Jump to content

Interesting AMI call w/NTG debate


Recommended Posts

Ahhhh...... what? Useful how?

Including this call, I've seen lidocaine appear to reduce ventricular ectopy a few times. I keep hearing the general consensus is that it doesn't help, but my county still uses it both in the ambulance and in the hospitals. I had another patient whose AICD had shocked them some 17 times before arrival for what appeared to be a recurring v-tach (was really hard to see because the AICD shocked so quickly). I gave lido and the patient went from getting shocked ever 30 seconds or so to once every 5-10 minutes (for a total of once during transport). At the hospital the MD tried to switch to amiodarone and the v-tach started re-occuring. He then switched to a lidocaine drip and the number of AICD shocks once again reduced dramatically. It was a real world situation where it appeared to work.

Edited by treaux
Link to post
Share on other sites

It wasn't really the lidocaine part that has me scratching my head, it's the AMI with ectopy. I agree that the evidence supporting amiodarone over lidocaine is pretty damn poor, so that doesn't bother me. However there is a vast difference between recurrent VT and ventricular ectopy.

I'm sure many here will remember the days of "Holy crap, 3 PVCs and 6 second strip, start the lidocaine!" (or something similar) We used to think that ventricular ectopy was bad, and would lead to ventricular arrhythmia, via the magic of the R on T phenomenon, so we would go jumping on any PVCs as soon as we saw them. Eventually we realised that it was an absolute load of crap, so it mercifully went away. There's really no need to cause further problems by loading up on pro-arrhythmic drugs unless there is actually an arrhythmia (such as you describe above)

Link to post
Share on other sites

I am going to go against the flow on this one....

1. There is no absolute contraindication against NTG....I agree to use it cautiously...but NTG is commonly used in IV form post arrest. I am confused if the patient is continueing to have the tingling or not. If he is......Since the patients tingling in the chest is considered an aginal equivalent...NTG may be considered.

(that said....I do understand the idea that sometimes we should leave good enough alone as well. )

2. Kudos on the Lido..Im a big fan myself.

3. In our protocols we not only have lido, but procainimide for recurrent VF (defined as VF that comes back AFTER termination) where we start with lido first for "persitant" VF (VF with no ROSC in between. )

Link to post
Share on other sites

However, this is an established STEMI, not an anginal episode. I have no problem with using nitrates for an anginal episode to address supply/demand problems, but there is no benefit in nitrates for STEMI, only risk.

Procainamide is interesting, not something that is seen often in the field, although it's the more effective drug. Does it get used often? How do you manage the issues with the infusion and potential side effects? I presume you have long transport times?

Link to post
Share on other sites

However, this is an established STEMI, not an anginal episode. I have no problem with using nitrates for an anginal episode to address supply/demand problems, but there is no benefit in nitrates for STEMI, only risk.

Procainamide is interesting, not something that is seen often in the field, although it's the more effective drug. Does it get used often? How do you manage the issues with the infusion and potential side effects? I presume you have long transport times?

RE: NTG - NTG still has benefit in STEMI, I am curious your reasoning behind the statement that there is only RISK. Not all STEMI is embolic, and even if one of the coronary arteries is indeed clogged, the resulting strain of the event on the remainder of the myocardium, as well as most the these patients have co-existing CAD, means NTG in my mind is of benefit.

Comments welcome.

RE: Procainimide: Our transport times are highly variable , from 5 minutes to 45, depending on weather and locations (Winter can be a b!tch in Idaho). However we work 99% of our adult codes on scene until ROSC, so transport times only come into play during the maint. infusion phase or procainimide. I wouldn't say it gets used a LOT, because the incidence of recurrent VF (as opposed to refractory) is (relatively) uncommon. Once we get ROSC we tend to be able to keep it for the next 15 minutes or so. By contrast, most of the time I give it is as a second line drug if I exhaust Lidocaine, yet their ETCO2 still indicates viability...wich is admittedly rare. But it does happen.

It wasn't really the lidocaine part that has me scratching my head, it's the AMI with ectopy. I agree that the evidence supporting amiodarone over lidocaine is pretty damn poor, so that doesn't bother me. However there is a vast difference between recurrent VT and ventricular ectopy.

I'm sure many here will remember the days of "Holy crap, 3 PVCs and 6 second strip, start the lidocaine!" (or something similar) We used to think that ventricular ectopy was bad, and would lead to ventricular arrhythmia, via the magic of the R on T phenomenon, so we would go jumping on any PVCs as soon as we saw them. Eventually we realised that it was an absolute load of crap, so it mercifully went away. There's really no need to cause further problems by loading up on pro-arrhythmic drugs unless there is actually an arrhythmia (such as you describe above)

I remember those days, though I recall it was 6/minute , non-perfusing, with agina/ACS s/s. As a side thought:

I actually gave it once recently for 10-15/minute PVCs, multi-focal, with chest pain, diaphoresis, etc and a Hx of previous sudden cardiac arrest 6 months prior. I still got the beginning of an ass chewing from a doctor who is known for her (usually justified) EPIC ass chewing, but even she (reluctantly) admitted that I had a point and "at least you had a thought process". I think that was a compliment. :punk:

Edited by croaker260
Link to post
Share on other sites

I fear there has been a bit of misinterpretation in what I posted.

Using lidocaine to reduce the development of ectopic beats, in the setting of a presumed AMI, is reasonable. It should not take precedence over managing the underlying problem, but reducing the occurrence of ectopic beats, and rhythm, should be a consideration. Limit the ischemia/injury, limit the development of dysrhythmias, and maximizing the cardiac output are still measures to shoot for with an active MI.

Link to post
Share on other sites

I fear there has been a bit of misinterpretation in what I posted.

Using lidocaine to reduce the development of ectopic beats, in the setting of a presumed AMI, is reasonable. It should not take precedence over managing the underlying problem, but reducing the occurrence of ectopic beats, and rhythm, should be a consideration. Limit the ischemia/injury, limit the development of dysrhythmias, and maximizing the cardiac output are still measures to shoot for with an active MI.

Sorry for taking so long to reply, the silly season has indeed been silly this year.

Azcep, I am still unsure what you mean by reducing ectopic beats with lidocaine in an AMI. This is exactly the scenario where we used to start lidocaine infusions, with the rationale being that ectopics can lead to R on T, R on T leads to VF, VF kills people. Seems reasonable, until we found out that it didn't make any improvement to mortality or morbidity, so we stopped pouring a pro-arrhythmic cardiac depressant into people with a vulnerable myocardium.

What would be your trigger to give lidocaine in someone with AMI? How many ectopics, or what type? What about re perfusion arrhythmia and ectopy, do you treat that with lidocaine?

Croaker, given this is an established inferior infarct, who tend to have a high likelihood of RV involvement, and that there is no evidence that nitrates improve outcomes (if there is I would be happy to recant, but there is none that I am aware of), all there seems to me to be is a 50/50 chance that one will tank this patient's BP due to them having impaired RV function and being preload dependant. (Right sided leads not being given here, and the incidence of RV dysfunction being arounf 40-60% depending on whom you read)

I could go with nitrates if you had a nice lateral or anterior with a booming blood pressure, but not for an inferior.

Link to post
Share on other sites

Lots of things "seem reasonable" but turn out to be harmful. Consider this video from the father of evidence based medicine.

Fast-forward to 5:00.

I fear there has been a bit of misinterpretation in what I posted.

Using lidocaine to reduce the development of ectopic beats, in the setting of a presumed AMI, is reasonable. It should not take precedence over managing the underlying problem, but reducing the occurrence of ectopic beats, and rhythm, should be a consideration. Limit the ischemia/injury, limit the development of dysrhythmias, and maximizing the cardiac output are still measures to shoot for with an active MI.

Link to post
Share on other sites
  • 3 weeks later...

I was reading about Nitro and Wellens Syndrome where in a right sided MI Nitro would definitely be contraindicated.

Link to post
Share on other sites
This thread is quite old. Please consider starting a new thread rather than reviving this one.

Join the conversation

You can post now and register later. If you have an account, sign in now to post with your account.

Guest
Reply to this topic...

×   Pasted as rich text.   Paste as plain text instead

  Only 75 emoji are allowed.

×   Your link has been automatically embedded.   Display as a link instead

×   Your previous content has been restored.   Clear editor

×   You cannot paste images directly. Upload or insert images from URL.

×
×
  • Create New...