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Posted

Got into a chat recently with another EMT and once everything had shaken out, I realized that I wasn't actually sure whether nitro had been definitely associated with positive outcomes in well-powered research. The gold standard here might be aspirin -- having an MI, take ASA, the data shows more live tissue and better survival to discharge. Does this sort of evidence exist supporting similar use of nitrates? Or is it just "one of those things" that in reality is done mainly as palliative care?

I recognize the theoretical mechanism here, but that it makes sense doesn't mean that it works. And this is not an academic issue, since it is potentially important to deciding priorities when rendering care.

Anyone know of any studies?

  • Like 2
Posted

Imrpoving outcomes in an MI? Haven't seen anything.

Now I could be wrong but I don't really think GTN has a role in myocardial infarction in the context of sublingual application in ambulance practice.

Although I have no research to cite at the moment there are two main mechanisms which can be researched.

Dilation of collateral circulation.

Reduction of preload

Posted

Although I have no research to cite at the moment there are two main mechanisms which can be researched.

Dilation of collateral circulation.

Reduction of preload

The only research I could find said either M&M was increased (first link) or that a bunch of studies happen to include GTN as part of thier treatment but was not specifically related to GTN. It also does not say if it was talking about carefully titrated intravenous nitrates or sublingul application.

I certianly agree that in theory yes reduction in preload and increasing coronary artery dialation sound quite useful it has not proven to be effective at reducing M&M in the context of prehospital application of sublingual nitrates.

Perhaps I am guilty of "says-so" syndrome in that the consensus of our clinical group is that GTN doesn't really have a role in MI and I sort-of agree but can't really find any good evidence to support this claim.

Posted

If you read the drug information, the manufacturers of sublingual nitroglycerin tablets state that nitro is in fact contraindicated in the presence of an acute myocardial infarction. These people, who are, at least in theory, the experts on the drug, do not want it given in the setting of AMI While I do not have any studies in front of me, I believe that the evidence is increasingly showing that despite the theoretical benefits, there is little statistical benefit, if any.

Second, as to the theory of the reduction in preload - there is a reason that you should ALWAYS obtain a 12-lead prior to NTG administration. Early aspirin is very beneficial, however, early nitroglycerin can in fact be fatal. Should the patient be experiencing an AMI with RVI, then they are probably preload dependent - and reducing this can certainly cause death. This (and the training/education to detect aortic stenosis) are the reasons that BLS should never carry their own nitroglycerin - should they assist the pt with their own pre-prescribed NTG, much, if not all, of the liability can be shifted to the prescribing physician. On the other hand, if you give your own, you would not have a legal leg to stand on if the pt received NTG, had an adverse reaction, and had one of these two conditions. Even worse, if you are an ALS tech, and you didn't bother to check/perform these simple assessments.

Posted

Gawd I hope we can get through one Nitro discussion someday without someone bringing this up.

This is not cutting edge information here, notice we are discussing collateral circulation and preload? It should be safe to assume we do not need a lecture on RVI MI.

Do you have any supporting evidence of the BOLDED segment above?

Not trying to personally attack you bro, but every freaking thread on 12 leads, IV's or Nitro ends up this way and it is getting frusterating.

  • Like 3
Posted

I don't know what to say here; I want to be a puppet for "CMG-say-so" sydrome and agree with what our clinical group says; that GTN has no role in an MI. That said I also am capable for thinking independantly and questioning that theory.

This study does not support GTN as reducing infarct size

http://www.sciencedirect.com/science?_ob=ArticleURL&_udi=B6WK6-4MHPC3V-3&_user=10&_coverDate=02%2F28%2F2007&_rdoc=1&_fmt=high&_orig=search&_sort=d&_docanchor=&view=c&_searchStrId=1194483771&_rerunOrigin=google&_acct=C000050221&_version=1&_urlVersion=0&_userid=10&md5=5f5c05aee69bef7e020ac3c056413abf

This one shows increased mortality and echos the careful need for monitoring and titration

http://circ.ahajournals.org/cgi/content/abstract/54/4/624

This study DOES support intravenous GTN

http://www.springerlink.com/content/q4p5v41652241175/

This study sort-of supports the use of intravenous GTN and not SL

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC483883/?page=4

I've had this discussion before and the apparent outcome seems to be that SL GTN is not appropriate and may be harmful whereas intravenous GTN may be of benefit. IV GTN can also be carefully titrated and monitored invasively which SL GTN in the back of an ambulance cannot.

Also our Technician (BLS) level has had GTN for years and they don't have 12 leads (if working with another Technician)

Posted (edited)

quote name='usmc_chris' date='04 February 2010 - 10:19 PM' timestamp='1265339990' post='235353']

Second, as to the theory of the reduction in preload - there is a reason that you should ALWAYS obtain a 12-lead prior to NTG administration. Early aspirin is very beneficial, however, early nitroglycerin can in fact be fatal. Should the patient be experiencing an AMI with RVI,

Gawd I hope we can get through one Nitro discussion someday without someone bringing this up.

This is not cutting edge information here, notice we are discussing collateral circulation and preload? It should be safe to assume we do not need a lecture on RVI MI.

Do you have any supporting evidence of the BOLDED segment above?

Not trying to personally attack you bro, but every freaking thread on 12 leads, IV's or Nitro ends up this way and it is getting frusterating.

Do you ever consider that this keeps coming up because it is a valid point. Although rare, this is a etiology that can be easily found with proper assessment and diagnositcs.

As far as NTG actually reducing the size of the infarct, I agree with Kiwi. I do not think that NTG is as beneficial as people think. However, I think where we make our money is by preventing further infact, and reducing overall oxygen consumption, (which has been proven to have a positive effect on patient outcome) (I will try to find the study).

Edited by armymedic571
Posted

Do you ever consider that this keeps coming up because it is a valid point. Although rare, this is a etiology that can be easily found with proper assessment and diagnositcs.

Agreed

As far as NTG actually reducing the size of the infarct, I agree with Kiwi. I do not think that NTG is as beneficial as people think. However, I think where we make our money is by preventing further infact, and reducing overall oxygen consumption, (which has been proven to have a positive effect on patient outcome) (I will try to find the study).

Look forward to reading it

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