Toxicology Question

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Phenytoin is itself arrhythmogenic.

What's the question, and is bicarbonate the answer?

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I thought norepi + benzo was the answer and then glucagon if the patient is really bad. and you can't use dopamine because the endogenous stores of norepi are depleted by the TCA OD.

well the reason xiphoid was wrong is that phenytoin isn't effective for drug-induced seizures. Benzos, benzos, benzos are.

Glucagon isn't used for TCA overdose, but in the case presented to us, high-dose insulin was used successfully. Glucagon is usually used for Beta-Blocker overdoses and high-dose insulin was first used for calcium channel blockers.

Sodium Bicarbonate works by both alkalinizing the serum, which decreases the affinity of the TCA for the cardiac sodium channels, and providing a sodium load, thereby flooding the sodium channels.

For a patient who is alkalotic from too much bicarb there are case reports (the big one is from my alma mater) of using hypertonic saline and hyperventilation, so you can titrate the alkalinity and sodium separately. But that is not common practice.

For once I was not on my phone and could actually answer things.

Originally Posted by Praziquantel86

Phenytoin is itself arrhythmogenic.

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All antiarrhythmics can cause arrhythima, that's just the nature of the beast. You just need to use the right ones.

Originally Posted by njac

well the reason xiphoid was wrong is that phenytoin isn't effective for drug-induced seizures. Benzos, benzos, benzos are.

Glucagon isn't used for TCA overdose, but in the case presented to us, high-dose insulin was used successfully. Glucagon is usually used for Beta-Blocker overdoses and high-dose insulin was first used for calcium channel blockers.

Sodium Bicarbonate works by both alkalinizing the serum, which decreases the affinity of the TCA for the cardiac sodium channels, and providing a sodium load, thereby flooding the sodium channels.

For a patient who is alkalotic from too much bicarb there are case reports (the big one is from my alma mater) of using hypertonic saline and hyperventilation, so you can titrate the alkalinity and sodium separately. But that is not common practice.

For once I was not on my phone and could actually answer things.

Cool, learns something everyday. Nobody told me phenytoin didn't work for drug induced seizures before. Is there a reason behind that?

pharmdstudent,

I don't think you give lidocaine (sodium channel blocker to treat a sodium channel blocker??) or dopamine in that situation.

I think it's bicarb for arrhythmias and norepi as a pressor. Bicarb infusion can help treat hypotension as well.

for seizures, phenytoin should not be used in a tca overdose. benzos are the drug of choice.

happy hunting!

NE is b/c TCA's induced alpha blockade and bp drop in OD. Dopa will not work (unless you crank the rate up to at leat 15-20 mcg/kg/min, which then they will start tachying away and induce some other type of arrhthymia)-plus you've depleted your indogenous resevere of dopa to initiate the relase of your own NE). NE is the most most potent alpha agonist to help with hypotension. Bicarb is because of the QRS widening affect of TCA's and has nothing to do with the bicarb componet but the NA content, b/c if you are blocking Na+ channesl with the TCA, in theory, giving Na+ will overcome that, hence even using NS is a viable option. Also phenytoin is never used. Drug OD's pretty much are gaba mediated, and bz can supress firing faster than Na+ channels that pheny works on.

Originally Posted by PharmD2MD2

NE is b/c TCA's induced alpha blockade and bp drop in OD. Dopa will not work (unless you crank the rate up to at leat 15-20 mcg/kg/min, which then they will start tachying away and induce some other type of arrhthymia)-plus you've depleted your indogenous resevere of dopa to initiate the relase of your own NE). NE is the most most potent alpha agonist to help with hypotension. Bicarb is because of the QRS widening affect of TCA's and has nothing to do with the bicarb componet but the NA content, b/c if you are blocking Na+ channesl with the TCA, in theory, giving Na+ will overcome that, hence even using NS is a viable option. Also phenytoin is never used. Drug OD's pretty much are gaba mediated, and bz can supress firing faster than Na+ channels that pheny works on.

Addendum: bicarb does have a role in treating hypotension, through narrowing the QRS and through secondary volume expansion (just as using NS would help pts that are hypovolemic), pts are normally given boluses of bicarb (1-3 amps (50-150 ml) separated by a few minutes, then started on a drip in which 3 amp (132 mEq) are put in a liter D5W and run continuously. There is also some thinking the alkalinization helps for the OD. NS (1 L =154 mEq), however, is still the first thing for hypotension in pts that are hypovolemic, followed by NE (or vasopressin if not responsive or pt is acidotic).

Lidocaine is in fact 2nd line for TCA induced dysrhythmias, although there are no controlled human studies proving its efficacy. Class IA and IC are contraindicated b/c they have similar actions of TCA’s and may exacerbate Na channel inhibition more so than lido.

For seizures, bz’s (lorazapam/diazepam/midazolam) are fist line b/c they elevate the seizure threshold (GABA mediated), followed by barbiturates/propofol. Phenytoin limits the spread of sz activity and reduces propagation, but does not elevate the threshold. It is of course used for pts with epilepsy or unknown unprovoked seizures that need long term therapy, but for an OD and sequential recovery pts will not be on any anticonvulsants at discharge.

Cholinesterase inhibitors (physostigmine) are not used 2/2 to potentially inducing bradycardia and asystole. They were used in the past to reverse the anticholinergic CNS properties (delirium, confusiont, etc) of TCA’s.