The improper incorrect thread: what do you do that's not in the protocols but WORKS?

[46Young]

I assume you still have some sort of air flowing to that NRB, or that you mean a simple mask / partial rebreather.




Not saying I've seen it, but I've heard medics say they've hinted to patients to say they are nauseous from morphine so they can give phenergan as to potentiate the morphine.

Maybe 2 liters. I'm trying to raise their CO2, after all.

 

[emtbill]

And I am sure you can provide the study to prove this? I am sure a lot of cardiologists would love to read up on it!

The fluids are given to keep cardiac output up (starling's law) while the NTG keeps coronary arteries dilated to increase blood flow and oxygen delivery to the myocardium. The right sided MI patient needs NTG so that they will get more oxygen, however also needs something to compensate for the reduction of preload and afterload. That's what the fluids are for. If the two are not in balance (ex: a bolus of NTG sublingually) the cardiac output will drop and the patient will be in trouble!

This is how many cardiac patient are treated in my CCU. I'm sure there are studies out there supporting this.

 

[Shishkabob]

Show me some studies that state the huge dose of NTG isn't dangerous in the right-sided MI.

Do you have studies that show 400mcg is bad for a rightsided MI?


It goes both ways.

 

[emtbill]

Ok here, I spent 90 second on pubmed and found this:

The literature on isolated right ventricular infarction is reviewed and local experience is reported. Chronic lung disease is an important risk factor. Chest pain and breathlessness are common. Syncope and sudden collapse can also occur. Rhythm disorders include sinus bradycardia, atrial fibrillation and ventricular tachycardia or fibrillation. Atrioventricular block is rare. Hypotension and a right-sided fourth heart sound are common. Cautious use of slow-release nitroglycerin is not hazardous in the absence of hypotension. High doses of steroids and anticoagulants can be helpful. The prognosis is usually good, although sudden collapse can occur due to ventricular fibrillation, rupture of the right ventricular free wall or massive pulmonary embolism.

Key word is slow release.

 

[Hockey]

When I get annoyed with someone thats talking out of their behind about how I should give them pain meds (Yes I know) and they have every medical condition in the world, I just stare at them


It works everytime and they stop talking and asking for meds

 

[paccookie]

The sub-lingual dose of NTG is 400 mcg whereas I can titrate a NTG drip to begin at as low as 10 mcg/min and control the increase in relation to my patient's pain and blood pressure.

Show me some studies that state the huge dose of NTG isn't dangerous in the right-sided MI.

When I was an intermediate, long before 12-leads, I had a patient's very good blood pressure tank on me after administering NTG for his chest pain. We never got him back, despite aggressive fluid resuscitation. I later found out that he had a right-sided MI, however since I didn't have 12-lead capabilities and was but an intermediate anyway, all I could do was follow the protocol (I didn't have the education not to) and kill my patient.

I want proof. I want to see studies. Until I see them, I remain firm that a dose of 400 mcg is a bit extreme when dealing with that type of MI. I'm not in the business of jacking with homeostasis. It's bad enough you're battling an MI, but lets add battling hypovolemia to the mix.

I agree with you. I had a STEMI patient not too long ago that was given 3 SL NTG by his wife prior to EMS arrival. BP was 70/30 when we arrived. 12 lead showed ST elevation in II, III and AVF and depression in several of the V leads. BP came up after a fluid bolus (I think 300 cc brought it to 110/60?). Gave him 324 ASA and 3 mg Morphine (morphine by online med control) and O2. He went straight to the cath lab table.

I'm not saying that NTG is bad for MI patients, but sometimes you do need to look at more than just "he's having chest pain, he needs NTG." I've personally seen too many medics do no more assessment than "tell me where your chest hurts, when did it starts hurting, describe the pain" and then give a NTG without ever checking vitals or putting the pt on the monitor, let alone start an IV.

 

[Shishkabob]

I agree with you. I had a STEMI patient not too long ago that was given 3 SL NTG by his wife prior to EMS arrival. BP was 70/30 when we arrived

That's part of the problem right there, and as such your story really doesn't prove NTG to be detrimental.

We don't know what the BP was before she administered the first dose, let alone the 2 subsequent dosages. For all we know, all 3 doses could have been given one after the other, over a few seconds.

 

[emtbill]

That's part of the problem right there, and as such your story really doesn't prove NTG to be detrimental.

We don't know what the BP was before she administered the first dose, let alone the 2 subsequent dosages. For all we know, all 3 doses could have been given one after the other, over a few seconds.

I disagree; you're just speculating about the interval between dosages and since we know the patient was having an inferior STEMI we should assume the patient has a proximal occlusion of the RCA, and the right ventricle is infarcted (this occurs in 40-50% of inferior MI's). NTG is usually well tolerated in people with angina, and it's not uncommon for patient to take 3-4 tablets prior to EMS arrival and still be normotensive. In fact, most patient are told to call 911 if 3 tablets do not relieve their angina. I think you'll find with a little more experience you'll be more judicious in your medication delivery for STEMI patients as well.

 

[Ridryder911]

Not to be off topic but NTG is not contraindicated but should be used cautiously with inferior & right side involvement. Now, with that saying if you lower your patients blood pressure to the point of preload has to catch-up then you have a problem because of increasing demand on a damage muscle.

Sure, fluids may help resolve the problems but you may have caused an increase in size by doing so. Many clinicians much rather not take the chance and rely on other pharmakinetics.

R/r 911

 

[Smash]

The fluids are given to keep cardiac output up (starling's law) while the NTG keeps coronary arteries dilated to increase blood flow and oxygen delivery to the myocardium. The right sided MI patient needs NTG so that they will get more oxygen, however also needs something to compensate for the reduction of preload and afterload. That's what the fluids are for. If the two are not in balance (ex: a bolus of NTG sublingually) the cardiac output will drop and the patient will be in trouble!

This is how many cardiac patient are treated in my CCU. I'm sure there are studies out there supporting this.

If there are studies, by all means post them. If not, the physioogical rationale doesn't make sense. As MelClin succinctly pointed out, GTN is for dropping preload, thus workload, thus MvO2. Arterial dilation is variable and dose related and coronary artery dilation even more so as we are dealing with sclerosed vessels that amy or may not have collaterals to actually dilate anyway.

The RVI patient needs preload at all costs so they don't die. Dropping that preload, then jacking it up with medications or fluids that will also increase MvO2 just isn't good thinking.

Do you have studies that show 400mcg is bad for a rightsided MI?


It goes both ways.

Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?

 

[Hockey]

Do I get to talk like this with big words and medications and accronyms once I go through my Paramedic class too?

 

[Shishkabob]

Do I get to talk like this with big words and medications and accronyms once I go through my Paramedic class too?

No.




"Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?"

Do you have studies that show an increase?



We can do this all day

 

[JeffDHMC]

No data to back it up, but I have seen SL NTG do bad things when given to a pt. presenting with inf. AMI with RV involvement. Because of that, I am a touch careful if I feel the need to go that route.

 

[Meursault]

Do I get to talk like this with big words and medications and accronyms once I go through my Paramedic class too?

I'll let you in on my secret:
Take a few undergrad classes (physio, immuno, various public health, etc.) and you can do it beforehand!

(not that I can play with the medics, though)

 

[Ridryder911]

No.




"Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?"

Do you have studies that show an increase?

Yes...just Google Scholar or read any advanced level cardiac book above Paramedic level (even ACLS) . If you had learned pathophysiology, we would not be having this discussion of preload vs. afterload effects.

R/r 911

 

[Melclin]

The sub-lingual dose of NTG is 400 mcg whereas I can titrate a NTG drip to begin at as low as 10 mcg/min and control the increase in relation to my patient's pain and blood pressure.

Show me some studies that state the huge dose of NTG isn't dangerous in the right-sided MI.

When I was an intermediate, long before 12-leads, I had a patient's very good blood pressure tank on me after administering NTG for his chest pain. We never got him back, despite aggressive fluid resuscitation. I later found out that he had a right-sided MI, however since I didn't have 12-lead capabilities and was but an intermediate anyway, all I could do was follow the protocol (I didn't have the education not to) and kill my patient.

I want proof. I want to see studies. Until I see them, I remain firm that a dose of 400 mcg is a bit extreme when dealing with that type of MI. I'm not in the business of jacking with homeostasis. It's bad enough you're battling an MI, but lets add battling hypovolemia to the mix.

I agree with a number of things you said. I think titrating up to the minimum dose they need is a very good idea. Although, the venous dilation will come before the arterial dilation, so if you are going to aim for the coronary artery dilation (I'm still not quite sure about the efficacy of GTN in CA dilation) then you would need to give substantially more than what you gave to just drop their preload, so you would end up having the same problems with RVI/low preload anyway. I.

We don't have 12-leads (only MICA have twelve leads). I don't agree with it. I understand it's difficult for the older medics to catch up with more clinical requirements, considering some of them started when CPR and bandage selection was the extent of their knowledge, but with three years of university education, we have plenty of time to learn 12 lead interpretation, to the benefit of our pt.'s hopefully. We were talking today about how we basically just have to guestimate an RVI from the 3 lead, when considering GTN, despite it being marked as a contraindication to RVI/Inferior STEMI.

400mcgs seems a bit extreme anyway as a bolus dose if they've never hat nitrates before.

If there are studies, by all means post them. If not, the physioogical rationale doesn't make sense. As MelClin succinctly pointed out, GTN is for dropping preload, thus workload, thus MvO2. Arterial dilation is variable and dose related and coronary artery dilation even more so as we are dealing with sclerosed vessels that amy or may not have collaterals to actually dilate anyway.

The RVI patient needs preload at all costs so they don't die. Dropping that preload, then jacking it up with medications or fluids that will also increase MvO2 just isn't good thinking.

Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?

+1

 

[Smash]

"Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?"

Do you have studies that show an increase?



We can do this all day

We could, but I refuse to have a battle of wits with an unarmed opponent.

ISIS-4, GISSI-3, ESPRIM.

You might also want to find out why RVI is a strong independant predictor of mortality in ACS and extrapolate from there.

In the meantime, if you want to pop nitrates to your RVI patients whilst staving off cardiogenic shock with volume loading and pressors, you go nuts. I just hope I don't infarct in your service area.

 

[emtbill]

Do you have studies that show use of nitrates decreasing mortality and morbidity in ACS?

Seven randomized controlled trials of intravenous nitroglycerin in a total of about 850 patients have been reported. Overall, there were 51 deaths (12.5%) in the nitroglycerin group and 87 (20%) in the control group. This indicates a 48% reduction in the odds of death (P less than 0.001, 95% confidence limits (25% to 64%)). 2. There are five randomized trials of oral nitrates after acute myocardial infarction. In these trials, 11.8% of the patients in the nitrate group compared with 13.3% in the control group died. This indicates a nonsignificant 12% reduction in the odds of death but the 95% confidence interval overlaps widely with the i.v. trials. If all trials of i.v. or oral nitrates are considered the reduction in the odds of death is 32% (P less than 0.01). 3. Nitrates have a beneficial effect on haemodynamics in heart failure but the data on mortality effects are sparse. In combination with hydralazine, however, long-term mortality was reduced in the V-HEFT trial of chronic heart failure.

I've posted two articles so far. NTG is beneficial in ACS, but in a proximally occluded RCA it needs to be titrated IV with fluids to keep the patient hemodynamically stable. Also, remember that I said this is how some patients are treated in hospital. I agree that a sublingual bolus of nitrates in the field for RVI patients is too risky and I do not do it.

 

[Ridryder911]

I've posted two articles so far. NTG is beneficial in ACS, but in a proximally occluded RCA it needs to be titrated IV with fluids to keep the patient hemodynamically stable. Also, remember that I said this is how some patients are treated in hospital. I agree that a sublingual bolus of nitrates in the field for RVI patients is too risky and I do not do it.

What you have failed to recognized is those studies were not discussing RVI. Sure nitrates are beneficial in ACS but so is having a CABG over having stents; but you will not see me posting lit reports on it, since that is a mute point as well.

Do I give nitrates in RVI? Sometimes. Sometimes I have seen it be very beneficial and other not so. What I do not want to portray is that giving fluids and titrating NTG is the end of all when considering administering NTG especially those with right sided involvement. Dropping the pressure where one has to give fluid replacement is placing demand already on a damage heart.. and why should you? That's bad care.

Consider other options and treatments.

R/r 911

 

[DV_EMT]

needle sticks to check blood glucose.... yeah, we can give po glucose but cant see if they're hypoglycemic... pretty lame huh?

i'd say also starting LR, NS, and D5W drips would be nice... not necessary, but nice