Last night I was asked to speak at the Australian Catholic University Student Paramedic Society’s clinical night. Someone I have previously worked with dobbed me in, and I felt I couldn’t say no…
(Photo by The Zeke: @xzcion)
Actually it was an honour to be asked to speak and it was thrilling to see so many students giving up an evening to come and listen to me blather away about ECGs. It is nice to know that the future of paramedicine is in the hands of such enthusiastic and dedicated people.
So I gave a little chat about ECGs. Specifically about the things that I was never taught about ECGs; those few little things that can make the difference between a good outcome for a patient and a poor outcome. So what were they?
First of all, the importance of proportionality in ECGs. We are given a set of (somewhat arbitrary) rules that state there must be ST elevation of > 2mm in V1 & V2 or greater than 1mm in other leads. The trouble with this is that it does not hold true for all situations.
Some ECGs are very subtle – think of the electro-cardiographically silent high lateral infarct where depression in the inferior leads is the first, or only, sign that something is amiss.
Or the posterior infarct, where in the standard 12 leads there will be no elevation at all, just depression in anterior leads, and only a tiny amount of elevation in the posterior leads.
Or the patient with Wellen’s Syndrome, who again will have no clear ST elevation, but are at high risk due to the location of their lesion (Wellen’s Syndrome is indicative of a missed LAD occlusion. The classic biphasic, or deeply inverted T waves are also known as ‘reperfusion T waves, as they occur when the clot has spontaneously resolved. The patient needs a trip to the cath lab due to the risk of re-infarcting and the huge amount of real-estate at risk. Check out this page from Dr Smith for the classic evolution of Wellen’s Syndrome. These waves can also appear in inferior leads)
These patients don’t have the ‘classic’ pattern of infarct, but they nonetheless need a trip to the cath lab. These are also situations I was never formally taught, but had to find out for myself.
The above images are all from Dr. Smith’s ECG Blog
The next issue was that of Left Bundle Branch Block and STEMI. Where I work it is ambulance dogma that LBBB is equivalent to STEMI because in the presence of a LBBB one cannot diagnose true STEMI. This is nonsense. Check out my post here as to why that is.
Finally the one dogma to rule them all was laid to rest (I hope). That is the enduring (at least where I work) and just plain wrong idea that ST depression is ‘ischaemia’ and that it localises. This is not the case. Ischaemia does not localise in the way the ST elevation in STEMI does. I don’t know why (I’m not sure if anyone does) but you cannot pick a culprit artery, or even region of ischaemic myocardium from ST depression. So if you see localised ST depression in someone you suspect of having a cardiac complaint this must be assumed to be reciprocal changes from the facing leads. If someone has global ischaemia from hypoxia, or from a left main coronary artery/triple vessel/ostial occlusion, then you will see depression everywhere (except maybe aVR – the most important ‘forgotten’ lead)
This needs to be said again as it is an absolutely vital concept that we need to understand:
Localised ST segment depression must be considered to be reciprocal changes.
And once more with feeling! Localised ST depression = reciprocal changes.
This really is a terribly important concept and one that was neglected in my training. It is also important to realise that reciprocal changes may be apparent even when ST elevation is minimal (eg the high lateral infarct or posterior infarct as above). Reciprocal changes may also show up before the typical signs of ST elevation, so can clue you in to a potentially sick patient earlier if you know what to look for.
From Dr. Smith’s ECG Blog, here is an example of how subtle lateral infarcts can be. This provides a good demonstration why we need to be alert to the significance of ST depression.
And from Life in the Fastlane, another example of how subtle infarcts can be:
So this was my chat to the students last night. It was met by a deathly silence and a lot of blank stares. That made me feel good… although I actually expected as much. These are concepts that were not taught to me in my previous 15 odd years of driving ambulances, and I did not expect them to be all over electrophysiology at this early stage of their training. What I hope is that when the time comes, a light bulb will go on in their heads and they will recall some of the goobledegook I was spouting and it will all suddenly make sense.
I’m still waiting for that moment myself.
I hope this is useful to someone out there. If you would like to explore ECGs in all their intricate subtlety further, head on over to Dr. Smith’s ECG Blog, or EMS12Lead. The people running these sites have much more idea than I about all this stuff. Dr Smith in particular is my go to when I want to go a little cross-eyed staring at funny little bumps.
As always, let me know if this is any use, or what you would like to hear about in future posts. And while you are out there, check out the “Code STEMI” web series on YouTube, starting off with the London Ambulance Service
And remember: Localised ST depression = reciprocal changes. That is: infarct!