TCA OD Flashcards
Acute toxicity symptoms of TCA OD: CV
Hypotension and ventricular dysrhythmia including sinus tachycardia and wide-complex tachycardia
Prolonged PR interval, QRS complex, QT interval
Acute toxicity symptoms of TCA OD: CNS
Delirium, agitation, psychotic behaviors with hallucinations, seizures, lethargy, coma
Acute toxicity symptoms of TCA OD: anticholinergic
dilated pupils that are minimally responsive to light, dry mouth, drug-flushed skin, urinary retention, ileus
Acute toxicity symptoms of TCA OD: other symptoms
ARDS, aspiration pneumonitis, multisystem organ failure
Is chronic TCA toxicity life-threatening?
No
Signs/symptoms of chronic TCA toxicity
Sedation, sinus tachycardia
Diagnostic testing of TCA OD
ECG, TCA serum concentration, electrolytes, glucose, venous or arterial blood gas
ECG changes in TCA OD
Abnormal aVr, prolonged QRS
Caveat about obtaining a TCA serum concentration
Quantitative concentrations may not be readily available and there’s limited utility early after ingestion
Membrane stabilizing effect: normal cardiac conduction
sodium depolarizes the cell → cardiac depolarization, opening the voltage-dependent calcium channels
Membrane stabilizing effect: in the presence of TCAs
sodium channel is altered slowing the rate of rise of action potential
Membrane stabilizing effect: doing what will speed up the action potential?
Increasing the sodium gradient (administering large volumes of sodium or large concentrations of it)
Effects of increasing the sodium gradient
Drug-induced effects are counteracted; it removes TCAs from the binding site on the sodium channel
Doing what will remove TCAs from the binding site on the sodium channel?
Increasing the pH (by administering large amounts of sodium)
Patho/chemistry behind TCAs getting kicked off their binding site
TCAs bind to sodium channels in an ionized state → increases pH and TCAs become ionized → TCAs will be removed from their binding site on the sodium channel → moves into lipophilic tissue
TCA OD management: GI decontamination- when to use it and in what patients
AC is recommended in ALL patients with a TCA OD who present within 2 HOURS of ingestion with a normal mental status or patients with altered mental status with a protected airway
A repeat dose can be considered several hours later if needed
TCA OD management: serum alkalization and sodium loading- what’s the purpose of it?
Membrane stabilizing effect
TCA OD management: serum alkalization and sodium loading- what’s it useful for?
Wide-complex dysrhythmias (QRS complex duration >100ms)
TCA OD management: serum alkalization and sodium loading- what’s used for serum alkalization?
Sodium bicarb (preferred) or hypertonic saline
TCA OD management: serum alkalization and sodium loading- dose of sodium bicarb
Bolus or rapid infusion over several minutes: 1-2mEq/kg
Additional boluses q3-5min until QRS duration narrows (monitor serial ECGs!) and hypotension improves, then consider initiating continuous infusion to maintain pH
Target pH for serum alkalization in TCA OD
7.5-7.55
What to monitor during serum alkalization in TCA OD
Potassium and ionized calcium (they may be affected by alkalemia)
TCA OD management: serum alkalization and sodium loading- what else is used for this and when to use it
Hypertonic saline, use when sodium bicarb administration isn’t possible or CI’ed
TCA OD management: serum alkalization and sodium loading- dose of hypertonic saline
Same as sodium bicarb (1-2mEq/kg bolus)
TCA OD management: arrhythmia control- what medications can you use for it?
Lidocaine, magnesium sulfate
TCA OD management: arrhythmia control- lidocaine indication
Ventricular dysrhythmias not responsible to sodium bicarb therapy
(AKA your first backup option)
TCA OD management: arrhythmia control- magnesium sulfate indication
Consider after alkalization, sodium loading, and a trial of lidocaine fails
TCA OD management: arrhythmia control- which drugs are CI’ed?
Class 1A, 1C, and III antiarrhythmics
Why are Class 1A and 1C antiarrhythmics CI’ed?
Their chemical structures are similar to TCAs
Why are Class III antiarrhythmics CI’ed?
They prolong the QT interval…when the QT interval is already prolonged
TCA OD management: hypotension- what treatments can you consider for this?
NS, sodium bicarb
Also extracorporeal membrane oxygenation
TCA OD management: hypotension- what to do if you administered fluids and the patient is still hypotensive
NE, vasopressin can be added PRN
TCA OD management: seizures- what’s first line treatment?
BZDs, like lorazepam 4mg IV push in adults; can repeat q3-5mins if they continue
TCA OD management: seizures- what’s second line treatment if BZDs don’t work?
Propofol or a barbiturate
TCA OD management: seizures- what drugs are CI’ed?
Phenytoin
Flumazenil
Physostigmine
TCA OD management: seizures- why is phenytoin CI’ed?
Fails to terminate seizures, enhances CV toxicity
TCA OD management: seizures- why are flumazeil and physostigmine CI’ed?
They both induce seizures
TCA OD management: seizures- seizures can do what to serum lactate levels?
Cause an acute increase, which decreases serum pH, increases risk of cardiac toxicity, bradycardia, and systole
TCA OD management: an decrease in serum pH leads to what?
TCAs becoming ionized and binding more to sodium channels
TCA OD management: ILE
Salvage therapy used when CV therapy is refractory to standard therapies
TCA OD management: ILE is only effective for what kinds of TCAs?
Lipophilic drugs (amitriptyline, clomipramine)
ADEs of ILE
ARDS, pancreatitis
