Antidepressant/Lithium/BZD Toxicity Flashcards
TCA is not really used for depression anymore. Why?
Due to high risk of toxicity, and safer alternatives
T or F: Srs TCA toxicity can appear to be trivial.
T (which is why TCA’s are particularly dangerous)
How well are TCAs absorbed?
Well absorbed
TCA tmax?
up to 12h (OD dosing)
What kind of effect do TCAs have on gastric emptying?
Delays it due to anticholinergic effects
How extensive is plasma protein binding of TCAs?
V. extensive 85-98%
TCAs are…
- lipophilic
- hydrophilic
- amphipathic
- lipophilic (highly)
normal t1/2 of TCA? t1/2 in toxicity?
6-24h (up to 72h in toxicity)
Why is TCA toxicity variable in the pop?
bc it’s metabolized by enzymes that are subject to genetic polymorphisms
What is the main enzyme that metabolizes TCA?
2D6
T or F: If the pt ingested a little TCA, then no need to worry too much
F
Dose ingested is a poor predictor of outcome
CV signs/sx’s of TCA tox
Hypotn, cardiac dysrhythmias
How do TCAs cause hypotn?
by antagonizing peripheral alpha-1 receptors on blood vessels
by causing dysrhythmias
by directly suppressing myocardial activity (binds Na channels)
What’s important to do early on during TCA tox?
Take early ECG track heart’s electrical activity
CNS signs/sx’s of TCA overdose?
agitation
seizures
coma (can be rapid)
T or F: serum TCA levels are essential for TCA overdose dx
F
Single most important diagnostic tool during TCA overdose
ECG
TCA overdose: what does a QRS < 100ms tell us?
no seizure or ventricular arrhythmia
TCA overdose: what does a QRS > 100ms tell us?
26% risk of seizure
TCA overdose: what does a QRS > 160 ms tell us?
50% risk of ventricular arrhythmia
What’s used to tx the hypotn assoc w/ TCA tox?
fluid boluses
What’s used to tx dysrhythmias assoc w/ TCA tox?
NaHCO3
How does NaHCO3 help with dysrhythmias?
The Na helps overcome the Na channel blockade induced by TCAs
AND
blood alkalinization > reducing TCA binding to myocardial Na channels
T or F: NaHCO3 is used to enhance elimination of TCA faster from the body, much like it enhances elimination of salicylates
F
-NaHCO3 does NOT enhance elimination of the TCAs > we’re just treating sx’s and hoping for elimination of toxicity (this is unlike salicylates, which IS eliminated faster with NaHCO3)
When would we give lidocaine to a pt suffering from TCA-induced ventricular fib or ventricular tachycardia?
If they’re unresponsive to NaHCO3
If NaHCO3 isn’t helping w/ dysrhythmias assoc w/ TCA tox, what can we use?
lidocaine, hypertonic saline, magnesium sulfate
What do we AVOID in TCA-induced dysrhythmias?
BBs, class IA and IC antiarrhytmics (may worsen cardiac depression/hypotn)
What can we give for additional hypotn management during TCA toxicity (if NaHCO3 isn’t enough)?
Vasopressors (NE is the best one), DA (not as effective)
During TCA tox, what would make a pt’s hypotn worse?
B-agonists (B2, specifically)
During TCA tox, if a seizure arises, what should we give?
BZDs (diazepam)
What is recommended for decontamination of TCAs?
Single dose activated charcoal
Gastric lavage for TCA tox is reasonable in a certain situation.
Adults w/ intentional ODs
Is hemodialysis useful for TCA tox? Why?
No > TCAs have extensive plasma protein binding, are lipophilic, and hence also distribute widely in tissues
Antidote for TCA?
IV lipid emulsion (don’t use if not life-threatening)
-Based on case reports only
What must be tx’ed right away during an MAOI-induced toxicity?
Hyperthermia
Decontamination strats for MAOI-induced toxicity
SDAC, gastric lavage
Elimination strats MAOI-induced toxicity
?MDAC
hemodialysis = not effective
