NTG and Morphine I’m Inferior AMIs

[michael150]

Alright guys, I know this has been covered before but I want to restart the conversation. With recent studies, (I will try to find them and link them) I want to kind of talk with the more experienced medics and leave an in-depth discussion for those in medic and learning.

During school, it was drilled into our heads to not give a SL nitro or morphine in patients that are presenting with inferior AMIs because of the potential of RVI and dropping their pressure through the floor. I have read studies proving this false and that with the supplement of NS boluses, we can effectively raise theBP back to therapeutic levels. I have also been told by attending ED docs that they don’t hesitate to give it or start a drip anymore. Just now, I cleared off of an IFT interior MI with 2 boxes of elevation in all 3 leads. He had heparin and NTG running. NTG at 5mcg/min on a pump. I got into an argument with the ED medic saying that it’s been proven that we can raise their BP. He says that we can’t do it quickly enough and he has seen patients crash with the administration of NTG.

What are your experiences with this? Anyone have protocols to still give NTG and supplement with a liter or 2? Thanks guys. I’m still within my first year of being a paramedic but I feel like withholding these two meds is an old wive’s tale.

 

[Aprz]

I cannot give you any science to back this up, but I consider the whole do not give nitroglycerin to inferior wall MIs to be sort of a medical/EMS dogma thing. If the patient is hypertensive, it is probably fine to give nitroglycerin. n=1 paramedic experience, but I've given several inferior wall MI patients nitroglycerin with zero issues. For any MI, not just inferior wall only, being borderline to low blood pressure is risky to administer nitroglycerin. I think that nitroglycerin has such a short half life that they aren't going to remain permanently hypotensive after administration unless straight up code, lol. By the time you finish giving them a fluid bolus, the nitroglycerin will be wearing off anyways. Even though I am saying that it is probably OK to give nitroglycerin to these patients, I think nitroglycerin (and morphine) haven't even been shown to decrease morbidity, mortality, or have any real effect on the amount of damage done to the myocardium anyways. For me, the only reason I give it is to treat chest pain.

 

[VFlutter]

A patient with a true RV infarct is extremely preload dependent and very much can have hemodynamic collapse after nitro administration. Having said that, with appropriate fluid resuscitation, low does nitro drips shouldn't hurt anything. 5mcg/min is nothing. SL nitro is 400mcg over a few minutes. Some of these patients require 2-3L or more so there is some truth to the fact that you likely can't dump enough fluid in fast enough if they are tank their pressure and are under resuscitated.

 

[hometownmedic5]

How’s this for a wild idea. Shoot the right sided cardiogram and see if there’s RV involvement. If there is not, we’re arguing about nothing and if there is, chances are excellent their pressure isnt going to support NTG anyway.

 

[PotatoMedic]

https://www.ncbi.nlm.nih.gov/m/pubmed/26024432/

The dogma to whithold ntg on an inferior mi is old and outdated. Yes if you do drop their pressures you have to compensate quickly, but you have just a good a chance of bottoming an inferior mi as you do other mi's.

 

[Tigger]

I guess I don't understand why would be giving nitro in any form to these patients? The primary benefit of nitro is assist with pain control. There are other medications that can do that with significantly less chance of inducing hypotension so why not use those?

 

[PotatoMedic]

I guess I don't understand why would be giving nitro in any form to these patients? The primary benefit of nitro is assist with pain control. There are other medications that can do that with significantly less chance of inducing hypotension so why not use those?

Our medical directors are actually thinking of getting rid of ntg because of that.

 

[StCEMT]

I don't think I've given it at all this year for a STEMI. It's usually pretty low on my list and the first I brought in had respiratory problems that took precedence. I suppose I'd consider it if I had longer transport times, but in my setting I usually don't have time or desire. I have many other things that are actually helpful at improving outcomes or keeping the transfer/continuity of care going smoothly.

To spin off Tigger, I'm much more comfortable with the effects of Fentanyl in sick people than Nitro.

If we are gonna discuss meds in MI's, is anyone giving Metoprolol in the field? We have it in our regional box, but don't currently give it.

 

[Tigger]

A patient with a true RV infarct is extremely preload dependent and very much can have hemodynamic collapse after nitro administration. Having said that, with appropriate fluid resuscitation, low does nitro drips shouldn't hurt anything. 5mcg/min is nothing. SL nitro is 400mcg over a few minutes. Some of these patients require 2-3L or more so there is some truth to the fact that you likely can't dump enough fluid in fast enough if they are tank their pressure and are under resuscitated.

I guess I don't understand the use of low dose NTG when we can just give fent for the same effect. 5mcg/min isn't really going to cause much coronary vasodilation as I recall. And if you're giving fluids at the same time, I guess I don't understand what we are trying to accomplish.

We carried NTG drips for years and they were used so infrequently that we let the waiver expire. I think their best use was for CHF exacerbations but alas no one with more importance cared enough to save them.

 

[VFlutter]

I guess I don't understand the use of low dose NTG when we can just give fent for the same effect. 5mcg/min isn't really going to cause much coronary vasodilation as I recall. And if you're giving fluids at the same time, I guess I don't understand what we are trying to accomplish.

We carried NTG drips for years and they were used so infrequently that we let the waiver expire. I think their best use was for CHF exacerbations but alas no one with more importance cared enough to save them.

Not necessarily advocating for it is use but supposedly does offer some mortality benefit, not great studies. Aside from a RVI a little less preload, reduced ventricular wall stress, and increased coronary perfusion probably helps in most AMIs. But lots of ways to approach it with analgesia, beta blockers, nitroprusside, etc

http://rebelem.com/death-mona-acs-part-iii-nitroglycerin/

Nitroglycerin should still be kept around for APE patients. Massive IV doses with Bipap works wonders.

 

[KingCountyMedic]

If we are gonna discuss meds in MI's, is anyone giving Metoprolol in the field? We have it in our regional box, but don't currently give it.

We carry it and do use it for Acute MI. 5mg IV every 5 minutes up to 15mg (in our guidelines)

It's not used very frequently, if the patient is hypertensive and HR is above 60 we discuss it with the Doc and will usually only give the first dose, we are usually at the hospital pretty quick with most of these folks.

As far as Nitro and Inferior we always do a right sided 12 lead on Inferior MI and would usually just give MS if the right side was positive but we have now finally made the switch to Fentanyl.

 

[StCEMT]

We carry it and do use it for Acute MI. 5mg IV every 5 minutes up to 15mg (in our guidelines)

It's not used very frequently, if the patient is hypertensive and HR is above 60 we discuss it with the Doc and will usually only give the first dose, we are usually at the hospital pretty quick with most of these folks.

As far as Nitro and Inferior we always do a right sided 12 lead on Inferior MI and would usually just give MS if the right side was positive but we have now finally made the switch to Fentanyl.

That's probably how it would be for me. At best I could manage two doses , all three would require inclement weather or something drastic. I'm still curious about the idea of us starting it in the field if there is good research behind it, which it seems like there is compared to NTG from what I recall.

 

[Bullets]

Like others have said, we have started to move away from nitro in MIs, which right now largely depends on the doc we're talking to. Either way we always get that 12lead first so we know if we need to hang fluid and prepare for hypotension. Most of the inferior MIs ive seen have started hypotensive which precluded NTG anyway, but we do give it on a case by case basis depending on their BP. We almost exclusively use fentanyl for pain control and only carry morphine in our backup narcs bag if we run out

If we are gonna discuss meds in MI's, is anyone giving Metoprolol in the field? We have it in our regional box, but don't currently give it.

Yes we carry it on our trucks and our outstations with longer transport times have been giving it

We carried NTG drips for years and they were used so infrequently that we let the waiver expire. I think their best use was for CHF exacerbations but alas no one with more importance cared enough to save them.

This is really what we are carrying it for. Usually if we have acute CHF patients they are getting some SL nitro while we get CPAP ready and start an IV then switch to a nitro drip. Some of our docs are talking about moving to push dose nitro so we can drop the big nitro bottle in our bags

 

[epipusher]

We were giving ntg and asa long before 12 leads.

 

[VFlutter]

We were giving ntg and asa long before 12 leads.

So? And I am sure a few patients suffered because of it.

 

[Aprz]

How’s this for a wild idea. Shoot the right sided cardiogram and see if there’s RV involvement.

I personally don't bother with doing right sided 12-leads/lead V4R; The 12-lead provides us already an excellent view of what is going on. It's the same concept as determining a posterior wall MI seeing the reciprocal changes in the anterior leads or slight ST elevation in lead V6 (since V6 is more posterior than other leads). For recognizing significant right ventricular involvement (RVI), lead V1 already sits over the right side of the heart, so if it has ST elevation, that is a sign of significant RVI. Sometimes it is isoelectric, but lead V2 will have reciprocal change/ST depression since it is on the left side of the heart. On top of that, lead II (white right arm lead to red foot/left leg lead) looks more closely to the left and lead III (black right arm lead to red foot/left leg lead) looks more closely to the right. They are both witnesses to the infarction, but when one has a better view of injury like lead III has more ST elevation than left II, than it is reasonable to believe that the right side has more injury than the left or vise versa when lead II has more ST elevation than lead III. Although it is just an extra electrode/sticker and takes maybe a minute to print another 12-lead, it's still waste of time to me, and lead V4R is more of an unnecessary confirmation.

 

[StCEMT]

I personally don't bother with doing right sided 12-leads/lead V4R; The 12-lead provides us already an excellent view of what is going on. It's the same concept as determining a posterior wall MI seeing the reciprocal changes in the anterior leads or slight ST elevation in lead V6 (since V6 is more posterior than other leads). For recognizing significant right ventricular involvement (RVI), lead V1 already sits over the right side of the heart, so if it has ST elevation, that is a sign of significant RVI. Sometimes it is isoelectric, but lead V2 will have reciprocal change/ST depression since it is on the left side of the heart. On top of that, lead II (white right arm lead to red foot/left leg lead) looks more closely to the left and lead III (black right arm lead to red foot/left leg lead) looks more closely to the right. They are both witnesses to the infarction, but when one has a better view of injury like lead III has more ST elevation than left II, than it is reasonable to believe that the right side has more injury than the left or vise versa when lead II has more ST elevation than lead III. Although it is just an extra electrode/sticker and takes maybe a minute to print another 12-lead, it's still waste of time to me, and lead V4R is more of an unnecessary confirmation.

I feel like I am one of very few people who do this. Largely due to urban EMS transport times, but I can get pertinent info without extra steps.

 

[Tigger]

Not necessarily advocating for it is use but supposedly does offer some mortality benefit, not great studies. Aside from a RVI a little less preload, reduced ventricular wall stress, and increased coronary perfusion probably helps in most AMIs. But lots of ways to approach it with analgesia, beta blockers, nitroprusside, etc

http://rebelem.com/death-mona-acs-part-iii-nitroglycerin/

Nitroglycerin should still be kept around for APE patients. Massive IV doses with Bipap works wonders.

From the link

• The evidence for SL NTG in acute coronary syndromes appears to be extrapolated from IV nitrate dosing
• Nitrates studied in most of these trials were IV nitrates and oral long acting nitrates (i.e. isosorbide dinitrate) not SL nitroglycerin
• In patients with ischemic chest pain, IV nitroglycerin initiated within the first 24 hours of symptom onset reduces overall mortality.

To me this is not enough reason to mess around with nitro in any patient that is close to hypotension unless I still had access to IV (we switched to paste which I am not sure what to make of).

 

[Peak]

I think that you have to look at the goals of treatment with Nitro in order to really address the risks and benefits in MIs. Nitro is given to reduce the work of the myocardium and therefore oxygen demand by reducing blood pressure (reducing afterload). If patients have poor vascular return (especially in cases of dehydration) then yes, you can drop the amount of blood being fed into the right ventricle, impairing the effects of Starling's law, and thusly causing less blood to be fed into the pulmonary vasculature and subsequently the left ventricle; when this is coupled with right ventriclar or atrial dysfunction from ischemia we can see a rather large drop in blood pressure. The nitro in and of itself does not have some magical property that tanks pressure specifically in right sided MIs, you would see similar effects if you gave the patient a large dose of lopressor, nicardipine, or even if they had a decent histamine response to morphine.

From a management standpoint even a 300 mcg tab of SL nitro is a rather large dose (although most systems use 400 mcg tabs), when we give IV nitro we typically start patients at 5-10 mcg/min which over the 5 minute period that we would have given one tab would only be 25-50 MCG nitro. Often NTG is better tolerated in IV or paste than as massive sublingual doses.

I also wouldn't assume that simply because the patient doesn't have right sided EKG involvement that they won't have a drop in their blood pressure, EKGs are only about 90% sensitive and 80% specific for right sided MI even with right sided leads. Further I have had multiple patients drop their pressure from normotensive to the 50s systolic from one 400 mcg SL NTG who on catheterization had no right sided involvement.

From a EMS/ED perspective these patients are unlikely to be significantly detrimented by 1-2 liters of fluids, however I also wouldn't start them unless I actually needed to as it can potentially cause cardiac strain and systemic fluid overload, especially considering that a pretty good number of ACS patients are not the people that we would describe as healthy or athletes. Fluid management also has really implications in the ICU/CCU, although alive now and later on CRRT or a home script of Dig is a lot better than dead now. I wouldn't plan on giving nitro knowing that I need to give fluids, then we are just stacking more problems on the patient. The effect of fluids is directly providing volume to the right side of the heart negating the above detriments to preload.

In my opinion we should be anticipating potential hypotension in ACS, whether is be from NTG, response to narcotics, heart/valve failure, and so on. I don't give nitro without IV access, and I don't give nitro without having at least one bag of NS or LR strung up on a pressure bag. If the patient is significantly hypertensive and could potentially benefit from nitro then I would go for it, but even on a classic lateral STEMI I don't see a lot of benefit of giving nitro to a patient with a pressure of say 120/70 (excluding trialing NTG for CP relief and increasing the index of suspicion of ACS vs benign eitiology, but that isn't really something we need to do in the field).

As far as your Doc's concerns about NTG being deadly, we do plenty of things for patients that carry very real risk. Would he withhold TPA in a thrombotic stoke since it is the most deadly prescribed/ordered drug in medicine? Would we only go defensive on a working structure just because going in is dangerous? Would cops sit outside of an active shooter because they might get shot or accidentally shoot a bystander? Risk always needs to be balanced with benefit, but to say that we won't do something simply because it carries some risk is ridiculous.

In regards to protocols, back in my fire days were were certainly discouraged from giving nitro to inferior/right sided MIs, but it wasn't a contraindication. In my current ED I don't see the 911 agency giving a lot of nitro, but they also have very short transport times. We certainly still see a fair amount of nitro given in tabs from farther agencies and no shortage of drips from HEMS/CCT. Since almost all of my prehospital time is pediatric I don't really give it anymore, but we can give it under protocol.

 

[Bullets]

we switched to paste which I am not sure what to make of.

Huh, any specific reason? We're talking about ditching the paste since its rarely used and we have it in tab, spray, drip and push dose