# Nitro/Aspirin in conjunction



## Jonnyola87 (May 23, 2014)

Can anyone think of an instance in which nitro and aspirin would be given together? Maybe lack of a response to one or the other. It seems that even though aspirin is a platelet inhibitor, the potential drop in bp wouldn't be significant enough to worsen the effects of nitro.  Research has shown that aspirin can enhance the effect of nitro, I'm wondering if anyone has ever heard of it worsening the negative effects. 

Thanks.


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## STXmedic (May 23, 2014)

Umm... When are you not giving them together?... Unless the BP is too low for NTG, or they're allergic to ASA.


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## Jonnyola87 (May 23, 2014)

I apologize, there should be an "n't" at the end of that "would". The last sentence is the most concise question: any experience with a drop in bp associated with ASA which would contraindicate nitro? Any examples of negative interactions at all?


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## JPINFV (May 23, 2014)

Is there a time when you wouldn't give ASA and nitro together? The only think I can think of is the cheeky "if there's a contraindication to one." Otherwise, no.


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## STXmedic (May 23, 2014)

A quick search reveals one study from 30 years ago, with 7 subjects and 3x the dose of ASA given to most patients.


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## Jonnyola87 (May 23, 2014)

I had the same concerns with that paper (Pubmed, E. Rey, et al?) I couldn't imagine a response to ASA to such a degree that nitro would be off the table.  I appreciate the responses, both.


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## blindsideflank (May 23, 2014)

Didn't read article yet but high dose Asa can inhibit prostacyclin potentially causing vasoconstriction


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## Jonnyola87 (May 23, 2014)

From what I understand, the effects of NSAIDs would cover for the degradation of the prostacyclin pathway until transcription resumes, which is pretty rapid.  So use of ASA would have to be pretty extensive to counteract prostacyclin. All in all, there shouldn't be a scenario in which vitals are so affected as to warrant holding off on another dilator (nitro).


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## JPINFV (May 23, 2014)

Jonnyola87 said:


> From what I understand, the effects of NSAIDs would cover for the degradation of the prostacyclin pathway until transcription resumes, which is pretty rapid.  So use of ASA would have to be pretty extensive to counteract prostacyclin. All in all, there shouldn't be a scenario in which vitals are so affected as to warrant holding off on another dilator (nitro).




Another dilator? ASA isn't considered a, or used for, vasodilation.


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## Jonnyola87 (May 23, 2014)

No, but prostacyclins are.


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## FLdoc2011 (May 23, 2014)

The only time I worry about NSAIDS in light of hemodynamic instability/ hypotension is there deleterious effects on renal perfusion.


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## TheLocalMedic (May 26, 2014)

Okay...  Am I missing something here?  Aspirin is neither a vasoconstrictor nor vasodilator, at least at therapeutic doses.

Sounds like the OP may just simply be uneducated about what NTG and ASA are and what their effects are.


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## SeeNoMore (May 26, 2014)

I think the key phrase is "therapeutic doses". Obviously Nitro and ASA are commonly given together without an increase in concern for hypotension. I don't think there are many real world situations in which patients are being given far higher than standard does of ASA in conjunction with nitrates. Even when given for typical reasons,  standard doses of ASA may not confer a benefit over low dose ASA therapy. Out of curiosity  what made you ask this? Were you just curious because of the study you read?


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## Drax (May 26, 2014)

Jonnyola87 said:


> I had the same concerns with that paper (Pubmed, E. Rey, et al?) I couldn't imagine a response to ASA to such a degree that nitro would be off the table.  I appreciate the responses, both.



The course still has us giving them in conjunction...well, one after the other.

I know M.O.N.A is standard treatment for ALS capable levels, EMT-B's go O.A.N. if I'm not mistaken.

If you're not seeing signs of improvement by the time (or 5 minutes following) you've administered your last doses (per protocol), you're supposed to treat as a heart attack, right?


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## Medic Tim (May 26, 2014)

Drax said:


> The course still has us giving them in conjunction...well, one after the other.
> 
> 
> 
> ...




Hopefully you aren't just blindly putting O2 on everyone. If so your program is outdated( like most). Even nr now tests titrated o2. 
We use nitro for acute coronary syndrome. Even though it and morphine don't decrease morbidity and mortality. If we suspect chest pain or pressure is cardiac in nature we give nitro in most cases . 
At the BLS level you won't have 12 lead (in most cases ) or poc labs. So most all chest pains are treated as "heart attacks"or ACS.

Do you know how nitro works? What effects it has in the body? What are we trying to accomplish by administering it?

If you can't answer the above questions you shouldn't be giving it.


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## JPINFV (May 26, 2014)

Drax said:


> If you're not seeing signs of improvement by the time (or 5 minutes following) you've administered your last doses (per protocol), you're supposed to treat as a heart attack, right?




As an EMT, chest discomfort without obvious etiology ("I just took a baseball bat to the chest") is acute coronary syndrome until proven otherwise. There is no "If the pain goes away 5 minutes after treatment, we're good." You shouldn't be waiting 5 minutes to see if there is a response to your treatment. 

Additionally, ASA is not given to relieve pain. You shouldn't expect to see the patient's pain level decrease with it because that isn't ASA's job.


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## Drax (May 26, 2014)

retracted


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## Drax (May 26, 2014)

JPINFV said:


> As an EMT, chest discomfort without obvious etiology ("I just took a baseball bat to the chest") is acute coronary syndrome until proven otherwise. There is no "If the pain goes away 5 minutes after treatment, we're good." You shouldn't be waiting 5 minutes to see if there is a response to your treatment.
> 
> Additionally, ASA is not given to relieve pain. You shouldn't expect to see the patient's pain level decrease with it because that isn't ASA's job.



So you're saying, treat and transport without delay then?


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## JPINFV (May 26, 2014)

Drax said:


> So you're saying, treat and transport without delay then?


An EMT with a chest pain patient? Yes. However, in general, I can't really think of very many situations where an EMT shouldn't treat and transport since the disposition is going to be the same. There really isn't a place for EMTs to "treat and wait to see a response."


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## Drax (May 26, 2014)

JPINFV said:


> An EMT with a chest pain patient? Yes. However, in general, I can't really think of very many situations where an EMT shouldn't treat and transport since the disposition is going to be the same. There really isn't a place for EMTs to "treat and wait to see a response."



It absolutely makes more sense to move out right away. I just feel like there was a different process that I was taught...something to do with up to three separate doses, then calling for upgrade...bah nevermind. What the hell was a I taught? <_<


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## JPINFV (May 26, 2014)

Drax said:


> It absolutely makes more sense to move out right away. I just feel like there was a different process that I was taught...something to do with up to three separate doses, then calling for upgrade...bah nevermind. What the hell was a I taught? <_<




Patients are taught that they should take 3 doses of nitro, and if their chest pain isn't resolved (i.e. it's not stable angina), then call 911. This, for some reason and including the 3 dose nitro treatment, has made it into EMS. The problem is that the 3 dose nitro rule shouldn't apply to medical professionals, and the standard placed on medical professionals, especially those in emergency medicine, are much higher. No one is going to give a chest pain patient nitro in the ED and do nothing else if the pain goes away in 1-3 doses.


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## Drax (May 26, 2014)

JPINFV said:


> Patients are taught that they should take 3 doses of nitro, and if their chest pain isn't resolved (i.e. it's not stable angina), then call 911. This, for some reason and including the 3 dose nitro treatment, has made it into EMS. The problem is that the 3 dose nitro rule shouldn't apply to medical professionals, and the standard placed on medical professionals, especially those in emergency medicine, are much higher. No one is going to give a chest pain patient nitro in the ED and do nothing else if the pain goes away in 1-3 doses.



Would you mind going a little into what they would do?


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## JPINFV (May 26, 2014)

Drax said:


> Would you mind going a little into what they would do?


Chest pain workup?

Chest x-ray, 12 lead ekg, serial troponins. Depending on the presentation, patient's history (TIMI score), and the physician's experience, you're going to see everything from a "delta troponin" (second troponin 2-4 hours after the first, if both are negative, then discharge with PMD followup), to admission with troponins q8 hours x 3 followed by an inpatient stress test (EKG while either on a treadmill or after given a medication to increase the patient's heart rate), or possibly a stress echo (same concept, except with echocardiogram). 

Of course if anything is positive, then that's a different situation completely. Additionally, the differential for chest pain is about 3 pages long, hence why every chest pain is going to get a chest x-ray.


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## rugbyguy (May 27, 2014)

Jonnyola87 said:


> I apologize, there should be an "n't" at the end of that "would". The last sentence is the most concise question: any experience with a drop in bp associated with ASA which would contraindicate nitro? Any examples of negative interactions at all?



So let's break down the 2 drugs.

Nitro is a vasodilator. As a basic you can only "assist" a pt with their own, which means they have to be prescribed Nitro. First you must check the BP. We check the BP because it is a vasodilator, so we need to make sure the pressure is <90 systolic first as to not knock them out. Nitro is usually prescribed for angina pectoris, which is usually caused by atherosclerosis of the arteries coming off the heart. Nitro dilates the arteries when they wont them self, thus allowing more blood to be pumped into the systemic system, and relieving the patient's pain.

Aspirin is an anti-platelet. This inhibits thromboxin, the chemical that encourages platelets to stick and form clots over cuts in vessels. This way there is less chance of platelets clotting, and then breaking off, forming an embolus, then getting caught in the system later down the line. Also it can make blood less viscous, allowing for easier flow.

These are the main points covered in my EMT class if I remember right on each of these drugs. While they do a lot more, let's focus on these as the others are irrelevant at this time. According to that, why would they not always be given together for chest pain? Nitro for the angina, angina pain means blood is not flowing and properly feeding the heart, so dilate the blood vessels to allow more in, use aspirin to make the blood less viscous and able to move through the body easier.

I knew killing myself the last 3 weeks for my blood and cardiology A&P test would pay off.


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## Brandon O (Jul 25, 2014)

Perhaps the OP has a background in biochem, or just took a good A&P class. Strictly from the pharmocodynamics, it might seem to follow that aspirin could cause vasodilation, given that it's blocking thromboxane A2, a vasoconstrictor. On the other hand, its broader anti-inflammatory effects in blocking the COX-1 pathway might be expected to do the opposite (triad asthma is a cool example of this). Regardless, neither effect has much of a _hemodynamic_ effect in vivo. We use aspirin for the antiplatelet effects.

The idea of nitro being diagnostic for MI is a tricky one. It's probably true that a patient who gets some relief from nitro is more likely to have an ischemic cause (i.e. ACS), but probably LESS likely that it's a total occlusion (i.e. STEMI). Most folks agree now that nitro rarely dilates the actual blocked artery; the body's pretty good about locally regulating bloodflow to manage hypoxia, so odds are that vessel's already fully dilated. (Versus a partial stenosis which does get relief, more like a stable angina.) Nitro's role is more in dilating the peripheral vessels and decreasing cardiac preload, thus reducing work on the heart -- reducing oxygen demand, not increasing supply.

Long story short, it's not much help diagnostically.



JPINFV said:


> There really isn't a place for EMTs to "treat and wait to see a response."



Cardiac arrest.


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## JPINFV (Jul 25, 2014)

Brandon O said:


> Cardiac arrest.




...touche... (even if it isn't ACS being treated at that specific time).


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## Bearamedic (Jul 25, 2014)

Brandon O said:


> Perhaps the OP has a background in biochem, or just took a good A&P class. Strictly from the pharmocodynamics, it might seem to follow that aspirin could cause vasodilation, given that it's blocking thromboxane A2, a vasoconstrictor. On the other hand, its broader anti-inflammatory effects in blocking the COX-1 pathway might be expected to do the opposite (triad asthma is a cool example of this). Regardless, neither effect has much of a _hemodynamic_ effect in vivo. We use aspirin for the antiplatelet effects.




I was medic-taught that asa helps prinzmetal's because it alleviates vasospasm 
(txa2, can cause vasospasm?; formation inhibited via asa cox blocking )
Matches up with your initial pharmacodynamics hypothesis.


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## Brandon O (Jul 25, 2014)

Bearamedic said:


> I was medic-taught that asa helps prinzmetal's because it alleviates vasospasm



Sounds... duuuubious.


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## Bearamedic (Jul 25, 2014)

Brandon O said:


> Sounds... duuuubious.



Yep, but i dont know enough to say that this definitely isnt the case. I can only rely on what some preceptor said that one time.


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## Brandon O (Jul 25, 2014)

Yeah. I haven't played around with the Prinzmetal's literature enough to know anything for sure, but the choices I've heard recommended include nitro and CCBs. I suppose aspirin could work but that would be rather bizarre compared to its effects elsewhere, and in fact (briefly checking some references now) it looks like it might be deleterious -- due to the aforementioned anti-inflammatory effects.


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