Ntg

[Uclabruin103]

So I'm in my last month of didactic of school and was just curious of a few cardiac things. In class we were shown four serial 12-leads of an AMI that received pur full repetoire our EMS cardiac drugs; three NTG, MS, and ASA. The second 12-lead showed decreased ST elevation, and by the forth the 12-lead no longer showed infarction taking place. So that brings me to scenarios we were running today with atypical AMI presentations of flu-like and general malaise symptoms.

When I think about treatment I can't help but think about those serial strips getting rid of infarcting tissue and want to strive for that when I get in the field.

Finally the question, if a PT presents with atypical signs and symptoms and an absence of CP will you treat with NTG? I know its main indication is for cardiac CP, but if they are having an infarction dont we want to increase perfusion through coronary dilation even in the absence of pain?

Sorry if this does't make too much sense. Can't type too coherently on an iPhone.

 

[KellyBracket]

First off (and I won't be the only guy to point this out), nitro has not been shown to "get rid of infarcting tissue," reverse an AMI, or decrease mortality. There are a number of cases where ST segments have normalized after NTG, but I don't think anyone believes that the essential process has been reversed.

In other words, the MI has likely just been temporarily masked, not treated.

There might be some diversity of opinion on who, or what symptoms, should get NTG. Probably anyone with symptoms that you suspect to be ischemic in origin. Epigastric pressure, new heartburn, backache - whatever. Now, even though hiccups can be a symptom of an AMI, it would feel odd to treat them with NTG, I admit.

Wouldn't worry about it too much though, since NTG isn't really a life-saver in AMI.

 

[Uclabruin103]

First off (and I won't be the only guy to point this out), nitro has not been shown to "get rid of infarcting tissue," reverse an AMI, or decrease mortality. There are a number of cases where ST segments have normalized after NTG, but I don't think anyone believes that the essential process has been reversed.

In other words, the MI has likely just been temporarily masked, not treated.

There might be some diversity of opinion on who, or what symptoms, should get NTG. Probably anyone with symptoms that you suspect to be ischemic in origin. Epigastric pressure, new heartburn, backache - whatever. Now, even though hiccups can be a symptom of an AMI, it would feel odd to treat them with NTG, I admit.

Wouldn't worry about it too much though, since NTG isn't really a life-saver in AMI.

I know it's isn't curing the problem by any means, just a temproary fix (along with our ASA stopping platelet aggregation) to just halt the dying tissue until definitive care can be done, i.e. cath lab or thrombolytics.

Just curious if we can give in thr absence of chest pain to get the coronary dilation. Ours skills instructors give conflicting info.

 

[Uclabruin103]

So I'm in my last month of didactic of school and was just curious of a few cardiac things. In class we were shown four serial 12-leads of an AMI that received pur full repetoire our EMS cardiac drugs; three NTG, MS, and ASA. The second 12-lead showed decreased ST elevation, and by the forth the 12-lead no longer showed infarction taking place. So that brings me to scenarios we were running today with atypical AMI presentations of flu-like and general malaise symptoms.

When I think about treatment I can't help but think about those serial strips temporarily halting the infarcting tissue and want to strive for that when I get in the field.

Finally the question, if a PT presents with atypical signs and symptoms and an absence of CP will you treat with NTG? I know its main indication is for cardiac CP, but if they are having an infarction dont we want to increase perfusion through coronary dilation even in the absence of pain?

Sorry if this does't make too much sense. Can't type too coherently on an iPhone.

Edited to clarify NTG not thought to be curing the infarction.

 

[KellyBracket]

I would not think of NTG as providing even a "temporary fix." It's used for pain control, essentially. Aspirin in MI, however, saves 1 life out of every 50 patients who get it. (Well, at least in the pre-lytic, pre-PCI era)

Besides the obvious stuff you know (don't give in hypotension, after sildenafil, etc.), NTG doesn't have a huge downside.

I have heard of at least one patient who denied any and all symptoms, even though his ECG showed a large inferior MI. After getting NTG (not sure who gave it, or why), he said he felt better... So, I think you could be justified in giving it with atypical symptoms, just don't think that you are treating anything besides discomfort. The plaque & thrombus are still hanging out, doing their thing!

 

[Uclabruin103]

I would not think of NTG as providing even a "temporary fix." It's used for pain control, essentially. Aspirin in MI, however, saves 1 life out of every 50 patients who get it. (Well, at least in the pre-lytic, pre-PCI era)

Besides the obvious stuff you know (don't give in hypotension, after sildenafil, etc.), NTG doesn't have a huge downside.

I have heard of at least one patient who denied any and all symptoms, even though his ECG showed a large inferior MI. After getting NTG (not sure who gave it, or why), he said he felt better... So, I think you could be justified in giving it with atypical symptoms, just don't think that you are treating anything besides discomfort. The plaque & thrombus are still hanging out, doing their thing!

Copy that! Danke for the info!

 

[Handsome Robb]

So n=1 but I gave NTG to a pt with a STEMI on the 12 lead who's only complaint was shortness of breath. His shortness of breath was relieved by the NTG.

Like Dr. Brackett said, NTG isn't going to be a game ruiner when given correctly. If they have signs and atypical symptoms there's no reason you can't trial it. If it isn't relieving the symptoms though I wouldn't keep giving it to them, personally.

Serial 12-leads are a huge part of ACS care that many medics, unfortunately, don't do,

 

[Merck]

I've seen ST segments resolve with standard pre-hospital treatment and I don't think it's a stretch to say that NTG might be part of that in select cases. Consider what we're doing with NTG - a decrease in myocardial O2 demand brought about through preload reduction, coupled with a slight increase in coronary perfusion may well be enough to put the patient on the happy side of the availability vs. demand scale.

As for treating an atypical presentation, sure, why not? So long as other pertinent points are there to support a provisional diagnosis of ACS a trial of NTG is justified.

 

[Carlos Danger]

First off (and I won't be the only guy to point this out), nitro has not been shown to "get rid of infarcting tissue," reverse an AMI, or decrease mortality. There are a number of cases where ST segments have normalized after NTG, but I don't think anyone believes that the essential process has been reversed.

In other words, the MI has likely just been temporarily masked, not treated.

There might be some diversity of opinion on who, or what symptoms, should get NTG. Probably anyone with symptoms that you suspect to be ischemic in origin. Epigastric pressure, new heartburn, backache - whatever. Now, even though hiccups can be a symptom of an AMI, it would feel odd to treat them with NTG, I admit.

Wouldn't worry about it too much though, since NTG isn't really a life-saver in AMI.

Interesting. This is the first time I've heard this.

Obviously NTG isn't going to reverse the process or "fix" the problem, but it seems that the reduction in cardiac work and improvement oxygen supply:demand ratio would help significantly. I've seen ST changes reverse with NTG many times.

What about opioids in AMI? I keep hearing that "morphine doesn't improve mortality", and I wonder if that's because we don't give enough to attenuate the SNS response? I suppose that's what b-blockers are for, though in my experience it seems rare to see enough lopressor or esmolol given to make a significant different in HR.

When I used to fly we gave ASA, SL or IV nitro, fentanyl, lopressor or labetolol in that order.

 

[Akulahawk]

My take on that statement is that NTG is basically a temporizing measure. It causes some vasodilation, lowers cardiac workload, maybe encourages some collateral circulation... but it won't actually treat the underlying cause of the problem and it won't resurrect the infarcted tissue but it might result in some reperfusion of the ischemic tissue. Take the NTG away and all the stuff kicks off again.

IMHO the opiates simply relieve the pain and serve as an anxiolytic, reducing psych stress and calming down the SNS, thus decreasing the cardiac workload that way.

To me, it just seems that those measures just slow things down enough so that the real "magic" can be done using other, more definitive measures in a less urgent manner.


And as always: I reserve the right to be completely wrong and change my mind (and understanding) based on scientific findings.

 

[KellyBracket]

Interesting. This is the first time I've heard this.

Obviously NTG isn't going to reverse the process or "fix" the problem, but it seems that the reduction in cardiac work and improvement oxygen supply:demand ratio would help significantly. I've seen ST changes reverse with NTG many times.

What about opioids in AMI? I keep hearing that "morphine doesn't improve mortality", and I wonder if that's because we don't give enough to attenuate the SNS response? I suppose that's what b-blockers are for, though in my experience it seems rare to see enough lopressor or esmolol given to make a significant different in HR.

When I used to fly we gave ASA, SL or IV nitro, fentanyl, lopressor or labetolol in that order.

I was speaking a bit glibly - if you look back in the literature, you'll be able to find a number of studies that suggested a benefit with nitro, but it didn't pan out. The 2013 AHA STEMI guidelines summarize that "it generally does not attenuate the myocardial injury associated with epicardial coronary artery occlusion," and is used mostly for symptoms.

To me, it just seems that those measures just slow things down enough so that the real "magic" can be done using other, more definitive measures in a less urgent manner.

Yes, the magic of big catheters being jammed in the groin!

 

[Brandon O]

The general impression you get (or I get, anyway) when you look at the literature and rationale behind nitro is, it probably has a small beneficial effect, but for total or near-total occlusions it's small, and when it comes to actual outcomes it's largely balanced by the occasional adverse effects (i.e. tanking systemic pressure enough that you're causing a net loss in coronary oxygen balance).

The sad thing is that when compared to other dubious interventions (tPA for stroke, epi for cardiac arrest, etc), it almost seems like a resounding endorsement for nitro just to be able to say that we're pretty sure it's not actually harming people.

 

[Akulahawk]

Then again, maybe all we're really doing is giving the patients a headache to act as a counter-irritant (sort of) to make the patient think the chest pain is less than it is...???

 

[Undaedalus]

I gave NTG to a pt with a STEMI on the 12 lead who's only complaint was shortness of breath. His shortness of breath was relieved by the NTG.

Dypsnea secondary to pulmonary edema may resolve after administration of NTG. If the dyspnea was related to LHF caused by the STEMI, then I would suspect the patient may respond as you describe.

 

[Handsome Robb]

Dypsnea secondary to pulmonary edema may resolve after administration of NTG. If the dyspnea was related to LHF caused by the STEMI, then I would suspect the patient may respond as you describe.

I would generally agree.

Except for the fact that he was clear to auscultation bilaterally.

I had an APE pt the other day, it took a lot of nitro to make a small dent in her dyspnea.

 

[18G]

There is also a phenomenon called spontaneously reperfused STEMI. Nobody is really sure what happens here.

Nitro is really a temporizing measure as others point out. Reduce the pain, decrease sympathetic/catacholamine response = slow down progression and stress of the already starving heart. The studies I have read show no improvement in mortality with nitro. Does this make it not important? I don't think so. I think nitro is important.

Aspirin is the most important drug an MI patient can receive early on. The sooner you get aspirin onboard the better chance of survival. One study shows a 30% reduction in mortality just with aspirin.

 

[systemet]

There is also a phenomenon called spontaneously reperfused STEMI. Nobody is really sure what happens here.

I think that's the thing -- NTG was given, so the change in ST segments are often attributed to the NTG --- but what if the thrombus was unstable and going to spontaneously lyse anyway?

My guess is that these cases of ST-segment resolution following NTG just represent a point on the UA-NSTEMI-STEMI continuum when someone took a 12-lead at the right time before the clot resolved.

 

[Melclin]

Nitro Administration

This:

... nitro has not been shown to "get rid of infarcting tissue," reverse an AMI, or decrease mortality.

...Probably anyone with symptoms that you suspect to be ischemic in origin. Epigastric pressure, new heartburn, backache - whatever. Now, even though hiccups can be a symptom of an AMI, it would feel odd to treat them with NTG, I admit.

Wouldn't worry about it too much though, since NTG isn't really a life-saver in AMI.

I don't have a high opinion of nitro and I don't know that I agree that it is entirely benign. My opinion is purely anecdotal, but the caffeine filled monkeys on type writers in my head have produced the following:

The amount of times I have backed crews to a pt who has dropped their bundle after a nitro scares me. You take your average b-blocked, dehyrated nanna with CP, and you suddenly vasodilate her. Its not a shock that she becomes hypotensive and altered conscious for a little while and I wonder how detrimental this may be to some of our more frail patients and pts actually infarcting. How about those patients in whom you produce hypotension and a reflex tachycardia. Surely that produces a rise in MvO2.

When you combine the lack of proven benefit, a lack of relief from symptoms in my experience, and its potential to cause perfusion issues, I am very conservative with my nitro dosing and use in general.

I am usually very cautious with nitro. A Esp in the STEMI pt. nd I withhold it from a lot of pts to whom I certainly could administer it according to my guidelines. I'm a fan of a conservative trial of nitro and moving straight to opiates if there is no improvement. If there is some improvement, I may continue cautiously. However, I almost never see acute coronary syndrome patients who don't end up getting at least a little morph or fent from me at some stage.

Atypical symptoms
As far treating atypical ACS symptoms with nitro, I will happily trial nitro in anything that I consider to be an anginal equivalent. SOB, back pain, heavy arms/shoulders. If the whole clinical picture points to it being ACS then I'll give a little nitro a shot.