12 Lead STEMI suspicion w/ LBBB and PPM's

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46Young

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My medical director rode with us not too long ago. Among the many questions I asked him was if there is a way to definitively interpret a STEMI w/ a pacemeaker. What he told me is this:

Typically, w/ a vent. PPM, the T-wave will run in the opposite direction of the QRS. For example, you should see an upright T-wave w/ the QRS running the opposite direction. If the T-wave has a negative deflection, you should see a large, upright QRS. Again, this is considered normal. If you see the QRS and the T-wave moving in the same direction, you can strongly suspect a STEMI. My OMD said "That's the ECG trying to tell you there's a STEMI." He also said that the same holds true for LBBB.

Comments?

Also, we discussed NTG for ACS and APE. Boatloads of NTG are desired for the APE. For ACS, recent studies have not shown NTG to be of any (maybe negligible) benefit for short txp times, as in < 30 mins. ASA admin was of high importance, however. This conversation started with me saying that I found it foolish to give NTG for anything that suggests RCA involvement. I find it foolish to give NTG, then fluids, playing that teeter-totter game. The OMD agreed. NTG and opiates are beneficial for pt comfort/pain reduction, but not so much for pt outcomes. Prompt PCA and ASA are where it's at, is what I was told. We'll still give NTG per protocol, of course, but if there's suspected RCA involvement, or even just a SBP in or around 100, I can withheld w/o consequence.

Comments?
 
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I HAVE heard the T-wave / LBBB thing before, just never really checked in to it.


As for NTG in MI--- Some of the studies I've been reading have shown a decrease in infarct size and a decrease in ST-elevation with IV Nitro infusion... though not as much (or at all) in SL Nitro. Granted most of the studies I'm finding are from the late 80s, early 90s, or have small patient groups. I think a much bigger benefit of nitro is helping to rule in / out a thrombus vs a vessel spasm.


Now, as for NTG in AMI with the RCA involving the RV, I'm all for it still. Care needs to be taken, IVs established to be careful, of course. I think if you suspect RVI, IV Nitro should be used as opposed to SL nitro--- much more control.


http://www.ncbi.nlm.nih.gov/pubmed/7633178
http://content.karger.com/ProdukteDB/produkte.asp?Doi=174483
http://www.ncbi.nlm.nih.gov/pubmed/6407314
http://www.springerlink.com/content/901j534p06826728/


We aren't limited to just SL NTG, ASA and an opiod (though they have seen worse outcomes with Morphine in MI. Havent seen anything on Fentanyl yet)... we have IV Nitro, Heparin and Beta Blockers as well.
 
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Linuss said:
I HAVE heard the T-wave / LBBB thing before, just never really checked in to it.


As for NTG in MI--- Some of the studies I've been reading have shown a decrease in infarct size and a decrease in ST-elevation with IV Nitro infusion... though not as much (or at all) in SL Nitro. Granted most of the studies I'm finding are from the late 80s, early 90s, or have small patient groups. I think a much bigger benefit of nitro is helping to rule in / out a thrombus vs a vessel spasm.


Now, as for NTG in AMI with the RCA involving the RV, I'm all for it still. Care needs to be taken, IVs established to be careful, of course. I think if you suspect RVI, IV Nitro should be used as opposed to SL nitro--- much more control.


http://www.ncbi.nlm.nih.gov/pubmed/7633178
http://content.karger.com/ProdukteDB/produkte.asp?Doi=174483
http://www.ncbi.nlm.nih.gov/pubmed/6407314
http://www.springerlink.com/content/901j534p06826728/


We aren't limited to just SL NTG, ASA and an opiod (though they have seen worse outcomes with Morphine in MI. Havent seen anything on Fentanyl yet)... we have IV Nitro, Heparin and Beta Blockers as well.
Click to expand...

Yes, if we could start Tridil drips in the field here, I'd be less hesitant to start nitrates for the susp. RVI. I feel that the upside to SL ntg is too limited compared to the risks as it is, given that ntg in general s being shown to have little effect on positive outcomes. The OMD did mention some ongoing studies on ace inhibitors for ACS management, but also saw little benefit for prehospital b-blockers. We routinely use fentanyl in lieu of MS, but it's the medics discretion. I've read the chest wall rigidity thread, but we don't push benzos along w/ fent as of yet. I could call for orders of a benzo/fent (or MS) combo for the ext. fx, to relax the musculature and possibly use less opiods, but I haven't come across any pts that truly needed that type of intervention. A standard 1 mcg/kg, up to 100, w/ one repeat is usually more than enough (half of that protocol is our cardiac dose, btw).

Do you have IV ntg, heparin, and blockers for 911, or is that what you carry for IFT only?
 
Also, this doesn't really go along with the thread, but my OMD recommended not tubing peds at all, since tube dislodgement is commonplace with this pt population due to anatomy and frequent movement in the prehospital environment. For adult manual ventilation, the OMD said that even he cannot effectively bag a pt by himself, and has only seen one anesthesiologist do it well consistently. He recommends one provider using two hands for head tilt/mask seal, and the other squeezing the bag w/ one hand, and applying cric if necessary with the other.
 
We have Enalaprilat as our ACE inhibitor, but use it only for CHF and not MI.

I'm doing 911 where we have Tridil (NTG drip) Heparin and Labetalol. Sadly, per our guidelines, if we suspect an RVI we're to withold nitrates, which means med control gets a phone call from me. I LOVE Tridil... I like having a lot more control with nitro and being able to skirt it on down to a BP I'm comfortable with.


If we're on the topic of discussions with med control: I dropped a patient off at the ER yesterday and my med control came and shot the breeze with another medic and I for about 15 minutes just talking medicine (LOVE that a doc would do that). I asked him about IN Fent (because as per our protocols we only have IV Fent) and he said he had no problem with us doing it, just to be ready to give more than normal because of the non-guaranteed absorption.

Even after telling them, a couple other medics were like "You still have to call in as we don't have that route for fent written in our protocols!"... which kind of defeats the whole purpose of doing something IN: Get it in fast without an IV. If I'm going to call in just to do it IN, I might as well have an IV established.
 
Im kinda on the fence about NTG with RVI. The patients require extra preload with lots of fluid to ensure a good CO. The NTG does seem to be counter productive however, NTG does cause some coronary artery dilation which could improve blood flow... how much is not known and prob negligible but still prob of benefit from all that I have read.

How about a preemptive fluid bolus prior to giving the NTG? We have in our protocols to give NTG continuously every 5mins dependent on B/P. SL spray of 0.4mg NTG every 5mins equals 80mcg/min NTG infusion. We don't have IV NTG... what dose do you guys start the NTG drip out at?

As far as the cric pressure with BVM... the new AHA guidelines are advising not to perform cric pressure when using a BVM.... they claim it doesnt help and can impede ventilation.
 
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The problem I see with people wanting to withhold nitrates completely in MI with RVI is that, while yes the RV is pre-load dependent, the goal shouldn't be to decrease preload drastically, which is why I'm a fan of NTG drip.

You lower the BP as much as is safe, then hold it there, hopefully causing some systemic arterial dilation to reduce afterload to take the myocardial oxygen demand off the heart as much as you can, which is where I think it helps the heart the most.

A hypoxic heart that doesn't have to work hard is a slightly-less angry heart.



I like infusion because it is much more controlled and constant as opposed to SL which is a big bump in medication that wears off after a while. We start off at 10mcg/min and titrate up to 200mcg/min to get the desired results.
 
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^^^^ Agree... dosage wise 0.4mg SL every 5mins equals 80mcg/min.
 
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@46, yes you absolutely can diagnose STEMI in new LBBB and paced rhythms. you need to look at the QRS morphology, it will be ugly. anyway serial 12 leads are a must because you have to have change over time. look for the direction of travel for the J point (the start of the S-T seg). in a typical LBBB the j point will be discordant (opposite direction of the QRS), you are looking for concordant movement of the j-point. 1mm of concordant movement will indicate STEMI. this is mostly true for paced rhythms as well. there are tons of resources on the interwebs about this exact topic.

Just a word of caution about MDs, some know there stuff about 12 leads some just think they do, and some will openly tell you that they have no idea what to look for except ST elevation (not a slam, but some are old fashioned). if you transport to a cath lab hospital regularly try to get with the INTERVENTIONAL cardiologist, he will have the most up to date info and they are usualy more than happy to teach ems about 12 leads. I spent more than a few days in the cath lab during my internship and let me tell you there are tons of things to look for in a 12 lead.

http://link.brightcove.com/services/player/bcpid2219261001?bclid=0&bctid=68454127001

http://library.med.utah.edu/kw/ecg/index.html

the second link has some good pics that you can print and take with you to the doc for explanation.
 
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46Young said:
My medical director rode with us not too long ago. Among the many questions I asked him was if there is a way to definitively interpret a STEMI w/ a pacemeaker. What he told me is this:

Typically, w/ a vent. PPM, the T-wave will run in the opposite direction of the QRS. For example, you should see an upright T-wave w/ the QRS running the opposite direction. If the T-wave has a negative deflection, you should see a large, upright QRS. Again, this is considered normal. If you see the QRS and the T-wave moving in the same direction, you can strongly suspect a STEMI. My OMD said "That's the ECG trying to tell you there's a STEMI." He also said that the same holds true for LBBB.

Comments?


Comments?
Click to expand...

This is called scgarbosa criteria, and the same is true for LBBB. It is a part of our STEMI protocol. Google it, it is a good bit of info to become familiar with.
 
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Fish said:
This is called scgarbosa criteria, and the same is true for LBBB. It is a part of our STEMI protocol. Google it, it is a good bit of info to become familiar with.
Click to expand...

Yes, but it's spelt Sgarbossa's criteria. It apllies to LBBB & internally paced rhythms. The criteria when boiled down is:

If there is twave discordance, STE greater than 20% can indicate AMI.
If there is twave concordance, STE greater than 2mm can indicate AMI.
If there is ST depression 2mm in leads V1-V3, it can indicate AMI.

The best site to break it down more specifically is a blog by one of our members TomB (i think that's his user name). Anyways, the address is:

www.ems12lead.com
 
GTN does not really have a role in STEMI however the way most guidelines are written means that some GTN will be given before a 12 lead is obtained, or while being obtained.
 
Thanks for the input, everyone! The links were very helpful.
 
MrBrown said:
GTN does not really have a role in STEMI however the way most guidelines are written means that some GTN will be given before a 12 lead is obtained, or while being obtained.
Click to expand...

Most protocols say to perform a 12-lead before drug therapy, no? The way most protocols are written, meds are the last steps, past everything else. Besides, unless you've been living under a rock, you need to screen for inferior/V4 changes, and an initial prehospital 12 may be the only evidence of STEMI, and can get the pt to the table rather than being made to sit in the ED waiting for enzymes, etc.
 
46Young said:
Most protocols say to perform a 12-lead before drug therapy, no? The way most protocols are written, meds are the last steps, past everything else. Besides, unless you've been living under a rock, you need to screen for inferior/V4 changes, and an initial prehospital 12 may be the only evidence of STEMI, and can get the pt to the table rather than being made to sit in the ED waiting for enzymes, etc.
Click to expand...

You really only need a 12 lead OR IV access, so you can rule out RVI or control preload volume. The truth is that NTG is going to be helpful in angina, and possibly in AMI, but due to the risk of harm in using it with an inferior MI, you might as well just do the 12 lead first, since it only takes a minute.
 
Also helps greatly in potentially detecting Prinzmetal's angina.
 
46Young said:
Most protocols say to perform a 12-lead before drug therapy, no? The way most protocols are written, meds are the last steps, past everything else. Besides, unless you've been living under a rock, you need to screen for inferior/V4 changes, and an initial prehospital 12 may be the only evidence of STEMI, and can get the pt to the table rather than being made to sit in the ED waiting for enzymes, etc.
Click to expand...

I concur. Bob Page loves telling the horror story of taking a borderline B/P and killing the patient by dropping a right-sided MI's pressure.

I do 12 and 15 leads and have IV access before I'll give NTG. Risk vs Benefit isn't worth the rush, in my mind.
 
jjesusfreak01 said:
You really only need a 12 lead OR IV access, so you can rule out RVI or control preload volume. The truth is that NTG is going to be helpful in angina, and possibly in AMI, but due to the risk of harm in using it with an inferior MI, you might as well just do the 12 lead first, since it only takes a minute.
Click to expand...

That initial 12-lead in the first few minutes of pt contact is vital. It may be the only evidence of STEMI. It's important because it may get the pt right to the table for PCA, where otherwise, they'll remain in the ER. The ishcemic changes may very well resolve once we start treating, with a clean 12 at the ED.
 
Jon said:
I concur. Bob Page loves telling the horror story of taking a borderline B/P and killing the patient by dropping a right-sided MI's pressure.

I do 12 and 15 leads and have IV access before I'll give NTG. Risk vs Benefit isn't worth the rush, in my mind.
Click to expand...

Absolutely. We used to try and get ntg on board as fast as possible, but we now know why that's dangerous, and can alter the ER's tx of that pt.
 
Shoot, unless the chopper was auto-launched, I have 40+ minutes to work my way through deciding what is / is not best for the patient at any given time.

They get a 12-lead at their bed, with ASA right away. Everything else is done in the rig, from the IV, to the right-sided 12, to the posterior EKG, to the nitro drip and beyond.
 
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