ASA & Nitro

mikie

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For us basics in the area, we can administer 7 drugs (O2 is included). For chest pain, we have nitro spray and 'baby' asprin (4 tabs. for 324 mg)

My question is when to chose nitro or ASA and vise versa.

(per our protocol):

Nitroglycerin
Indication: Chest pain w/ Systolic > 100. Contraindications: Systolic < 100, altered LOC, Pt. Already taken max dose, erectile meds. within 48-72 hours)

Baby Aspirin (Chewable)
Indication: Chest pain, suspected angina or MI. Contraindication: Allergic to aspirin, active ulcer, asthma <30 y/o).

So other than if a contraindication is a problem, when would you use one over the other?

Thanks!
 
No offense, but if you don't know what your medicantions do, you shouldn't be administering them. If you knew what they did (acetylsalicylic acid is an anti-coaglent whereas nitro is a vassal dialater), then you probably wouldn't be asking this question. Those drugs are not either/or.
 
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When you suspect AMI or unstable angina, you can use "MONA" (morphine, oxygen, nitro, ASA)

These drugs can safely be used with each other. In most cases, ALS must provide the morphine administration, but some BLS crews may be able to provide the other three drugs.

The above poster is correct, you should try and learn more about the drugs you are giving before you give them. Now in days with google and wikipedia, there really is no excuse.
 
I know what the drugs do, I was just wondering the timing-but after reading into my local protocol it seems we would use both
 
No offense, but if you don't know what your medicantions do, you shouldn't be administering them. If you knew what they did (acetylsalicylic acid is an anti-coaglent whereas nitro is a vassal dialater), then you probably wouldn't be asking this question. Those drugs are not either/or.

Sorry, just a pet-peave of mine; it is "anti-coagulant" and Vaso-dilator

Also, let's be a tad more specific..

Aspirin is a thrombolytic that reduces overall mortality of AMI, reduces additional infarct, strokes and furthermore blocks formation of Thromboxane A2, which in turn causes platelets to aggregate and arteries to constrict

Contraindications are: Acute ulcer disease, GI or other bleeding disorders,
patients experiencing asthma attacks, hypersensitivity to ASA, or ASA prior to arrival.

Doses higher than recommended can interfere with Prostacyclin production.

while the exact mechanism of action is unknown, we do know that ASA inhibits prostaglandin sythesis, producing analgesia, anti-inflammatory, and
anti-pyretic effects, and irreversiby inhibits platelet aggregation (salicylate).

Metabolism: gut and plasma(aspirin), liver(salicylate) CYP 450 is currently unnown. Its excretion is usually through urine, of course with a half-life of 0.25h(aspirin), 2-6h (salicylate); though the half-life is dose dependent and the amount excreted is pH-dependent.

Now, Nitroglycerin(NTG) is a rapid smooth-muscle relaxant that causes decreased cardiac work. NTG dilates BOTH arterial and venous vessels and causes venous pooling of blood. I repeat, causes venous pooling of blood.
NTG also causes vaso-dilation of the coronary arteries thus, increasing perfusion(keyword) of ischaemic myocardium(bad ju ju).

While pain relief ocurs within two minutes, therapeutic effects can be observed up to 30 minutes later.


Indications: MUST HAVE ALL OF THE FOLLOWING S/S

Exhibits signs and symptoms of chest pain
Has physician prescribed sublingual tablets or spray AND
has specific authorization from medical direction unless standing orders exist.

Contraindications(AND THIS IS IMPORTANT)

Hypotension or blood pressure below 100 mmHg systolic, I repeat:

Hypotension or blood pressure below 100 mmHg systolic

Head Injury or increased ICP
Hypovolemia, severe bradycardia or tachycardia

Recent use within 24 hours of Viagra

Infants and Children(If you want to know a quick way to lose your license, this is it.)

Patient has already met maximum prescribed dose prior to EMT arrival.

NTG may induce headaches from vasodilation of cerebral vessels.

Pharmacology:

Metabolism: liver, erythrocytes(red blood cells), vascular walls
half-life is 1-3 min, 40 min(metabolites)
half-life: 1-3min, 40min (metabolites)

Mechanism of Action:

stimulates cyclic GMP production, resulting in vascular smooth muscle relaxation.

I think that is enough for now.
 
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No offense, but if you don't know what your medicantions do, you shouldn't be administering them. If you knew what they did (acetylsalicylic acid is an anti-coaglent whereas nitro is a vassal dialater), then you probably wouldn't be asking this question. Those drugs are not either/or.


Whoa!....

Sounds like you need to go back to your school and demand your money back! Sorry, but something is wrong ! Let's start back in cardiac care, when you should had been taught the general care of cardiac emergencies. As the poster describes.. if you don't know about the medications, then you probably should not be doing it... I am however; glad you are asking questions now.

Second I am sure JPINFV was being purposefully humorous it is vasodilator (don't know what a vassal dialater or coaglent is) (dilatation of the vessels i.e. veins, arteries, capillaries, venules) dilates. As well ASA is NOT a blood thinner, it is a anti-platelet which prevent clots from forming (which is NOT the same as a "blood thinner" such as Heparin/Coumadin) ....but does have a blood thinning coagulant effect. Yes, there is a MAJOR difference.

As well I have some REAL problems with anyone giving nitroglycerin (NTG) without having a 12 lead ECG interpreted prior to administration. The problem lies that patients are usually on or prescribed NTG for Angina not for having an AMI! Giving NTG blindly can be dangerous! Administering NTG to patients having a left ventricular infarct can actually cause more damage and YES.. potentially kill them! Thus the importance of a medical work up and referred to those that understand and treat cardiac care.

Again, the only reason we allow Basics to administer most medications is because the safety factor that most laymen could do the same without a percentage of risks. ASA is not going to effect the major population, as well most patients that do have NTG in their premise, have a history of angina... hopefully, that is all it is.

Medications are essential, just as essential they are to treat they all have potential dangerous side effects.

R/r 911
 
Rid,

What is your reasoning for wanting an interpreted EKG prior to administration of nitro? I've had old folks that pop nitro like they're tic tacs. I absolutely understand that nitro is a medication that requires proper administration and monitoring, but I've never seen an MD actually request a patient to assess any vitals before popping the magic pills.
 
Whoa!....
Second I am sure JPINFV was being purposefully humorous it is vasodilator (don't know what a vassal dialater or coaglent is)
Naw, I'm an idiot that needs to remember that Firefox spell checker + quick post box aren't friends... (i.e. it doesn't work for some reason in my browser). But (yea yea, conjunction violation), yea, it's not a peasant (vassal) dilator.
 
Rid,

What is your reasoning for wanting an interpreted EKG prior to administration of nitro? I've had old folks that pop nitro like they're tic tacs. I absolutely understand that nitro is a medication that requires proper administration and monitoring, but I've never seen an MD actually request a patient to assess any vitals before popping the magic pills.
I've never heard of a doc asking a patient to check ANYTHING before taking a medication. Why? Because the average person wouldn't know how, would do it wrong, or would ignore the request. Go figure. :rolleyes:

Luckily, we (some of us out there anyway) are just a leeeeetle better trained than the average person. Anyway, the reasoning behind the 12lead is pretty simple: give nitro the someone having the wrong kind of MI and you may very well kill them. Couple links if you want to get into all the details:
http://www.aafp.org/afp/991015ap/1727.html
http://www.emedicine.com/MED/topic2039.htm

In a nutshell, inferior wall MI's often happen at the same time as right ventrical MI's. When the right ventricle is affected, it stops pumping blood effectively, thus reducing the amout of blood available for the left ventricle to pump and thus maintain a BP. So these people may or may not allready have a low BP; either way, it's compromised. Now, if you throw nitro into the mix and decrease the preload to the heart, the amount of blood the right ventricle is moving is even less, and the BP really, really, REALLY takes a hit. Bad things tend to follow. Being able to read a 12lead will help you to decide wether or not you should be giving nitro to the patient.

Luckily right sided MI's are fairly rare, which is why people often get away with popping it or giving their patients nitro like it was candy. But trust me, do it once and you will never, ever do it again. ;)
 
Rid,

What is your reasoning for wanting an interpreted EKG prior to administration of nitro? I've had old folks that pop nitro like they're tic tacs. I absolutely understand that nitro is a medication that requires proper administration and monitoring, but I've never seen an MD actually request a patient to assess any vitals before popping the magic pills.


The physician are fools then, and I would hate to be there malpractice carrier. They are gambling that they are having Angina, and not an AMI. Remember there is a BIG difference. The patients medial history, as well as I am sure serial ECG's, U/S, stress test, etc. then they will make the determination that it is an Angina event, not an AMI. So when the patient has "chest pain" they are hoping, that there pressure will be high enough that they can sustain the NTG administration. Thus the reason to wait " five minutes" apart to re-administer. As well, they are assuming since the chest pain has been determined to angina in nature. If the pain does not go away... there is a great potential it is not angina rather an AMI (or other etiology).

In regards to an ECG prior let's review some basic cardiac physiology. Remember that the heart is filled by the venous system (inferior and superior vena cava-filled by the venule system) and dumps into the right chamber (right atrium)... right? Now, what happens if we were to dilate these vessels (in which NTG does) it would cause major vasodilation thus dilating or decreasing the peripheral resistance, and causing a decrease of the amount of blood and pressure entering the heart (preload factor). Now, what occurs if the heart does not sense there is enough blood or blood pressure? It increases the heart rate and stroke volume (contracts harder) thus increasing work demand .. thus if they are having an AMI causing the heart to work harder = increasing the AMI = infarct size larger... or basically in an inferior wall AMI or right sided AMI, possibly causing an major infarct size or death.

NTG is NOT a direct contraindication but definitely a STRONG CONSIDERATION not to administer. Thus, the reason for not giving NTG for patient with low B/P is because they might have a left sided AMI.
NTG is strong smooth muscle relaxer (hence the reason is also prescribed for esophageal spasms) and it dilates not just the coronary arteries but all smooth vessels.. hint: the reason people get a headache after NTG is administered- the cerebral arteries have just dilated and they got a head rush.

Remember, there are very few site medications, that just work upon specific receptors or sites. Each medication has it side effects or desired effects dependent upon what the reason it is administered makes the difference.

Even the most simplistic medications can be the most harmful.. ever seen a Tylenol or One-A-day overdose? .. thus the reason, medications administration as diagnosed by another provider is so dangerous.


* noticed an error in previous post- it should be right sided AMI, not left.
R/r 911
 
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well i know for RI the protocols are BP 90 or above for nitro and only with med contols approval, and only if its a prescription to that pt....but hey thats just RI lol
 
I remember when one of the common contraindications was P<50. Bradycardia is a common S/S of R-side MI.

I had a pt the other day that we were dispatched out to for VD (veak & dizzy). Got there and he was ashen color with cynosis around the lips and B/P of 80/60 (more or less here). He's pretty old and has a host of problems so we're kind of on high-alert with this gentleman.

So we assess and treat with O2 and get into the Hx. Anyway, find out that he developed chest pain earlier in the morning and his wife gave him his NTG. So that opens the door WIDE open and it's become quite obvious what has happened. We ask the wife and sure enough it is confirmed.

There's no chest pain complaint so I give ASA and attempted a line (unsuccessfully) and away we go to the H.

Now, I won't reveal it here but anyone that isn't sure, is welcome to guess at what happened. As most people with some experience will recognize the problem right away, I hope they won't say anything; let some of the less experienced ppl take a shot at it. I'd say I see this problem 2 or 3 times a year, so I think it's good for inexperienced rescuers to start to recognize it now.
 
thanks for all the answers, especially to Rid...very informational stuff, if i'm ever in need of EMS, i really hope you show up!

thanks again guys!
 
...hmmm..seeing as though im a basic whos never worked on a truck yet.. im not surprised im stumped, but im still thinkin.....
 
Whoa!....

Sounds like you need to go back to your school and demand your money back! Sorry, but something is wrong ! Let's start back in cardiac care, when you should had been taught the general care of cardiac emergencies. As the poster describes.. if you don't know about the medications, then you probably should not be doing it... I am however; glad you are asking questions now.

Second I am sure JPINFV was being purposefully humorous it is vasodilator (don't know what a vassal dialater or coaglent is) (dilatation of the vessels i.e. veins, arteries, capillaries, venules) dilates. As well ASA is NOT a blood thinner, it is a anti-platelet which prevent clots from forming (which is NOT the same as a "blood thinner" such as Heparin/Coumadin) ....but does have a blood thinning coagulant effect. Yes, there is a MAJOR difference.

As well I have some REAL problems with anyone giving nitroglycerin (NTG) without having a 12 lead ECG interpreted prior to administration. The problem lies that patients are usually on or prescribed NTG for Angina not for having an AMI! Giving NTG blindly can be dangerous! Administering NTG to patients having a left ventricular infarct can actually cause more damage and YES.. potentially kill them! Thus the importance of a medical work up and referred to those that understand and treat cardiac care.

Again, the only reason we allow Basics to administer most medications is because the safety factor that most laymen could do the same without a percentage of risks. ASA is not going to effect the major population, as well most patients that do have NTG in their premise, have a history of angina... hopefully, that is all it is.

Medications are essential, just as essential they are to treat they all have potential dangerous side effects.

R/r 911

Rid, I am in Pm school right now, and remember them talking baout how nitro can be bad for a pt with a right anterior MI. Is this the same thing or is there some different pathophys behind the nitro be bad for a left infarct. They said that giving nitro to a pt with a right anterior would bottom the b/p out, and that could lead to dysrythmias etc.

Here is what I think could cause problems. If there is a right side MI, then it would drop the B/P because it is reducing the amount of blood being sent to the pulmonary arteries already, because of the ischemic tissue, thereby less blood volume is making it to the left side of the heart and to the body reducing stroke volume and lowering the b/p. So giving nitro would dramatically increase this effect by reducing the preload which is one of the effects of nitro.
Now the left infarct I am thinking this would be bad because the nitro would decrease the afterload, because of lowered peripheral vascular resistance, to the point where it is going to seriously reduce the coronary circulation.


These are the ways I am trying to reason this out, I may be totally off base and if I am, please guide me in the right direction. Thanks for the info.
 
What you witnessed, was one of those rare occurrences in EMTLife Hx -- Rid made an error.

Of course, he later corrected himself. He never meant to say Left-sided AMI, he intended to say Right.

That's assuming I read your post correctly. As per Hx, I make my share of mistakes all the time.
 
...hmmm..seeing as though im a basic whos never worked on a truck yet.. im not surprised im stumped, but im still thinkin.....


If you think about chest-pain as a blockage (partial or complete), then what effect does that usually have on a pt's blood-pressure? Is that consistent with what we see here? Why?
 
Lot of helpful info, Rid....thanks for the good read.

-Matt
 
For us basics in the area, we can administer 7 drugs (O2 is included). For chest pain, we have nitro spray and 'baby' asprin (4 tabs. for 324 mg)

My question is when to chose nitro or ASA and vise versa.

(per our protocol):

Nitroglycerin


Baby Aspirin (Chewable)


So other than if a contraindication is a problem, when would you use one over the other?

Thanks!

Wow... as a basic, i can tell you you got away light out here... but... are you thinking about the big picture? is it stable angina? relieved by rest? was it sudden onset at rest? has the pt taken their own Nitro? what were the effects?

if you just look at indications, and give meds without understanding how they work or seeing the bigger picture, you are not providing a good level of care... sorry to say it, but as a Basic, you can kill someone if you don't know what you are doing with these meds.

also, i find it hard to believe you would be able to administer Nitro without a line in place... what happens if the BP bottoms out? is it your Nitro you are administering, or are you saying you can help the patient administer his own? HUGE difference there... please clarify that for me...

thanks
 
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