the bucket on you between strips, but I’ve seen enough tracings where posterior leads were not run for some reason that I end up using it quite a bit.

I could honestly live without the V6 sign by just relying on the more concrete signs of posterior MI discussed elsewhere, especially at Dr. Smith’s ECG Blog and Life in the Fast Lane. Sometimes, however, we all just need a little extra convincing, and that’s where this comes into play. In fact, I could probably just as well call it the “lead III, aVL, or V6 sign” because those other two leads often show similar subtle changes, but in my experience V6 is slightly more useful during truly “isolated” posterior MI, so I’m going with that. Here’s a great “aVL sign” case posted last week by Dr. Brooks Walsh of Mill Hill Ave Command at EMS12Lead.com that proves V6 isn’t the only lead you should be looking at.

Lest I be accused of carelessly putting out information without context, let’s discuss some more of the shortcomings of the V6 sign:

  • I just made this up based on the case series that is my experience and study. It has not been previously studied or validated as far as I’m aware. If someone wants to study this (or especially my next topic of the “normal V6 sign,” please contact me.
  • It’s just a piece of the puzzle. You need to use this in combination with other ECG findings to make any diagnoses or decisions.
  • It’s not even a unique sign, but just a common result of the other findings you see with a posterior wall MI. I’m not being overly creative here.
  • As I’ll discuss in my next post, perhaps you should actually expect V6 to be NORMAL during a posterior MI, but this is for those cases when you get lucky.
  • ST-elevation in the posterior leads is often focused towards V8 and V9, so it may not always extend out to V7 and V6. This is not even close to being a substitute for running posterior leads.

I’ve already gone on for way too long at this point. Make sure you check out Part II in a couple of days (or tomorrow or whenever I get around to it) for some more tracings and hopefully less reading! And don’t forget to let me know what you think in the comments!

8 thoughts on “Posterior MI Part I – The Abnormal V6 Sign

  1. RyanTee says:

    Great input..Really looking forward to your next post about “normal V6 sign” !!!

  2. @Vince – NICE POST! I really like the concept of lead V6 at times serving as a posterior lead that may on occasion manifest ST elevation when there is acute Posterior MI. This may indeed be very helpful in certain cases.

    That said – I’d add the following considerations to Vince’s excellent post:
    - V6 isn’t always only about “posterior MI”. V6 is also a lateral precordial lead – which means that with lateral MI (as might occur with acute circumflex occlusion) – that V6 may also show ST elevation.

    - About 10% of patients have a left dominant circulation. In such patients – the circ is a larger vessel, and acute occlusion may result in acute infero-postero-lateral MI (reflecting the areas of the heart supplied by a dominant left circumflex vessel).

    - Therefore – seeing an acute infero-postero-lat MI might be due to acute RCA occlusion (more likely when the ST elevation in III > II and there is marked reciprocal ST dep in aVL – with perhaps the ST elevation in V6 being more a reciprocal change than true “lateral” infarction) – vs – acute circumflex occlusion in a dominant left system …

    - I DO like Vince’s suggestion to regularly incorporate lead V6 into one’s active assessment when contemplating acute posterior MI. BUT – I maintain that for each of the tracings you give in this post – use of the “mirror test” plus close scrutiny of inferior leads and aVL were enough for me to be comfortable with the diagnosis of acute posterior MI without either getting posterior leads or depending on V6. That said – incorporating Vince’s pearl to scrutinize subtle, potential hyperacute ST changes in V6 is a GREAT tool to enhance one’s diagnostic acumen that much more.
    Here’s a link to a brief pdf on ECG-Mirror Test-List 5 from my Dropbox:

    https://www.dropbox.com/s/quydaxs4o9azixh/ECG-Pg%2053-54-Mirror%20Test-List%205%20%287-17.1-2011%29-LOCK.pdf

  3. [...] Chi volesse¬†approfondirePosterior myocardial infarction in LTFLPure (isolated) posterior STEMI… su Dr Smith’s ECG blogPosteriore MI part I… in The Medial Approach to Emergency Medicine [...]

  4. Vince… Excellent article! I do agree with Dr. Grauer that I too felt very comfortable diagnosing each of the ECG examples without using V6. However, the concept is very interesting and you can never have too much supportive information when you are making decisions such as these. I hope to see if someone does a study to assess the validity of your concept.

    By the way, thanks and congrats on an excellent new blog (or “community”)!

    • Vince D says:

      Thanks for the kind words!

      There was actually supposed to be a Part II to this post about picking up truly subtle acute posterior wall MI, but when I realized there might be a real opportunity to study a related form of this “sign” and that it might have clinical utility, I held off on posting. Hopefully I’ll be the one spearheading some real V6 publications if I get my act (and enough cases) together. STEMI is a hard thing to study and get right, but trying to look at isolated posterior STEMI makes it 10x harder. Cases aren’t extraordinarily rare, but the low incidence really makes specificity a concern with so many causes of secondary ST-abnormalities on the EKG that can get in the way.

  5. Ken Grauer, MD says:

    I had not thought about this post for a while – until Jerry Jones made his comment yesterday (= March 3, 2014). In between time – I’ve become familiar with another possible reason for associated ST elevation in V5,V6 – namely that either the RCA or a dominant LCx may have disproportionately large posterolateral branches arise from the PDA (Post. Descending Artery). In such cases of acute infero-lat-postero stemi – one can suspect a dominant LCx as the “culprit” lesion if: i) ST elev in II > III; ii) ST dep in aVL is minimal; and iii) there is at least 2mm ST elev in V5,V6 (esp. if ST elev in V6 is equal or greater than the amount of ST elev in lead III).

    In contrast – one may suspect the RCA as the “culprit artery” for acute inf-post-lat stemi if: i) ST elev in III > II; ii) ST dep in aVL is marked (and more than in lead I); and iii) there is acute RV mi; and iv) ST elev in V6 is less than the amount of ST elev in lead III.
    (Kosuge et al- Am J Cardiol 109:314-319,2012).

    • Vince D says:

      I’ll have to check out the Kosuge study. Recently I’ve resigned myself to the notion that maybe discerning RCA from LCx on the EKG with any reliability is a losing endeavor, though your recommendations are quite reasonable.

      Clear RCA’s are easy to pick out when V1 is affected, and playing the odds will still lead you to RCA most of the time, but it’s that relatively small number of inferior LCx occlusions that we want to weed out and I’m presently not on board with any convincing way of doing so. That can change however, like my intra-reader reliability when it comes to discerning RCA from LCx; I love going back and forth.

      • Ken Grauer, MD says:

        The above criteria I wrote is my synthesis of what I believe is there, though not obvious from the literature I’ve read. I like the above criteria – but don’t yet have a good “feel” for how reliable they will turn out to be in practice – though to me they make the most sense of any I’ve seen up to now.

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