# Atypical STEMT Treatment



## JwL (Oct 8, 2019)

Scenario:

60 y/o diabetic woman with a Chief complaint of weak, diphoretic, and nausea. 
No chest pain 
12 lead shows ST Elevation in the anterior leads . 

Would you administer Nitro assuming BP is good ?


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## DrParasite (Oct 8, 2019)

Define a good BP...  how is the pulse rate? 

What are you giving NTG for?


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## JwL (Oct 8, 2019)

DrParasite said:


> Define a good BP...  how is the pulse rate?
> 
> What are you giving NTG for?


BP is 160/90, HR 88
Patient is a diabetic experiencing a "silent" MI. 
Typical chest pn resolved using NTG is the result of restoring blood flow to an ischemic area.  So, if you ID a stemi, Wouldn't the patient benefit  even in the absence of chest pn?


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## Rano Pano (Oct 8, 2019)

I think where @DrParasite is coming from is your opening post doesn’t describe a confirmed MI. It would be in my index of suspicion, but you’ve provided a fraction of a pt assessment. Low BGL causes these symptoms. Reciprocal changes on that 12? 12 lead imposter?

If you’re saying you have a confirmed Anterior STEMI & all vitals are within a range you feel comfortable giving your STEMI meds then why wouldn’t you?
A big reason we treat pain is because of the added workload it puts on a heart that’s already oxygen deprived. NTG reduces this by decreasing preload.


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## DesertMedic66 (Oct 8, 2019)

I think jwl  is meaning more from the standpoint that the patient is having a STEMI but having no chest pain. All of my agencies that I work for only want NTG given to relieve chest pain. So if there is no chest pain then no NTG will be given.


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## JwL (Oct 8, 2019)

Yes, my scenario is a confirmed STEMI. Our protocols indicate NTG for chest pain only. I was debating a co-worker regarding atypical presentations giving NTG with no pain during a Hot MI. The pain is just a symptom of the underlying issue which is ultimately why you are administering NTG. So yes, I have always administered it in the absence of pain if I have a confirmed STEMI. I was just curious if anyone else was onboard with the idea.


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## Tigger (Oct 9, 2019)

I thought we had established that SL NTG doesn't improve outcomes much if at all?


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## FiremanMike (Oct 9, 2019)

Tigger said:


> I thought we had established that SL NTG doesn't improve outcomes much if at all?



There was a block about nitro this past year at Eagles..  Some docs supported it, some docs talked about higher dosing of nitro, it was really all over the place...


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## SpecialK (Oct 9, 2019)

Why? GTN doesn't treat STEMI.

There's your answer.


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## JwL (Oct 9, 2019)

SpecialK said:


> Why? GTN doesn't treat STEMI.
> 
> There's your answer.


Ok, so you wouldn't give NTG for chest pain if your pt was experiencing a STEMI in the prehospital setting ? As of today,  we use NTG to tx chest pn. All variables aside, the question was in reference to prehospital administration of NTG for a silent MI.  Reduction of preload and coronary artery dilation are the ultimate goals even in the absence if chest pn.


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## DrParasite (Oct 9, 2019)

Tigger said:


> I thought we had established that SL NTG doesn't improve outcomes much if at all?





SpecialK said:


> Why? GTN doesn't treat STEMI.


That was what I getting at.  NTG is given to relieve chest pain, however your patient is currently pain free.  It doesn't "fix" the STEMI, nor does it improve patient outcomes (although, it does help to relieve the any cardiac pain the patient is feeling).

So I ask again, what is your goal when administering NTG on this STEMI who isn't having chest pain?


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## FiremanMike (Oct 9, 2019)

Bonus question - what is the actual etiology of the pain which is associated with cardiac ischemia..


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## VentMonkey (Oct 9, 2019)

ASA anyone? As @Tigger mentions, it's substantially more beneficial in the ACS crowds than NTG. Whenever I've had these patients with atypical presentations, high cardiac-origin suspicions, and all the classic co-morbidities I'd feel much better having given the ASA in lieu of any NTG.


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## JwL (Oct 9, 2019)

DrParasite said:


> That was what I getting at.  NTG is given to relieve chest pain, however your patient is currently pain free.  It doesn't "fix" the STEMI, nor does it improve patient outcomes (although, it does help to relieve the any cardiac pain the patient is feeling).
> 
> So I ask again, what is your goal when administering NTG on this STEMI who isn't having chest pain?


So again I will reiterate.  The atypical present resprents the fact that diabetic woman are infamos for having silent MIs. The diabetes results in them not perceiving pn as a patient without diabetes.  My point is, in the same scenario on a pt with no Hx will most likely have chest pn in the event of an MI. The diabetic pt may be experiencing the identical cardiac event with no pain. So why not tx the same? The only deterrent is you wont have a pn scale to judge effectiveness.


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## Tigger (Oct 9, 2019)

JwL said:


> So again I will reiterate.  The atypical present resprents the fact that diabetic woman are infamos for having silent MIs. The diabetes results in them not perceiving pn as a patient without diabetes.  My point is, in the same scenario on a pt with no Hx will most likely have chest pn in the event of an MI. The diabetic pt may be experiencing the identical cardiac event with no pain. So why not tx the same? The only deterrent is you wont have a pn scale to judge effectiveness.


Because the intervention is not shown to be helpful? It's quite rare to see ACS treated with NTG in this region. Maybe if the patient was quite hypertensive and/or not responsive to fentanyl I'd consider it. But now, even "classic" STEMIs don't routinely get NTG.


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## JwL (Oct 9, 2019)

Tigger said:


> Because the intervention is not shown to be helpful? It's quite rare to see ACS treated with NTG in this region. Maybe if the patient was quite hypertensive and/or not responsive to fentanyl I'd consider it. But now, even "classic" STEMIs don't routinely get NTG.


Gotcha.. this is interesting ...we r in Florida and routinely give NTG for chest pn


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## RocketMedic (Oct 13, 2019)

Aspirin, potentially heparin or Plavix, metoprolol, maybe nitro, quick trip to cath lab


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## E tank (Oct 13, 2019)

RocketMedic said:


> Aspirin, potentially heparin or Plavix, metoprolol, maybe nitro, quick trip to cath lab



If the patient ends up having a CABG because of inability to stent from whatever reason, plavix causes a lot of avoidable problems. If there would ever be a choice, choose heparin for that reason.


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## Akulahawk (Oct 14, 2019)

JwL said:


> So again I will reiterate.  The atypical present resprents the fact that diabetic woman are infamos for having silent MIs. The diabetes results in them not perceiving pn as a patient without diabetes.  My point is, in the same scenario on a pt with no Hx will most likely have chest pn in the event of an MI. The diabetic pt may be experiencing the identical cardiac event with no pain. So why not tx the same? The only deterrent is you wont have a pn scale to judge effectiveness.


NItroglycerin is used to treat chest pain. If there's no chest pain, what's the indication for the nitroglycerin? Given those vital signs and no other signs or symptoms that lead me to think that nitroglycerin is indicated, I would not give it. In short, if the only reason you're giving it is the STEMI on the EKG and she otherwise has zero signs or symptoms of a cardiac nature, then you're not doing her any favors. Nitroglycerin doesn't actually treat the cause of the STEMI. Same idea goes for using morphine or fentanyl. You're looking to treat the pain but neither actually treats the STEMI. 

The other night, my ED sent a patient out to a Cath Lab. STEMI, confirmed by labs. The morphine and nitroglycerin we administered didn't do anything to remove the clot that was causing the ischemia. They relieved the pain, and that's their only real job in this scenario.

The kicker of it all is that about 40 minutes of time could have been saved if the EMS crew had initially taken the patient to a facility with a cath lab when their 12-lead said "STEMI" instead of bringing the patient to my facility. We're good at this... My point: Know your local system well enough that you know what the hospitals are capable of so that you can make a good destination decision and potentially save mucho time because facilities that can't do what's needed must do their EMTALA stuff, arrange for appropriate transport... stuff that takes time. Just another instance where another 10-15 minutes transport = 40-60 minutes saved from onset of sx to balloon time.


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## FiremanMike (Oct 14, 2019)

Akulahawk said:


> NItroglycerin is used to treat chest pain. If there's no chest pain, what's the indication for the nitroglycerin?



I disagree with this.  Theoretically, nitro is given to vasodilate the coronary arteries to improve blood-flow to an area of the heart which is hypoxic due to a spasm or blockage.  The indication for giving nitro, then, is that you feel your patient is having a an event related to hypoxic cardiac tissue.

This is why my side-bar question earlier in the thread becomes pertinent, which is "what is the actual etiology of chest pain".  As of my last research on the topic, no one base been able to definitively say why hypoxic cardiac tissue leads to pain.  Ultimately, this leads into why some people can be having significant cardiac events without associated chest pain.

Whether you believe nitro is helpful, harmful, or a non factor in cardiac events is a slightly different topic, although I will again mention that there are studies in both directions on this topic.


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## E tank (Oct 14, 2019)

FiremanMike said:


> I disagree with this.  Theoretically, nitro is given to vasodilate the coronary arteries to improve blood-flow to an area of the heart which is hypoxic due to a spasm or blockage.  The indication for giving nitro, then, is that you feel your patient is having a an event related to hypoxic cardiac tissue.
> 
> This is why my side-bar question earlier in the thread becomes pertinent, which is "what is the actual etiology of chest pain".  As of my last research on the topic, no one base been able to definitively say why hypoxic cardiac tissue leads to pain.  Ultimately, this leads into why some people can be having significant cardiac events without associated chest pain.
> 
> Whether you believe nitro is helpful, harmful, or a non factor in cardiac events is a slightly different topic, although I will again mention that there are studies in both directions on this topic.


 
Agree that there are multiple advantageous effects of NTG outside of pain relief in the setting of myocardial ischemia. Not the least of which is preservation of the hypokinetic RV in the context of relative or actual pulmonary hypertension. If you can keep the RV sending blood to the LV you've won more than half the battle.


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## OKparamurse (Oct 19, 2019)

Okay, relatively seasoned paramedic asking here, though not nearly as smart as the frequent fliers on this board, I give ASA to almost all of my chest pain pts, but I only give NTG to suspected acute cardiac event pts. And by acute cardiac pts; I mean pts with non-reproducible chest pain, severe angina pectoris, cardiac hx, high risk cardiac event pts, and others.


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## Peak (Oct 20, 2019)

The amount of vasodilation from nitro in the presence of thrombotic occlusion is trivial at best. 

Pain relief from nitro largely from reducing after load on the heart decreasing the oxygen consumption and therefore reducing the ischemic process. 

An argument could certainly be made for giving a medication to reduce blood pressure and therefore the work being performed on the heart. Generally we would prefer for this to be achieved with a beta blocker as it lowers mortality unlike nitro, however that is not an option for most EMS services. I'm personally not a fan of SL nitro, I think it is a uncontrolled administration method compared to paste or preferably a drip. Between a rock and a hard place I would give SL nitro if I think it would be of benefit and I had no better option, but I think the role is extremely limited outside of as part of a rule out during chest pain evaluation and risk stratification.


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## MSDeltaFlt (Oct 24, 2019)

JwL said:


> Scenario:
> 
> 60 y/o diabetic woman with a Chief complaint of weak, diphoretic, and nausea.
> No chest pain
> ...




This sounds like a question best reserved for one's educator.  Because depending on your region, your service, and your protocols, nitroglycerine in this scenario is either stated as an absolute or is stated to consider.  Some service have to give while others don't.  So what does your medical director want you to do?  Does he/she want you to think critically and consider NTG?  Or does he/she want you to give the d@mn nitro?


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## Tigger (Oct 24, 2019)

I think I would rather be treating patients based on evidence as opposed to someone just telling me to do it.


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## Peak (Oct 24, 2019)

Tigger said:


> I think I would rather be treating patients based on evidence as opposed to someone just telling me to do it.



That would be the difference between being a technician and a clinician, and EMS should always be trying to advance in the latter.


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## CANMAN (Oct 24, 2019)

Tigger said:


> I think I would rather be treating patients based on evidence as opposed to someone just telling me to do it.



Rather yes, but deviating from an agency or state protocol despite evidence one way or another is an issue in the meanwhile. I may not 100% completely agree with all treatments and might be more up to date on evidence based research then someone writing a protocol that year, but until that protocol changes from a protocol submission/revision I'm bound to follow it if I want to keep a state license, as are most am I not correct?


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## Tigger (Oct 24, 2019)

CANMAN said:


> Rather yes, but deviating from an agency or state protocol despite evidence one way or another is an issue in the meanwhile. I may not 100% completely agree with all treatments and might be more up to date on evidence based research then someone writing a protocol that year, but until that protocol changes from a protocol submission/revision I'm bound to follow it if I want to keep a state license, as are most am I not correct?


Sure. I am not suggesting doing something that you have no guideline for. But if the guideline is crap, does your system require you to provide some sort of outdated treatment? I can't think of a time where I was dinged for withholding something that there was no evidence for. Perhaps I am just fortunate that our CPGs rarely mandate anything. We were never required to give NTG to ACS patients and when it was found that Fentanyl was just as good at treating actual pain in the ACS setting, many of us reevaluated how we gave it to patients.


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## CANMAN (Oct 24, 2019)

Tigger said:


> Sure. I am not suggesting doing something that you have no guideline for. But if the guideline is crap, does your system require you to provide some sort of outdated treatment? I can't think of a time where I was dinged for withholding something that there was no evidence for. Perhaps I am just fortunate that our CPGs rarely mandate anything. We were never required to give NTG to ACS patients and when it was found that Fentanyl was just as good at treating actual pain in the ACS setting, many of us reevaluated how we gave it to patients.



Gotcha, yup certain states (Maryland for example) say active chest pain that is potentially cardiac in nature should get NTG.


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## FiremanMike (Oct 25, 2019)

CANMAN said:


> Gotcha, yup certain states (Maryland for example) say active chest pain that is potentially cardiac in nature should get NTG.



But I think that is the crux of this debate, there is a likely cardiac event that is presenting without chest pain..


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## CWATT (Oct 26, 2019)

Tigger said:


> I thought we had established that SL NTG doesn't improve outcomes much if at all?



How are we defining outcomes?  Mortality?  Cardiac wall function post MI?


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## Lemur (Nov 9, 2019)

FiremanMike said:


> I disagree with this.  Theoretically, nitro is given to vasodilate the coronary arteries to improve blood-flow to an area of the heart which is hypoxic due to a spasm or blockage.  The indication for giving nitro, then, is that you feel your patient is having a an event related to hypoxic cardiac tissue.
> 
> This is why my side-bar question earlier in the thread becomes pertinent, which is "what is the actual etiology of chest pain".  As of my last research on the topic, no one base been able to definitively say why hypoxic cardiac tissue leads to pain.  Ultimately, this leads into why some people can be having significant cardiac events without associated chest pain.
> 
> Whether you believe nitro is helpful, harmful, or a non factor in cardiac events is a slightly different topic, although I will again mention that there are studies in both directions on this topic.


The idea that nitro dilates coronary arteries and that this is the mechanism responsible for its anti-anginal effects is probably not right. At least it’s not the full story. More likely it addresses the “demand” problem by reducing preload.

In stable angina, the mechanism of the chest pain is transient mismatch between oxygen supply and demand but the coronary circulation is patent (perhaps reduced in diameter in places but ultimately permits flow). In most STEMIs, there is near-total or total occlusion of a vessel with clot. You aren’t going to handle that with nitro. You may help the pain by reducing preload. But to my knowledge, it hasn’t been established that there is any benefit beyond analgesia.


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## E tank (Nov 9, 2019)

Lemur said:


> The idea that nitro dilates coronary arteries and that this is the mechanism responsible for its anti-anginal effects is probably not right. At least it’s not the full story. More likely it addresses the “demand” problem by reducing preload.
> 
> In stable angina, the mechanism of the chest pain is transient mismatch between oxygen supply and demand but the coronary circulation is patent (perhaps reduced in diameter in places but ultimately permits flow). In most STEMIs, there is near-total or total occlusion of a vessel with clot. You aren’t going to handle that with nitro. You may help the pain by reducing preload. But to my knowledge, it hasn’t been established that there is any benefit beyond analgesia.



NTG causes a fall in pulmonary vascular resistance which is just RV afterload. As a result it potentially causes a rise in RV stroke volume which increases cardiac output and therefore coronary artery flow.

 To the extent that this effect is mitigated by a fall in venous return in a particular patient, hard to say. 

 That there might be a single vessel acutely narrowed by a fixed defect doesn't mean that increasing collateral vessel flow won't help.


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## Lemur (Nov 10, 2019)

E tank said:


> NTG causes a fall in pulmonary vascular resistance which is just RV afterload. As a result it potentially causes a rise in RV stroke volume which increases cardiac output and therefore coronary artery flow.
> 
> To the extent that this effect is mitigated by a fall in venous return in a particular patient, hard to say.
> 
> That there might be a single vessel acutely narrowed by a fixed defect doesn't mean that increasing collateral vessel flow won't help.


I think the larger point is we just don’t know the precise contributions of these various effects of the drug in its use to relieve chest pain. In my mind there is no clear reason to give it to patient with MI not complaining of chest discomfort because maybe it will increase collateral flow. It’s not a bad thought but there isn’t evidence that it’s helpful.


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## E tank (Nov 10, 2019)

Lemur said:


> I think the larger point is we just don’t know the precise contributions of these various effects of the drug in its use to relieve chest pain.



We don't know the precise contributions to pain relief but we do know what the drug does in terms of the things we know are good for the stressed, ischemic heart and can infer them with reasonable confidence. 



Lemur said:


> In my mind there is no clear reason to give it to patient with MI not complaining of chest discomfort because maybe it will increase collateral flow. It’s not a bad thought but there isn’t evidence that it’s helpful.



Agree that a situation where empiric therapy with NTG in the absence of pain isn't 'a thing' but, not to put too fine a point on it, improving collateral flow is hardly the only reason that it would be useful.


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## Frank frankerson ESQ (Dec 13, 2019)

E tank said:


> We don't know the precise contributions to pain relief but we do know what the drug does in terms of the things we know are good for the stressed, ischemic heart and can infer them with reasonable confidence.
> How many STEMI’s you all seen? 1 call a day rural i would say one a year, a real one anyway. Not being insulting. ACS looks like alot of things. Repeat EKGs on the way to the hospital, SUBTLE things are key. STEMI is a RARE, time sensitive thing, it can change on paper quickly. Generally you catch subtleties before the monitor printout says its one, or you see them after ROSC.
> 
> 
> ...


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## Frank frankerson ESQ (Dec 13, 2019)

Whoops posted my reply in the middle of the posters quote


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## Frank frankerson ESQ (Dec 13, 2019)

Frank frankerson ESQ said:


> How many STEMI’s you all seen? 1 call a day rural i would say one a year, a real one anyway. Not being insulting. ACS looks like alot of things. Repeat EKGs on the way to the hospital, SUBTLE things are key. STEMI is a RARE, time sensitive thing, it can change on paper quickly. Generally you catch subtleties before the monitor printout says its one, or you see them after ROSC


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## Frank frankerson ESQ (Dec 13, 2019)

FiremanMike said:


> I disagree with this.  Theoretically, nitro is given to vasodilate the coronary arteries to improve blood-flow to an area of the heart which is hypoxic due to a spasm or blockage.  The indication for giving nitro, then, is that you feel your patient is having a an event related to hypoxic cardiac tissue.
> 
> This is why my side-bar question earlier in the thread becomes pertinent, which is "what is the actual etiology of chest pain".  As of my last research on the topic, no one base been able to definitively say why hypoxic cardiac tissue leads to pain.  Ultimately, this leads into why some people can be having significant cardiac events without associated chest pain.
> 
> Whether you believe nitro is helpful, harmful, or a non factor in cardiac events is a slightly different topic, although I will again mention that there are studies in both directions on this topic.


NTG is useful in some presentations, but inferior MI can first present with nothing, or subtle things on the EKG.


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## JwL (Dec 13, 2019)

Mike, I think you are 1 of 2 people replying who actually understood my question. Yes. In the scenario,  the cardiac event is due to a blockage indicated by ST elevation in the anterior leads on the 12 lead. I'm my experience, diabetic women sometimes do not perceive pain like the average individual but may be experiencing the same cardiac event. People are replying with transport destinations, other Tx meds, inferior MIs, etc. I'm wondering if anyone actually read the entire question I proposed.  Maybe I didn't present the question appropriately. I guess "silent MIs" are not apart of the curriculum? Next, people will be saying "cardiac asthma" should be treated with albuterol/atrovent and no NTG ...lol jk


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## JwL (Dec 13, 2019)

Frank, I dont work in a rural area. We tx and transport hot MIs all year long so I'm afforded the opportunity to view real time 12 leads and even 15 leads when indicated. So, the senario presented with with a 12 lead indicating anterior lead elevation and I will even throw in reciprocal changes in leads 2,3,aVF with the pt being diphoretic and vomiting.  All vitals are stable.  The question was would one give NTG in the absence of CP knowing your pt is a diabetic woman?


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## Frank frankerson ESQ (Dec 15, 2019)

_


JwL said:



			Frank, I dont work in a rural area. We tx and transport hot MIs all year long so I'm afforded the opportunity to view real time 12 leads and even 15 leads when indicated. So, the senario presented with with a 12 lead indicating anterior lead elevation and I will even throw in reciprocal changes in leads 2,3,aVF with the pt being diphoretic and vomiting.  All vitals are stable.  The question was would one give NTG in the absence of CP knowing your pt is a diabetic woman?
		
Click to expand...

You dont need reciprocal changes at all, you know that. If you’re 100% sure its a real MI and there are no contraindications its ok, but you must really think before you give NTG, and you are, which i respect. You have stable vitals, are you going 75 minutes on an IFT to a STEMI facility when youre not rural? The usual is you have a nitro drip, 2 docs, 10 residents, bilateral 14s, serial 12 leads, full hx, pads on, and instructions on what to do, before you even get to the patient. Might as well put a bow on it for you as well. When, in your urban “hot MI” IFT experience have you had to make the decision you are talking about? Diabetic woman out of the blue STEMI, during transport in URBAN IFT? It can happen, but like i said before its RARE. Youre already transporting a STEMI so i dont understand. Im addressing the issue that you seem to see it frequently. Lets talk about 911. A call with limited hx? Call medical control, send them the 12 lead. The monitor can print out ACUTE MI and it could look like one. Lead placement, artifact, early repol, BBB etc can make it look like, and make the monitor say, something that it isnt. Its not a simple decision in 911. If you stay current on 12 leads, think before you do something, and youre convinced its a STEMI, NTG will benefit the pt in your diabetic scenario. Be safe.._


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