NTG for chest pain... even when you're thinking respiratory.

[the_negro_puppy]

What about using your clinical judgement and assessments to try and narrow down most likely diagnosis?

Sure, we always lean towards treating CP as cardiac in nature as benefits outweigh the risks of an aspirin, GTN and perhaps even IV MS.

However if the call iis seemingly pleuretic/resp in nature i.e febrile 50 y.o basal rales/crackles, decreased Sp02, mild tachycardia with recent hx of chest infection and mild CP on inspiration, are you really going to start treating with aspirin, GTN etc? particularly if they have no risk factors or cardiac hx?

 

[T1medic]

I dont post often, mostly just read and absorb info. But I'd like to chime in on this one.

Ok first off, yea I know I have a cliche username. I made it back when I was a squirrel a few years ago.

It sucks that US EMS has brought everyone to think like this and all the sue happy people in this world don't help but most medics hear "chest pain"and automatically give NTG as a CYA. In school w are taught, "you see A,B,C you do X,Y,Z" not "you see A,B,C, you assess the pt,do X if appropriate, re-assess, do Y if appropriate, but revert to W if assessment deems appropriate, etc". So as soon as most hear the magic chest pain its straight to NTG. There is also the type that is constantly in fear of the "well my protocol says so." Who wants to be sitting in court trying to justify why you withheld NTG from a pt complaining of chest pain? I don't.

Having said that, I don't throw medications out without having a reason. If the pt complains of chest pain but presents as respiratory, I'm witholding NTG for the time being.

 

[Medic Tim]

Just finished a run where the cc was chest pain. With a little investigation we found it to be respiratory in nature and a few updrafts took care of the problem.

 

[EMSrush]

He is of the thought process "If they're complaining of chest pain, even if I think it's respiratory in nature, they get a nitro SL just to test it out".

Fascinating. Does he do a 12 lead or any other type of assessment first?

 

[usafmedic45]

well rob because you seem to not be a pompous douche like others who sit in the holy EMS Heaven that is EMTLIFE which is like being the coolest kid on the short bus.

Aww...cut Rob some slack, he'll get there eventually.

Seriously, if you're going to get into a debate on here, about the last two people you want to do it with are Smash and DV EMT. Even I stop and think before wading into that. Good luck man.

 

[18G]

Sometime ago (prob many years ago) I read that NTG has very little diagnostic ability. So giving it "just to see" if it lessens the pain (or not) doesn't carry a lot of weight in making the determination of etiology.

Chest pain carries many etiologies and all chest pain is not cardiac. I don't believe in blanket treatment of all chest pain with NTG. Sometimes it is hard to distinguish cardiac or not in the field and I don't have a problem with erring on the side of caution if something is nagging at you on the cardiac side. A 12-lead that is negative DOES NOT rule out cardiac causes. But a good assessment and history can tell an obvious respiratory or musculoskeletal cause most of the time.

The thing with NTG is that it is a pretty innocent drug and has a very short half life. Within 5-10mins the effects are gone. Same with ASA. If the FTO is giving NTG I hope he is giving ASA to or that makes the practice even more mindless.

 

[Handsome Robb]

Aww...cut Rob some slack, he'll get there eventually.

Shhh your going to get me into trouble h34r: I blame you for all my infractions :rofl:

NTG is pretty innocent like 18g said but I still don't think we should be using it as a diagnostic tool.

 

[Veneficus]

The thing with NTG is that it is a pretty innocent drug and has a very short half life. Within 5-10mins the effects are gone. Same with ASA. If the FTO is giving NTG I hope he is giving ASA to or that makes the practice even more mindless.

If I am reading this right, you are saying ASA is a relatively benign drug?

ASA permanantly binds to and inhibits COX 1 and 2.

That inhibits platelet aggregation, inhibits vasoconstriction via TXA2 (one of the more potent constrictors), prevents PGE 2 vasodilation, decreases the inflammatory response of neutrophils, decreases stomach mucosal barrier synthesis, and just for completeness but not important for discussion here decreases uterine contraction.

It takes about 24-48 hours for the body to reconstitute these permanantly inhibited products.

This has an impact on everything from clotting (in any pathology which causes bleeding) as well as reducing the acute immune response (which makes the patient more suseptable to infections).

Depending on your etiology (which I will limit to chest/GI pain) You could do everything from creating or enhancing a bleed to incite a severe infection or reactivate a chronic one.

I agree with you some times in the field you have to decide to give nitro and ASA based on less than perfect information or circumstances.

But that doesn't make it a benign decision. It makes it a prudent one based on risk/benefit analysis.

 

[Rettsani]

I try sometimes to answers
whom also my English is not great and you can misunderstand me.

Here we give only nitro for heart attack and angina symptoms after a thorough medical history and blood pressure measurement. For the addition of nitro spray, blood pressure should be 110/80 mmHg at least.

I think Nitro is not a bad drug, it should only apply it correctly and note the risks.

Nitro reduces the preload of the heart and the oxygen consumption.
The decrease in preload leads to improved blood flow and a decrease of capillary pressure, which explains the effect in cardiac pulmonary edema.
Nitro is capable of to limit the ischemia zone during a Infakt.

 

[Brandon O]

A 12-lead that is negative DOES NOT rule out cardiac causes. But a good assessment and history can tell an obvious respiratory or musculoskeletal cause most of the time.

Just want to add that the idea of a "negative" 12-lead is somewhat vague. There's this idea floating around that you can have a STEMI without any ECG changes, which IMO is largely wrong. (Okay, STEMI by definition has ECG changes, but we really mean any clinically significant coronary occlusion.) If what's meant is that you can have an occlusion without classic, textbook ST elevation, that is very true, but if you widen your net to encompass the many more subtle signs, you do approach 100% sensitivity.

The reason people are still unsure and fall back on things like biomarkers is that the cause of the ECG changes they see may not be clear. But it's pretty reliable that there will be some changes. I have never seen a confirmed MI with a properly-done 12-lead ECG that is truly textbook normal, or at least 100% unchanged from the patient's baseline.

 

[usafmedic45]

There's this idea floating around that you can have a STEMI without any ECG changes, which IMO is largely wrong. (Okay, STEMI by definition has ECG changes, but we really mean any clinically significant coronary occlusion.) If what's meant is that you can have an occlusion without classic, textbook ST elevation, that is very true, but if you widen your net to encompass the many more subtle signs, you do approach 100% sensitivity.

Hence the term "non-ST elevation myocardial infarction".

 

[NomadicMedic]

I have never seen a confirmed MI with a properly-done 12-lead ECG that is truly textbook normal, or at least 100% unchanged from the patient's baseline.

How often do prehospital providers in your area see a baseline 12 lead for comparison to the one obtained in the field?

 

[Shishkabob]

Good... I'm not the only one with this reasoning.



Sad part is I can't really refute it without coming off as a knowitall new employee. Meh.

 

[Dwindlin]

In my limited time off I volunteer with a FD based system and I too have had some issues with my QA/QI officer dinging me for not doing some really archaic things. While I die a bit inside every time I do them, I decided when I started it just isn't worth the headache to argue with him.

 

[Shishkabob]

In my limited time off I volunteer with a FD based system and I too have had some issues with my QA/QI officer dinging me for not doing some really archaic things. While I die a bit inside every time I do them, I decided when I started it just isn't worth the headache to argue with him.

And that's the decision I came to during my FTO period... but it was already too late and it's bit me.



Thing is, this is a progressive system with a fairly robust QA/QI group and direct involvement with the MDs who are very evidence-based medicine... but alas...

 

[DV_EMT]

Seriously, if you're going to get into a debate on here, about the last two people you want to do it with are Smash and DV EMT. Even I stop and think before wading into that. Good luck man.

Thanks, I take that as a compliment

 

[Brandon O]

Hence the term "non-ST elevation myocardial infarction".

Yeah... but I find it to be less than useful terminology at times. What we really care about isn't whether there's ST elevation or not; what we care about is the severity and risk of the occlusion. That's why lots of NSTEMIs still get cathed.

So prehospitally, is there an acute occlusion causing injury? (STEMI or NSTEMI, really either way? Even UA that may deteriorate?) Or is there, well, anything else? (Baseline cardiac changes on the ECG, a non-cardiac event, an acute but non-ischemic cardiac event, etc.) If this is the decision you're trying to make, you can apply a pretty broad ischemia-minded filter, place the results in their clinical context, and otherwise forget about the labels. At least IMO.

 

[themooingdawg]

Uh, yes it does



If its not indicated (see the DIICE pneumonic I used) then why would you give it. Linuss states that he wouldn't give it for a person without a HX of cardiac issues. You wouldn't just give a drug just cause you want to test the waters... especially if you can't reverse it.

Example - I had substernal Chest Pain w/ some shortness of breath on inspiration. I had been down with a cold x2 days prior to onset. I have no Cardiac History, but a Hx or Pneumonia...and I'm 22 y/o. My vitals were stable. If a paramedic had tried to give me Nitro prior to getting an EKG and a set of vitals, I would have refused it because I - the patient - knew that there was no way in hell that i was having angina pectoralisis or an MI given my HX.

Why give a drunkard or diabetic with slurred speech & loss of motor coordination a clot buster when they don't have an active stroke.

here is the problem, you have the mentality that just because you think its one thing, you shouldn't treat it as is, but the thing is, you're not out there to diagnose anything. If somebody, after questioning, still states chest pain, even if they have pain on palpation/inspiration, etc, you're more than likely going to give nitro than to not give it, because the point is you're still treating the chest PAIN, not trying to diagnose out in the field. Yeah, patient might be pleuritic in nature, but how are you gonna look when u come into the ER and say pt has chest pain, blah blah blah, pain of 9/10, oh but we didn't give any nitro because i think its pleuritic.... yeah, but the pt still has pain. and btw, where do you know that gives fibrinolytics out in the field prior to a ct scan to confirm stroke?

 

[themooingdawg]

maybe you can call base and see how they feel about you not wanting to give ASA/nitro, but i highly doubt any base is going to say withhold on everything if the pt states there is pain

 

[themooingdawg]

but then again, it all goes down to where you're working at, protocols, and who your micns are