Localizing Infarcts On a 12-Lead EKG
Hi all: here’s another in the FAQ series – this is one that a lot of people have been asking for. It’s been many years since I was on the CCU learning curve, and as usual there will probably be mistakes here – your job is to find them and report back so they can be fixed! As usual, please remember that this file is not meant to be any kind of official reference, but meant to reflect the kind of information a preceptor would give to a new orientee in the MICU.
1-What does localizing an infarct mean?
2-What are the stages of an MI, and what to they look like on a 12-lead EKG?
2-1- Acute Injury: ST elevations.
2-2- Necrosis: Q-waves.
2-3- Resolution: persistent Q-waves or flipped T’s.
3-What do EKG lead groups have to do with cardiac anatomy?
3-1: Inferior
3-2: Lateral
3-3: Anterior
3-4: Septal
4-What does ischemia look like on a 12-lead?
5-What is ‘electrical reciprocity’?
Reference EKGs:
- Normal 12-lead
- Acute Inferior MI
- Acute Anterior MI
- Resolved MI (“Old Inferior MI”)
1-What does localizing an infarct mean?
Localizing an infarct means using a 12-lead EKG to figure out where in the heart an MI is taking place. To do this, you have to do a little – but really not a whole lot – of memorization: you need to learn what the stages of an MI look like on an EKG, and you need to learn which EKG leads reflect which part of the heart. Less than your average Spanish final!
2-What are the stages of an MI, and what do they look like on a 12-lead EKG?
There are three general phases that an MI “evolves” through, and each phase has it’s own clear EKG characteristics. The underlying process took a long time to clarify, but finally in the 1980’s it was found that little clots were the culprits in causing MIs, suddenly occluding what was left of the lumen in a tight coronary artery lesion. The ‘tight lesions’ are the places along the lumen of the coronary artery where the cholesterol plaques have nearly – but not completely – closed the lumen to blood flow. As I understand it, the theory says that platelets, loving as they do to stick to rough places, tend to form clots that plug what small opening is left – which is what lies behind the whole method of ‘clot-busting’.
Apparently there’s a whole inflammatory aspect to the process of infarction, involving plaques rupturing, which doesn’t sound healthy at all. Also there’s a story around that bacteria from the mouth may be involved in plaque formation, and that flossing can help prevent it. Just something else grandma was right about.
2-1- Acute Injury (ST Elevations):
Now that there’s a clot occluding the lumen - assuming that the patient doesn’t get “clot busted” - the process of infarction begins. It turns out that there are three clear stages in the progression of the MI – the first is the period of the ‘acute injury’. This stage lasts some hours – I remember being taught that it’s roughly six- and represents the period of time between the acute blockage of the lumen, and the start of tissue death in the part of the heart that is distal to that plug. On an EKG, this stage of infarct will show as ST elevation in all the leads that reflect whichever part of the heart is being affected. This is the point in time when you want to get your TPA up and running – any later may be too late to salvage tissue. Look at the EKG of the acute inferior MI – there are clear ST elevations in II, III, and AVF.
2-2- Necrosis (Q-waves):
The second stage of an infarct is the actual process of tissue death, or necrosis – which makes sense, considering that the artery has now been plugged for more than six hours. Necrosis shows up as Q-waves on an EKG, again, in the leads that reflect the affected part of the heart.
Q-waves are actually easy to recognize: if you look at a normal EKG, you’ll notice that the QRS starts out upright in all twelve leads – that’s to say, the first move the normal QRS makes is always going up - check the normal reference EKG at the back of this FAQ. A “pathologic” Q-wave shows up as an initial downward deflection at the beginning of the QRS, that is bigger than 1/3 the total size of the QRS complex itself. Look at the EKG of the acute anterior MI – you should easily see big ugly Q-waves in V2 and V3. Do you see anything else in those leads? Notice the ST elevations – this person is evolving from the first stage to the second – moving from the stage of acute injury to the stage of necrosis. The ST segments will often come back down to the baseline (the “isoelectric” line) as the Q’s develop. The appearance of Q’s is not a happy thing – it means the patient has missed her window of treatment by lysis - that it’s too late to clot-bust, and the damage has been done. (“Look, she’s Q’d out already, inferiorly.”)
2-3- Resolution:
The resolution stage represents the development of scar tissue in the infarcted area, which happens roughly two weeks after the necrotic stage of the MI. The affected part of the heart will still show EKG changes, possibly forever – either what are called ‘persistent Q-waves’, or ‘flipped T-waves’ – if you look at the “Old inferior MI” EKG at the back of the FAQ, you’ll see Q’s in II, III, and AVF. Looking at a perfectly pain-free man having a routine EKG on a physical, who has Q waves or flipped Ts in a correct lead group – you would probably say that the Qs represented an old MI, rather than one he was in the middle of.
3-What do EKG lead groups have to do with cardiac anatomy?
A twelve-lead EKG looks at the heart from different directions, at the same time. Some areas (also called “territories”) of the heart that you might hear about in report, or in patient histories: anterior, lateral, (or sometimes antero-lateral), inferior, posterior (sometimes infero-posterior), and maybe septal. Each of these areas is perfused by it’s own respective artery (there’s some anatomical variation – can somebody explain to me and the group what “left or right dominance” means?). Remember that what you’re looking for is one or another of the characteristic EKG changes that shows up at one point or another in the evolution of an MI.(Or ischemia – the goal then being to treat the patient, and to see if the ischemic EKG changes go away. More on this below.)
Twenty seconds of review: there are two main divisions of the coronary arteries: the right (RCA), and the left, which starts as the left main. The left main artery divides into the left anterior descending, and the circumflex. (There are more arteries of course, and they’re important too, but these are the main ones, and knowing how they show up on a 12-lead will cover about 98% of the crucial territory that you have to worry about at 4am when your patient is having chest pain.)
The different groups of EKG leads reflect what’s happening in only one part of the heart (most of the time – to keep things simple we’ll pretend that this is true), and they’re usually uniform from one person to the next. Here’s where a little memorization comes in:
3-1: Inferior: II, III, AVF
The inferior leads look at the right side of the heart, which lies sort of on its side in the chest, with the RV downwards. This territory is perfused by the right coronary artery (RCA). It’s worth mentioning that the inferior part of the heart is innervated partly by the same structures that innervate the stomach – the wall of the one organ lying near the other – and I understand that this is why people with inferior ischemia or infarct often have nausea or vomiting, or sometimes hiccups in place of anginal pain.
3-2: Anterior: V2, V3, V4
The next time you do a 12-lead, look where you’re putting these electrodes – they look at the front: the anterior part of the heart, really the anterior part of the left ventricle, which is perfused by the left anterior descending artery (LAD).
3-3: Lateral: I, AVL, V5, V6
Look at these – all the way around the side of the chest, they reflect the lateral part of the left ventricle. This part of the heart is perfused by the circumflex artery (LCX).
If you were still awake several paragraphs up, you’ll recall that the left main artery divides into the LAD and the LCX, which between them perfuse most of the left ventricle. The killer lesion is a left main artery occlusion – this will threaten both areas of the LV at the same time, and will produce an antero-lateral MI, with characteristic EKG changes in V2-4, as well as I,L, and/or V5-6. Take another look at the EKG for “Acute anterior MI” – do you see the ST elevations in I and AVL, along with the anterior ones? Both territories are being threatened. The front of the heart is also sometimes called the “precordium” – and you’ll hear people say “Wow, Q-waves all the way around the precordium” – in an antero-lateral situation.
Make sense? This is a very bad thing, and is responsible for cardiogenic shock. There’s lots more on cardiogenic shock and its’ treatment in the PA-line and intra-aortic balloon pump FAQs.
3-4: Septal: V1, V2
These, right in the center of the chest, look at the septum between the ventricles. The septum is perfused partly by the RCA, and partly by the LAD. The septal leads also reflect activity in the posterior of the heart, and there are special EKG changes that reflect that: if a septal MI would show ST elevations (at first) in V1 and V2, then those same leads would show ST depression in a posterior MI, due to an EKG effect called “reciprocity” – more on that below.
4- What does ischemia look like on a 12 –lead?
A little more quick review: remember the difference between ischemia and infarct. Ischemia means that the artery, whichever one it is, does indeed have a tight lesion, but in this case it isn’t completely blocked – there’s no platelet plug, or clot, blocking what’s left of the opening.
The progression of anginal (ischemic) symptoms over a person’s life reflects the fact that the lesion is getting tighter as more plaque is deposited, leaving a smaller and smaller opening for blood to flow through. A person will start with “stable” angina, meaning that it can be provoked by stable, or predictable exertion. “I get the pain if I carry up two bags of dog food, but not one.” Then later, as the lesion gets tighter, the patient will progress to “unstable” angina, which comes with the patient at rest: “I was watching a show about deck painting, and I had the pain. Before, it only came when I watched the Cubs.” I was taught that unstable angina is caused by coronary vasospasm, which I guess happens all the time, but which apparently doesn’t cause a problem until the arterial lesion gets tight enough.
For whatever reason, the point is that there’s not enough blood getting through the artery to part of the heart to supply it with enough oxygen, and the lack of oxygen is what provokes the pain. There are a couple of ways around this – the memory trick is “LMNOP”, standing for: Lasix (these patients often “flash” into CHF), Morphine, Nitrates, Oxygen, and Position (sit a patient who is short of breath up in a high Fowler’s position, with pillows under the arms- helps a lot). These don’t fix the underlying problem though – this is why people get cathed, and angioplastied, or stented, or bypassed.
Ischemia has a different EKG picture: usually ST depression. Look at the EKG for the Acute Inferior MI: do you see the lateral ST depressions in I and AVL? This actually isn’t ischemia, but it looks like it, so what the heck.
Ischemia may also show up as “flipped T’s”, or sometimes as “pseudonormalized T’s” – which means that if a group of leads shows flipped T’s at baseline, (maybe representing an old infarct), and then they flip upwards during an episode of chest pain, then that change would represent the ischemia, always in an “anatomical” lead group – one of the groups we looked at above. As with ST depression, you would look for these changes to go away with treatment.
5-What is “electrical reciprocity”?
Reciprocity is sort of like looking at something through binoculars: if you look one way, the image is right side up – if you flip the binoculars and look the other way, the image is upside down, even though you’re still looking at the same thing. Some EKG lead groups act this way.
It turns out that several of the areas of cardiac territory are electrically reciprocal: the leads that look at the inferior area for example, will show STelevation if the person is in the acute injury stage of an MI. But the lateral leads, which are electrically reciprocal to those inferior ones, will show ST depression at the same time – normally you’d think that this would mean lateral ischemia, but no – it’s a reflection bouncing electrically across the heart from the inferior injury, showing up in reverse.
It happens the same way in the opposite direction: an acute lateral injury will show ST elevation, and will show up reciprocally as ST depression in the inferior leads. As I understand it, most reciprocity shows up between the lateral and inferior territories, and sometimes septal-to-posterior, as above in 3-4.
Look again at the examples of “ischemia” we looked at above- especially in the IMI EKG – the ST depressions in the lateral leads I and AVL represent reciprocal changes reflecting the MI going on inferiorly.
EKG #1- Normal EKG: No Q-waves, no ST elevations or depressions.
EKG #2: Acute Inferior MI (My ER-RN wife would call this a “not-so-cute” MI.)
Look at the ST elevations in leads II, III and AVF – pretty impressive. They’re not quite high enough to be called “tombstones”, but close. Do you see the ST depressions in I and AVL? Looks like ischemia – except that this is lateral reciprocity. There are other ST depressions here: what’s happening in V1-V4? Could there be a posterior MI happening too? Here’s a question – if a left-main lesion results in an antero-lateral MI, what lesion produces an infero-posterior MI?
EKG #3: Acute Anterior MI
ST elevations are clear anteriorly – and Q’s have developed too. Are there ST elevations anywhere else on this EKG? There they are in I and AVL, and V5 too – lateral leads. So where is the lesion, if the patient is infarcting in both areas? Get the balloon pump ready.
EKG #4: Resolved MI (“Old Inferior MI”)
In this EKG, look at the “persistent” Q-waves in II, III, and AVF. Do you see Q’s anywhere else on this EKG? Are they large enough to worry you?
Our sincere thanks for these EKGs go to: