Amiodarone & lidocaine: ineffective?!!

zzyzx

zzyzx

Forum Captain
Messages
428
Reaction score
90
Points
28
Recently I've read that lidocaine is 90% INEFFECTIVE at converting VT, while amiodarone is 70% INEFFECTIVE. I suppose I could find the studies myself, but I thought this might be an interesting topic for discussion. For me, this is the first I've heard of these drugs being so ineffective at treating VT.
 
That's why defib is the first choice. Think about the mechanisms that cause VF.

1: ischemic cells lose their ATP. this shuts the sodium-potassium pump down. Sodium gets trapped inside, while the potassium leaks out causing the cell to lose a majority of its positive charges. The cell becomes more negative, thus ST depression and T wave inversion. the negative cell becomes more likely to depolarize. PVC's.

2: the sodium -calcium exhanger , also ATP dependant, shuts down. Calcium sequestered in the SR stays there, and continues to sequester more with each contraction: as calcium flows in, but cannot flow out without its active transport mechanism. Calcium has more positive charges than potassium, so the cell becomes more positive if blood flow is witheld long enough. ST elevation. This is also why we know that ST elevation represents a complete occlusion. This is also why injured or abnormal tissue calcified over time. Arteriosclerosis? Why do we see cancer on x rays?

As this progresses, calcium becomes less and less available to the myocardium, due to massive sequestering. Now the cell is extremely positive, making it again more likely to depolarize. But since there's less calcium to use, the cells are less likely to contract.

What do we call a tissue that is depolarizing but not contracting? V-fib.

How does lidocaine and amiodarone work on these voltage-gated channels?

Raising the threshold for depolarisation keeps them from going back into V fib, and when combined with deb, CPR, and vasopressors may assist in conversion, but you can see that alone, theres not much going on for it.

V tach is a different story.
 
Nevermind, Doczilla posted a much better explanation
 
Last edited by a moderator:
Sorry for the crappy spelling , posted this on my phone after running in triple digit weather lol.
 
Doczilla, I was actually talking about their ineffectiveness in converting stable V-tach.

Does anyone have studies related to this? If I don't see anyone post them, I'll search for them and post a link.
 
zzyzx said:
Recently I've read that lidocaine is 90% INEFFECTIVE at converting VT, while amiodarone is 70% INEFFECTIVE. I suppose I could find the studies myself, but I thought this might be an interesting topic for discussion. For me, this is the first I've heard of these drugs being so ineffective at treating VT.
Click to expand...

CPR is 97% ineffective at leading to good outcomes.
 
Linuss said:
CPR is 97% ineffective at leading to good outcomes.
Click to expand...

Yeah, but there is no alternative to CPR. There is an alternative to antidysrhythmics--sedation and cardioversion.
 
zzyzx said:
Doczilla, I was actually talking about their ineffectiveness in converting stable V-tach.

Does anyone have studies related to this? If I don't see anyone post them, I'll search for them and post a link.
Click to expand...

When giving lido/amnio it is usually to prevent VT by prolonging the refractory period not with the hopes of chemically converting. Once V tach is sustaining I dont think the drugs MOA will really help.
 
zzyzx said:
Yeah, but there is no alternative to CPR. There is an alternative to antidysrhythmics--sedation and cardioversion.
Click to expand...

Open chest cardiac massage...And I think that some of the new mechanical CPR devices (Lucas) will eventually be the standard.
 
Just for clarification, what lead(s) were used to determine these stable V-tach rhythms? I ask because, according to some, Lead II has an accuracy rate of diagnosing ventricular based rhythms of 34% making them wrong 66% of the time.
 
MSDeltaFlt said:
Just for clarification, what lead(s) were used to determine these stable V-tach rhythms? I ask because, according to some, Lead II has an accuracy rate of diagnosing ventricular based rhythms of 34% making them wrong 66% of the time.
Click to expand...

That is a good point, Mike. I was also wondering if perhaps a flaw with these studies is that they may be only looking at the effectiveness of antidysrhythmics on any wide complex tachycardia. So maybe a lot of those werent VT. I havent seen the studies, so I am just speculating
 
Don't count procainamide out!

This has to be one of the best-kept secrets in emergency cardiology: for chemical conversion of stable monomorphic VT, the AHA actually recommends procainamide as first-line. (See ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death for details, references.)

Lidocaine is suggested if cardiac ischemia is the suspected etiology, and amiodarone if the patient is unstable, and, I dunno, your defibrillator is in the shop!

I wrote a review of not-well publicized indications for procainamide for my EM residents a while ago. Check it out for more details!

Procainamide - Hipster drug, or too mainstream?
 
Procainimide has the unique property of blocking sodium AND calcium channels. WPW afib anyone?
 
Okay, I found the studies, or at least the ones for amiodarone. Check out the link to RogueMedic's blog, where I first read about this topic:

http://roguemedic.com/2012/01/is-ketamine-an-ems-wonder-drug/

He is promoting the use of ketamine in, among other things, sedation prior to cardioversion. At the bottom of his article are the studies showing amiodarone's apparent ineffectiveness at converting VT. (I haven't yet had a chance to read those studies myself.)

By the way, the RogueMedic blog is really great and I encourage you guys to check it out.
 
It's pretty amazing how long Amio and Lido have remained top dog, yet the entire time they've performed poorly when compared to procainamide. I can act all cool because my service carries procainamide, but the honest answer is our medical director simply didn't want to change (re: a broken clock is right twice a day) which drugs we carried.

If only procainamide wasn't a bear to give I think we'd see less amio/lido. One "neat" way to administer it is to put it into a Volutrol/Buretrol. Or, if you're flush with cash, use a pump.

The way I always remember it, for the conversion of monomorphic VT:
  • Lidocaine works 1 out of 5 times
  • Amiodarone works 1 out of 4 times
  • Procainamide works 80% of the time (every time.)
  • Cardioversion--first shock--works 90% of the time
  • Adenosine works 1 out of 50 times!
 
DYK--It's called a countershock because the first uses of defibrillation were from induced v-fib in the lab. Scientists determined that an electrical shock could cause fibrillation and that a COUNTERshock had a chance to restore normal sinus rhythm.
 
You must log in or register to reply here.
Back
Top