amitriptyline overdose (drug interventions)

coolidge

Forum Crew Member
Messages
76
Reaction score
0
Points
6
What algorithm do you follow for an amitriptyline overdose?
 
Here is a link to DFW in service on TCA overdose and their protocols, (which is similar to what I use).

http://www.utsw.ws/guestquizindex.htm

Look at the TCA link, and it is narrated by a physician, with power point.

R/r 9011
 
Thank you very much.
 
Life sucks

Just let them die. Life sucks. No matter how hard one tries. Life sucks.
 
Bosco578, Merry Christmas!!

You get your butt kicked by an Elavil overdoser, too?
 
TCA od

Bicarb baby, Bicarb.
 
Why bicarb?

Watch the attached link for a good inservice from DFW EMS and the physician will give you the in and outs.

R/r 911
 
To combat the acidosis. Cool stuff.
 
Just let them die. Life sucks. No matter how hard one tries. Life sucks.

Completely inappropriate. Let them die? Really?

NaHCO_3 is the answer. Lots of bicarb. It's not completely an acidosis thing. For all intents and purposes, it's a QRS thing.
 
Well since this post has just been necro'd...anyone have a downloaded copy of the TCA lecture link Rid posted earlier that they can host elsewhere? The link on the site is dead.
 
amitriptyline OD

Did anyone discover the new web site for tricyclic OD tx?
Thanks
 
The administration of Sod Bicarb alkalinizes the blood, resulting in an increased binding of the TCA's, therefore (sounds pretentious, sorry :rolleyes:) a decreased bioavailability of the drug
 
Sodium bicarb as MediMike has said increases the alkalinity of the blood which increases protein binding of the TCA molecules making them unable to exert their effect. A drug that is protein bound is not able to exert its effect. The drug has to be free.

The sodium bicarb also increases elimination of the drug through urination.
 
The administration of Sod Bicarb alkalinizes the blood, resulting in an increased binding of the TCA's, therefore (sounds pretentious, sorry :rolleyes:) a decreased bioavailability of the drug

Bingo. It's not about acidosis.
 
Good. Without it they rev and spin and then

............collapse.
 
Sodium bicarb as MediMike has said increases the alkalinity of the blood which increases protein binding of the TCA molecules making them unable to exert their effect. A drug that is protein bound is not able to exert its effect. The drug has to be free.

The sodium bicarb also increases elimination of the drug through urination.
I never knew this, very informative :)
So TCA can only be active at a neutral/normal pH's? What causes the QRS widening? Is it a potassium deal?
 
It's my understanding that the QRS widening seen in TCA OD comes from the sodium channel blockade effect.


From eMedicine:
"Serum alkalinization to a pH of 7.45-7.55 appears to uncouple tricyclic antidepressant (TCA) from myocardial sodium channels, and the sodium load increases extracellular sodium concentration, improving the gradient across the channel."
 
OK, folks, I would say bicarb is a good choice if treating based on the ECG findings, however since Amitriptyline is an older tricyclic antidepressant/SNRI giving a dose of activated charcoal would be most beneficial if the OD was acute and you have supporting evidance that the dose would be given within one hour of the oral intake.

Since we are talking SNRI, we would have similar issues when comparing this to a Tramadol overdose, one reason why Elavil and Tramadol are contraindicated. Both (especially together but independently) will cause Serotonin Syndrome where each "piece" can be individually managed, e.g. benzos, airway management, epinephrine (to raise the pulse/BP to be WNL), etc.

Remember that in all of the above cases Serotonin Syndrome should resolve in <24 hours. The key is management of the symptoms if the initial interference such as activated charcoal and bicarb (if the ECG supports it) do not resolve it, once the drugs have tapered down in the system there may be some after-effects but generally things will look positive.

The only exception to the Serotonin Syndrome with an Amitriptyline OD and that of Tramadol is that Tramadol additionally acts on the μ-opioid receptor as well as causing the burst in serotonin. This in some cases can lead to a more intense withdrawal than that of other synthetic opioids (whether scheduled of not) and is *probably* why naloxone is not as effective at treating such an OD.
 
Back
Top