Atypical STEMT Treatment

[E tank]

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.

 

[OKparamurse]

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.

 

[Peak]

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.

 

[MSDeltaFlt]

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 ?

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?

 

[Tigger]

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

 

[Peak]

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.

 

[CANMAN]

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?

 

[Tigger]

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.

 

[CANMAN]

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.

 

[FiremanMike]

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..

 

[CWATT]

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?

 

[Lemur]

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.

 

[E tank]

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.

 

[Lemur]

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.

 

[E tank]

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.

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.

 

[Frank frankerson ESQ]

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.



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.

 

[Frank frankerson ESQ]

Whoops posted my reply in the middle of the posters quote

 

[Frank frankerson ESQ]

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

 

[Frank frankerson ESQ]

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.

 

[JwL]

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