NTG is a very safe medication and in my opinion it is overboard to have a 12-lead before NTG. Only a small percentage... a very small percentage... of patients would be adversely effected and MI exacerbated with NTG. I've been doing this for 12 years as a career and active volunteer and NEVER once experienced a death or worsening of an MI from NTG. Could it happen... sure. Can a COPD patient stop breathing from to much O2 even though hypoxic? sure.
What are the chances? What is the benefit vs risks? Should we withhold early nitro therapy from 99% of the population bcause of 1% that may have a worsening of their MI?
Are you sure there were no risks if you did not do a 12 lead? Why one only look at a small view of an ECG. As those that really understand cardiology say ..."those that view in three, do
NOT see".... And can you say there is a small percentage of inferior AMI's? Is this based upon your clinical experience or AMI's in the U.S.? What are you basing your data upon? As well, exactly how do you know you did not increase the size of the AMI? If you did not have a pre twelve lead, then you have nothing in comparison. Not all (especially in post-inferior wall AMI) are symptomatic as they increase in size. As well, NTG is usually not beneficial treatment in a true obstructive AMI in comparison to Angina.
So you much rather gamble and take the chance of even causing more harm than to await to perform a 30 second twelve lead, that will help aid in diagnostic of the type of an AMI. Again, I am quite aware it may not affect
ALL patients with an AMI, but just to cause increase work load in one patient is too many... all for an additional 30-45 seconds. I have seen many patients that "bottom out" when given just one dose of NTG.
Do you not establish an IV prior to NTG administration as well? If not you are foolish. Then I ask you; what is the primary treatment of an inferior AMI ?
Do you agree to give NTG prior to 12 lead in a BBB patient? (again only determined by a 12 lead) as well; knowing that those with a BBB (wider than 170ms) only have about a 25% ejection fraction. So what do you think happens to these patients when NTG is given?
This is the same philosophy of not also believing in checking for bifascicular block/LBB before administering Morphine? Realizing that even M.S. may or will further the slow conduction through the ventricles and having a high risks of inducing a complete heart block, possibly ventricular aystole.
Attempting to compare oxygen toxicity to an inferior AMI has nothing even similar to comparison. The etiology and duration of time, percentage of occurrences has no similar comparison and is a very poor analogy.
R/r 911