Reciprocal ECG changes???

[VirginiaEMT]

I am an EMT-I student. I am trying to study more about reciprocal ECG changes and I have looked at three textbooks and there is very little information in them about the subject, or just maybe I am freaking out over something that is really not that big of a deal. I ask other medics and to be honest, I'm not sure they know.

Here's my question. Will reciprocal changes only be seen in the same leads every time? As an example, if I have ST elevation in leads II and aVF, will I only see reciprocal changes in the same leads everytime? Would ST depression in ANY lead help verify the findings in the inferior leads?

Where can I go to find info about this subject? My concern is this, if I need to call in a STEMI alert, are the findings in the inferior leads enough info to base this decision on?

 

[Maine iac]

In answer to your question, yeah recip changes will be seen in the same leads every time. Think of the heart as a balloon. If I push one side of the balloon in, the opposite side of the balloon pushes out. The side that is being pushed in is where the active MI is occurring (ST elevation). Lots of damage causing destruction, but because of the balloon model the opposite side is also effected (in this case ST depression).

In real life if the infarct is bad enough you will see reciprocal changes. A classic example is your inferior MI (elevation in II, III, AvF) which causes changes in Avl and some of the other lateral leads. You won't see depression in V1 or V2 though because it is a different part of the heart and not opposite of the infarct.

(there are people here who can give you a clearer description)

In answer to your second question: it depends on what your STEMI protocol says. Mine is ST elevation greater than 1mm in two contiguous leads, cardiac symptoms, QRS less than 0.120, and the computer has to read ***Acute MI***. In my system I can't call a stemi alert based on depression alone, i have to have the elevation.

What might help you is to look at a vascular model of the heart to learn where an occlusion might occur and then picture how your leads look at that part of the heart.

 

[Brandon O]

I am an EMT-I student. I am trying to study more about reciprocal ECG changes and I have looked at three textbooks and there is very little information in them about the subject, or just maybe I am freaking out over something that is really not that big of a deal. I ask other medics and to be honest, I'm not sure they know.

Here's my question. Will reciprocal changes only be seen in the same leads every time? As an example, if I have ST elevation in leads II and aVF, will I only see reciprocal changes in the same leads everytime? Would ST depression in ANY lead help verify the findings in the inferior leads?

Where can I go to find info about this subject? My concern is this, if I need to call in a STEMI alert, are the findings in the inferior leads enough info to base this decision on?

Anatomically, the relationships should hold. Which exact leads within the region will have what degree of change is a more case-specific issue. But on the whole reciprocal changes along with primary ST elevation is both sensitive and specific for STEMI.

Remember, think anatomical region. Loosely speaking:

Anterior and inferior leads are reciprocal (anterior injury produces inferior reciprocal changes, and inferior injury produces anterior reciprocal changes)

Lateral and inferior leads are reciprocal (anterior and lateral are slices of the same pie, really)

Anterior and posterior leads are reciprocal


Now, if you see depression without corresponding elevation, we might be inclined to call it ischemia rather than reciprocal changes for injury elsewhere. But in that case, ischemic changes are not anatomically localized; the ischemia could be anywhere.

 

[MSDeltaFlt]

I am an EMT-I student. I am trying to study more about reciprocal ECG changes and I have looked at three textbooks and there is very little information in them about the subject, or just maybe I am freaking out over something that is really not that big of a deal. I ask other medics and to be honest, I'm not sure they know.

Here's my question. Will reciprocal changes only be seen in the same leads every time? As an example, if I have ST elevation in leads II and aVF, will I only see reciprocal changes in the same leads everytime? Would ST depression in ANY lead help verify the findings in the inferior leads?

Where can I go to find info about this subject? My concern is this, if I need to call in a STEMI alert, are the findings in the inferior leads enough info to base this decision on?

www.12lead.com

www.ecglibrary.com

No. You will not see reciprocal changes in the same leads everytime. Depends on which artery is occluded. Reciprocal ST changes will be on the opposite side of the heart from the ST elevation.

 

[Farmer2DO]

What might help you is to look at a vascular model of the heart to learn where an occlusion might occur and then picture how your leads look at that part of the heart.

Good advice. Remember also that vascular anatomy is specific to the patient. Some people have a dominant LAD, while others have a dominant RCA. Either one can cause a STEMI in the inferior wall, but with different consequenses. If an inferior MI is caused by an LAD lesion, you will be more likely to have lateral and possibly even anterior or septal walls be contiguous, and have the issues that accompany them, vs the RCA lesion which causes the inferior wall MI, which then often involves the right ventricle and the posterior wall. Remeber also that the distal RCA provides 100% of the perfusion to the posterior leaflet of the mitral valve, and if THAT infarcts, your patient is in a world of hurt and will develop critical mitral regurg, pump failure, and will need a mitral valve replacement. I've seen that several times. The RCA/inferior/RVI patients will tend to have problems with hypotension and be preload dependent. No fun.

 

[VirginiaEMT]

It's funny I asked this question and 2 hours later I am on a call that pertains to it, running as an EMT-I preceptor. Call for 55 y.o male with chest pains:

BP: 108 palpated
Rate: 40 bpm
pale, diaphoretic
NO HISTORY

ECG:

II- 4 mm ST elevation
III- 4 mm ST elevation
aVF- 4 mm ST elevation
Lead 1 - normal
aVL- 2mm ST depression
V1,V2,V3 - 3mm ST depression
V4- normal
V5,V6- 2mm ST elevation

ECG read ACUTE MI SUSPECTED, marked sinus brady with 1st degree AVB. Obvious inferior infarct but which of the other leads would have been most reliable as a reciprocal lead?



QUOTE=Farmer2DO;385284]Good advice. Remember also that vascular anatomy is specific to the patient. Some people have a dominant LAD, while others have a dominant RCA. Either one can cause a STEMI in the inferior wall, but with different consequenses. If an inferior MI is caused by an LAD lesion, you will be more likely to have lateral and possibly even anterior or septal walls be contiguous, and have the issues that accompany them, vs the RCA lesion which causes the inferior wall MI, which then often involves the right ventricle and the posterior wall. Remeber also that the distal RCA provides 100% of the perfusion to the posterior leaflet of the mitral valve, and if THAT infarcts, your patient is in a world of hurt and will develop critical mitral regurg, pump failure, and will need a mitral valve replacement. I've seen that several times. The RCA/inferior/RVI patients will tend to have problems with hypotension and be preload dependent. No fun.[/QUOTE]

 

[Aidey]

That sounds like an inferior-lateral with reciprocal changes in the anterior leads.

 

[Brandon O]

It's funny I asked this question and 2 hours later I am on a call that pertains to it, running as an EMT-I preceptor. Call for 55 y.o male with chest pains:

BP: 108 palpated
Rate: 40 bpm
pale, diaphoretic
NO HISTORY

ECG:

II- 4 mm ST elevation
III- 4 mm ST elevation
aVF- 4 mm ST elevation
Lead 1 - normal
aVL- 2mm ST depression
V1,V2,V3 - 3mm ST depression
V4- normal
V5,V6- 2mm ST elevation

ECG read ACUTE MI SUSPECTED, marked sinus brady with 1st degree AVB. Obvious inferior infarct but which of the other leads would have been most reliable as a reciprocal lead?

Nice learning case.

Notice elevation in inferior and low lateral leads, with depression in anterior and high laterals. Thus, inferolateral injury with anterior reciprocal changes.

Notice the AVB, bradycardia, and hypotension -- all classic in inferior injury.

What artery feeds the inferolateral area?

What further diagnostic information could be helpful here?

 

[Handsome Robb]

Nice learning case.

Notice elevation in inferior and low lateral leads, with depression in anterior and high laterals. Thus, inferolateral injury with anterior reciprocal changes.

Notice the AVB, bradycardia, and hypotension -- all classic in inferior injury.

What artery feeds the inferolateral area?

What further diagnostic information could be helpful here?

RCA would be inferior supply but wouldn't the left circumflex supply the lateral aspect?

 

[MSDeltaFlt]

It's funny I asked this question and 2 hours later I am on a call that pertains to it, running as an EMT-I preceptor. Call for 55 y.o male with chest pains:

BP: 108 palpated
Rate: 40 bpm
pale, diaphoretic
NO HISTORY

ECG:

II- 4 mm ST elevation
III- 4 mm ST elevation
aVF- 4 mm ST elevation
Lead 1 - normal
aVL- 2mm ST depression
V1,V2,V3 - 3mm ST depression
V4- normal
V5,V6- 2mm ST elevation

ECG read ACUTE MI SUSPECTED, marked sinus brady with 1st degree AVB. Obvious inferior infarct but which of the other leads would have been most reliable as a reciprocal lead?



QUOTE=Farmer2DO;385284]Good advice. Remember also that vascular anatomy is specific to the patient. Some people have a dominant LAD, while others have a dominant RCA. Either one can cause a STEMI in the inferior wall, but with different consequenses. If an inferior MI is caused by an LAD lesion, you will be more likely to have lateral and possibly even anterior or septal walls be contiguous, and have the issues that accompany them, vs the RCA lesion which causes the inferior wall MI, which then often involves the right ventricle and the posterior wall. Remeber also that the distal RCA provides 100% of the perfusion to the posterior leaflet of the mitral valve, and if THAT infarcts, your patient is in a world of hurt and will develop critical mitral regurg, pump failure, and will need a mitral valve replacement. I've seen that several times. The RCA/inferior/RVI patients will tend to have problems with hypotension and be preload dependent. No fun.

[/QUOTE]

Did V1 - V3 also have a large R wave? Sounds your man was having a major multi-vessel disease process. Definitely Inf, Lat, and possibly posterior as well. One sick dude.

 

[the_negro_puppy]

If the Inferior side of the heart is supplied by the RCA and the lateral the LAD or Lcx doesnt that mean that this person is having 2 x infarcts simultaneously? how is this possible?

 

[Handsome Robb]

If the Inferior side of the heart is supplied by the RCA and the lateral the LAD or Lcx doesnt that mean that this person is having 2 x infarcts simultaneously? how is this possible?

Really bad luck? Multiple emboli from a spontaneously converted a-fib in someone who isn't med complaint?

I honestly don't know, more guessing than anything.

It seems like it would be Lcx rather than LAD but depression in aVL and elevation in V5-V6 makes me think it might be the LAD. I'm somewhat confused about it. Especially with V-4 having no changes.

Unfortunately I don't have the greatest knowledge of the circulation of the heart other than major vessels.

 

[Brandon O]

You guys are on the right track. The circumflex is usually associated with the high lateral wall, a la lead I (normal here) and aVL. But with a fairly dominant RCA (that is, one that perfuses a relatively large area of the myocardium), it's not unusual for its influence to push up into the low lateral area of V5 and V6. Some people call this style of infarct an "apical MI."

If we took right-sided heart leads, I wouldn't be surprised to see injury there too -- and, as MSDelta alluded to, possibly posterior injury too if we looked there.

With that said, can occlusion to one artery cause injury elsewhere? Definitely. When we see widespread changes that cross "anatomical boundaries" (such as both anterior and inferior injury), we should be suspicious of an alternate explanation like pericarditis. However, what can happen is that a heart with generalized, chronic coronary artery disease -- perhaps 80% narrowing of the LAD, 85% narrowing of the RCA, maybe 90% narrowing of the LCX -- becomes very dependent on "collateral circulation." Blood finds a way to percolate around through roundabout small vessels, allowing you to survive from day to day. Then an acute occlusion totally blocks off one of those arteries, and suddenly, not only does the myocardium immediately downstream get hit, but everywhere else starts to fall apart too.

Imagine how an accident in a major city intersection causes traffic jams miles away on streets with no direct connection -- traffic backs up locally, which blocks the next street, which blocks a different route, and it all starts to gridlock. Even traffic on streets that don't use that intersection is still "dependent" its functionality. "Three vessel" disease, where all the major vessels have narrowing, is not uncommon, and when a STEMI occurs it can throw a big wrench in all the compensating that patient's been doing. This is one reason (anatomical variation is another) why our attempts to anatomically isolate the culprit artery are worthwhile, but not always entirely possible.

 

[Smash]

If the Inferior side of the heart is supplied by the RCA and the lateral the LAD or Lcx doesnt that mean that this person is having 2 x infarcts simultaneously? how is this possible?

You can have a wraparound left circumflex that supplies the inferior aspec of the myocardium. Or you could have triple vessel disease or an ostial occlusion.

 

[Brandon O]

Especially with V-4 having no changes.

I would expect this is a result of the reciprocal anterior depression meeting the low lateral elevation and summing to no visible change.

 

[MSDeltaFlt]

It's funny I asked this question and 2 hours later I am on a call that pertains to it, running as an EMT-I preceptor. Call for 55 y.o male with chest pains:

BP: 108 palpated
Rate: 40 bpm
pale, diaphoretic
NO HISTORY

ECG:

II- 4 mm ST elevation
III- 4 mm ST elevation
aVF- 4 mm ST elevation
Lead 1 - normal
aVL- 2mm ST depression
V1,V2,V3 - 3mm ST depression
V4- normal
V5,V6- 2mm ST elevation

ECG read ACUTE MI SUSPECTED, marked sinus brady with 1st degree AVB. Obvious inferior infarct but which of the other leads would have been most reliable as a reciprocal.

So, how did you treat this fellow?

 

[VirginiaEMT]

So, how did you treat this fellow?

When we arrived on scene the patient was walking to our unit. He was not having difficulty ambulating but he was definitely pale and diaphoretic. Complaining of substernal chest pain radiating into his left shoulder and arm.

We only had about a 4-5 minute transport time to the hospital. First he was directed by dispatch to chew 324 mg. of Aspirin which he did before our arrival. Upon entering the unit I immediately took a blood pressure and pulse as the medic started the 12 lead. I can do that as an EMT-B but that's just how it worked out. Pulse was 40 and B.P was 108 palpated. I made the decision that transporting this patient to the cath lab was far more important than sitting on scene especially because of the transport time. I put the patient on O2 and started an I.V of N.S to get his pressure and rate up a little. Our local protocols states that ALL stemi pts. have defib pads put in place during transport and that O2 is to be titrated to 94% so the medic stayed on top of this.

To be honest, as a new student, I was concerned about giving nitro with the inferior ST elevation without having a V4r to see if there was right sided issues, and the B.P so close to 100, based on a protocol limit of 100 SBP. Then I began thinking, do we really want to get this guys heart beating much faster and his B.P much higher with all of the with all of the elevation in the various leads, due to fear pumping more blood to an occluded artery, or arteries, making matters worse. For cardiac issues I could have given 50 mcg. of Fentynal for the pain but he seemed to be tolerating it well and we just didn't have time. The medic I was with was giving the N.S just about wide open.

The medic stated afterwards that he wanted to get the pressure up so that we could give nitro. I am not so sure that I would have done that. I would have started the N.S at a much slower rate to gradually get the B.P up and the pulse up a little higher , but not wide open. Not sure with the nitro with this guy but I have the ECG and was going to talk to my instructor about it tonight.

ANY CRITQUE OR ADVICE WOULD DEFINITELY BE APPRECIATED!!!!

 

[Aidey]

He isn't a very good candidate for nitro. As other people have pointed out there is a good chance there is right sided involvement and his BP is already low.

Also, increasing his BP with fluids isn't going to raise his heart rate. His HR is slow because of the massive damage going on. It doesn't look like you posted what his actual rhythm was, but it is possible he is in a junctions rhythm because the av node has been knocked out because of the location of the MI.

 

[VirginiaEMT]

He isn't a very good candidate for nitro. As other people have pointed out there is a good chance there is right sided involvement and his BP is already low.

Also, increasing his BP with fluids isn't going to raise his heart rate. His HR is slow because of the massive damage going on. It doesn't look like you posted what his actual rhythm was, but it is possible he is in a junctions rhythm because the av node has been knocked out because of the location of the MI.

Sinus Bradycardia at 40 BPM

 

[MSDeltaFlt]

OK, here's what I would do. Fluids and morphine. Pacer pads and spike/hang a dopamine drip. Wouldn't necessarily run it just yet, but I would Already have the drip rate calculated.

NTG SL is 400mcg. That's a big dose all at once. If I had it IV, I'd run it along with fluids and dopamine, but I can't here on 911, so it's a non-issue.

Granted you were real close to hospital and cath lab. And time is muscle. But looking at the big picture you still have time. An ounce of prevention is worth a pound of cure. If you're "b@llz to the wall", you'll miss something. And that's when pts risk paying the consequences.

Critically thinking and pt advocacy is what saves lives.

I hope this helps.