Alcohol and Nitro

[VirginiaEMT]

If you were on scene of a chest pain patient and this patient is simply plastered from alcohol abuse, how would you treat the chest pain? What are the effects with nitro?

I had this the other day and have looked through books every since trying to find a good answer.

I found out that it was not as bad as it was portrayed because I gained IV access and when I flushed it the patient said he felt better so I now know Normal Saline will cure chest pain. But it did get me to thinking about what I would do the next time and to be quite honest, I'm not sure. What type of effect will the blood alcohol play on the aspirin and nitro?

 

[NYMedic828]

Alcohol potentiates the effects of NTG.

It's a risk vs reward scenario. Like giving NTG in the presence of erectile dysfunction meds. It's doable but must be done with greater care.

Just monitor BP and use more sparingly.

 

[Eli]

I'd say that there is a reason why alcohol is NOT listed as a contraidication for the use of NTG. Don't overthink it, just follow your protocols. Nitro hasn't been proven to be either detrimental or benificial in pre-hospital care. But trying to find reasons not to treat chest pain like a cardiac patient has wound many a medic in the hot-seat both clinically and administratively.

Case in point, recently saw a 50+ male with worsening chest pain throughout the day. Family members (bunch of drama-teens) were worried and called EMS. This guy had a good looking unremarkable 12 lead ECG, right sided chest pain, well localized and even presented with some point tenderness. All of the hallmarks I was taught were indicators of "chest wall pain" vs. cardiac related chest pain. The patient tells me that he'll have his kids drive him to the ED because he doesn't have any insurance. My response was I could either drive him to the ED or go back to the station and finish watching my football game. (My team had a 3 point deficit just after the half when we were called.)

When we got this patient to the ED the 12 lead looked almost like tombstones! He was sent to the city for a cath and said he felt like a million bucks when I talked to him several hours later. Can you imagine the convesation with my higher ups had I not treated him with ASA, nitro, etc...? Or! Can you imagine the consequences had I left and he talked his kids into not taking him to the ED because he couldn't afford it?

Watch the docs in your hospitals. They take the BS chest pain patients and do cardiac workups on them too. So why shouldn't we?

 

[mycrofft]

I almost delayed seeing a known liar about a heart attack. He was in electromechanical dissociation (I can't remember the new name for it) from a massive MI and died under my hands. Heck yeah(!), evaluate them seriously and entertain the etiologies with similar complaints (ranging from chest wall pain, to early signs of pulmonary embolism and aortic dissection).

I'm curious as to why patients are given nitro tabs and report relief of angina when it is "not effective" as a prehospital medication? Just a scientific question.

 

[Eli]

I'm curious as to why patients are given nitro tabs and report relief of angina when it is "not effective" as a prehospital medication? Just a scientific question.

I don't understand the question. Are you referring to no change in mortality based on nitro use?

 

[NYMedic828]

I'd say that there is a reason why alcohol is NOT listed as a contraidication for the use of NTG. Don't overthink it, just follow your protocols. Nitro hasn't been proven to be either detrimental or benificial in pre-hospital care. But trying to find reasons not to treat chest pain like a cardiac patient has wound many a medic in the hot-seat both clinically and administratively.

Case in point, recently saw a 50+ male with worsening chest pain throughout the day. Family members (bunch of drama-teens) were worried and called EMS. This guy had a good looking unremarkable 12 lead ECG, right sided chest pain, well localized and even presented with some point tenderness. All of the hallmarks I was taught were indicators of "chest wall pain" vs. cardiac related chest pain. The patient tells me that he'll have his kids drive him to the ED because he doesn't have any insurance. My response was I could either drive him to the ED or go back to the station and finish watching my football game. (My team had a 3 point deficit just after the half when we were called.)

When we got this patient to the ED the 12 lead looked almost like tombstones! He was sent to the city for a cath and said he felt like a million bucks when I talked to him several hours later. Can you imagine the convesation with my higher ups had I not treated him with ASA, nitro, etc...? Or! Can you imagine the consequences had I left and he talked his kids into not taking him to the ED because he couldn't afford it?

Watch the docs in your hospitals. They take the BS chest pain patients and do cardiac workups on them too. So why shouldn't we?

It isn't listed as a contraindication per protocols but it is listed as having an interaction with alcohol in a epocrates. Whenever you are going to administer a treatment any possible adverse affect relevant to your treatment has potential to be a contraindication.

Again, risk vs reward.

Disregard protocols, acquire actual knowledge. You can treat to the limit of your protocol but you can also choose to withhold anything you deem non-beneficial or dangerous.

If someone has to rely on defending themselves with "I just followed the protocol" or they don't know what to do so they blindly follow a protocol they have no business treating a patient above anything but basic first aid and transport.

 

[the_negro_puppy]

I'm curious as to why patients are given nitro tabs and report relief of angina when it is "not effective" as a prehospital medication? Just a scientific question.

Nitro can be effective in reducing angina type symptoms hence why it is widely prescribed for home use. It is evident that it works to reduce pain symptoms associated with the condition however it has not been proven effective in reducing the morbidity and mortality in AMI.

Think about the pathophysiology. If you have a coronary artery blocked by a thrombus nitro generally will not fix this. It claims to try and help improve circulation through co-lateral channels and reduce pre-load and after load. It will not reduce or remove the thrombus, hence infarction and pain symptoms will continue.

 

[Aprz]

I'm slightky interested in knowing if alcohol potentiates the effect of nitroglycerin. Out of interest one time, I was trying to figure out the associating of nitroglycerin and the nuof mber methemoglobins, and if it was an actual concern giving a lot of nitroglycerin (it was the only reason I figured a limit existed), but then I read about nitroglycerin IV, and I believe I read that nitroglycerin IV is stored/mixed with alcohol, and figured the patient would probably die from alcohol poisoning befote having to worry about methemoglobinemia.

Guess this would be a good time to master nitroglycerin and figure this out together.

Nitroglycerin (NTG) = Glycerol Trinitrate (GTN) (you'll see people from outside of the US call it GTN, thry don't have it backwards)

Glycerol is propanol-1,2,3

Prop is from propane, an alkane, or fully saturated hydrocarbon group. Meth = 1, Eth = 2, Prop = 3, But = 4, Pent = 5, Hex = 6, Hept = 7, Oct = 8, Non = 9, Dec = 10. E.g. Methame is 1 carbon, and it's full saturated so when you draw it out, you can put a hydrogen on every side to every carbon. I think the gormula you could use is # of hydrogen = (# of carbon x 2) + 2, or something like that (going off my head amd typing this on my phone so hopefully not wrong, lol). Propane is C3H8.

The -ol ending would mean that it's an alcohol, or one of the hydrogen has a hydroxyl grpup instead (-OH). So propanol is C3H8O.

But the 1,2,3 would mean their is a hydroxyl group attached to the 1st, 2nd, and 3rd carbon. Propanol-1,2,3 is C3H8O3. So that should be glycerol if I did everything correctly (It's easier for me to draw).

Then glycerol trinitrate, or nitroglycerin, is a nitrate instead of the hydroxyl (that confused me, but whatever). So instead of -OH attached to each carbon, it's NO3. Nitroglycerin is C3H5O9N3 I think....

Anyhow, spray nitroglycerin into the body, something like aldehyde dehydrogenase cleaves off a nitrate from nitroglycerin, the nitrate (NO3) becomes nitric oxide (NO) which is a known vasodilator. I think the NO goes through the cell membrane, attaches to guanynyl cyclase, release cyclic guanosine monophosphate (cGMP), which is the thing that makes the vessel dilate.

Forgive me if I got some or all of this wrong, but this is what I think right now and it'll lead me to my question.

I think ethanol (Eth, 2 carbons, would be fully saturated with hydrogen ethane C2H6, but ends with -ol so one hydrogen is replaced with -OH hydroxyl group so C2H6O) becomes acetaldehyde (the thing that is toxic to our body and is reddish so makes some asians red if they drink a lot) becomes acetic acid by acetaldehyde dehydrogenase, acetic acid becomes acetyl-CoA, I forget the enzyme that does that. Acetyl-CoA gets used up by the Kreb's Cycle.

I think acetaldehyde dehydrogenase, or maybe it was aldehyde dehydrogenase, causes the vasodilation, and somehow causes an increase in cGMP.

So I wonder if they both use the same mechanisms to cause vasodilation, if this could increase the numher of cGMP significantly, or if alcohol and nitroglycerin kind of compete because I think they probably use the same enzymes, or something.

Some gaps in what I know, but think this would be interesting to fil in, and I am pretty sure nitroglycerin IV is stored/mixed with alcohol so in a sense, to me, makes me think it's okay to use nitroglycerin on somebody intoxicated.

 

[Aprz]

I'm home now. I feel like an idiot reading my previous post because of all the typos and accidentally using "their" instead of "there". It took me like an hour to type with my phone though, and it still makes sense for the most part.

I looked it up on Google, both alcohol and nitroglycerin uses the same enzyme, aldehyde dehydrogenase 2 (ALDH2), and then I thought it was even more interesting because I found that ALDH2 was also used to fight free radicals too, and then answered another one of my questions, why is there a limit on nitroglycerin (read this article, the author didn't like that there was a limit to nitroglycerin)? This would be a good reason why if true. We know that nitroglycerin hasn't reduce morbidity and mortality, why should we continue use it, and if we continue to use it, how much should we give before it is a problem? Is 3 too little or too much?

Anyhow, I think the answer to the question is alcohol is probably gonna use up ALDH2 and prevent nitroglycerin from working. That's my current thought right now.

 

[Shishkabob]

Think about the pathophysiology. If you have a coronary artery blocked by a thrombus nitro generally will not fix this. It claims to try and help improve circulation through co-lateral channels and reduce pre-load and after load. It will not reduce or remove the thrombus, hence infarction and pain symptoms will continue.

Though one often over-looked benefit is decrease in pain = decrease in catecholamine release, leading to less oxygen demand, vasoconsctricion, and work on the heart.

So even though there is minimal/no effect on the coronary vasculature of the heart, it can have some side benefits.

 

[AnthonyTheEmt]

I hope you are joking when you say this

 

[AnthonyTheEmt]

I found out that it was not as bad as it was portrayed because I gained IV access and when I flushed it the patient said he felt better so I now know Normal Saline will cure chest pain.

I hope you are joking about this