TCA OD

Question 1

Acute toxicity symptoms of TCA OD: CV

Answer 1

Hypotension and ventricular dysrhythmia including sinus tachycardia and wide-complex tachycardia

Prolonged PR interval, QRS complex, QT interval

Question 2

Acute toxicity symptoms of TCA OD: CNS

Answer 2

Delirium, agitation, psychotic behaviors with hallucinations, seizures, lethargy, coma

Question 3

Acute toxicity symptoms of TCA OD: anticholinergic

Answer 3

dilated pupils that are minimally responsive to light, dry mouth, drug-flushed skin, urinary retention, ileus

Question 4

Acute toxicity symptoms of TCA OD: other symptoms

Answer 4

ARDS, aspiration pneumonitis, multisystem organ failure

Question 5

Is chronic TCA toxicity life-threatening?

Answer 5

No

Question 6

Signs/symptoms of chronic TCA toxicity

Answer 6

Sedation, sinus tachycardia

Question 7

Diagnostic testing of TCA OD

Answer 7

ECG, TCA serum concentration, electrolytes, glucose, venous or arterial blood gas

Question 8

ECG changes in TCA OD

Answer 8

Abnormal aVr, prolonged QRS

Question 9

Caveat about obtaining a TCA serum concentration

Answer 9

Quantitative concentrations may not be readily available and there’s limited utility early after ingestion

Question 10

Membrane stabilizing effect: normal cardiac conduction

Answer 10

sodium depolarizes the cell → cardiac depolarization, opening the voltage-dependent calcium channels

Question 11

Membrane stabilizing effect: in the presence of TCAs

Answer 11

sodium channel is altered slowing the rate of rise of action potential

Question 12

Membrane stabilizing effect: doing what will speed up the action potential?

Answer 12

Increasing the sodium gradient (administering large volumes of sodium or large concentrations of it)

Question 13

Effects of increasing the sodium gradient

Answer 13

Drug-induced effects are counteracted; it removes TCAs from the binding site on the sodium channel

Question 14

Doing what will remove TCAs from the binding site on the sodium channel?

Answer 14

Increasing the pH (by administering large amounts of sodium)

Question 15

Patho/chemistry behind TCAs getting kicked off their binding site

Answer 15

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

Question 16

TCA OD management: GI decontamination- when to use it and in what patients

Answer 16

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

Question 17

TCA OD management: serum alkalization and sodium loading- what’s the purpose of it?

Answer 17

Membrane stabilizing effect

Question 18

TCA OD management: serum alkalization and sodium loading- what’s it useful for?

Answer 18

Wide-complex dysrhythmias (QRS complex duration >100ms)

Question 19

TCA OD management: serum alkalization and sodium loading- what’s used for serum alkalization?

Answer 19

Sodium bicarb (preferred) or hypertonic saline

Question 20

TCA OD management: serum alkalization and sodium loading- dose of sodium bicarb

Answer 20

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

Question 21

Target pH for serum alkalization in TCA OD

Answer 21

7.5-7.55

Question 22

What to monitor during serum alkalization in TCA OD

Answer 22

Potassium and ionized calcium (they may be affected by alkalemia)

Question 23

TCA OD management: serum alkalization and sodium loading- what else is used for this and when to use it

Answer 23

Hypertonic saline, use when sodium bicarb administration isn’t possible or CI’ed

Question 24

TCA OD management: serum alkalization and sodium loading- dose of hypertonic saline

Answer 24

Same as sodium bicarb (1-2mEq/kg bolus)

Question 25

TCA OD management: arrhythmia control- what medications can you use for it?

Answer 25

Lidocaine, magnesium sulfate

Question 26

TCA OD management: arrhythmia control- lidocaine indication

Answer 26

Ventricular dysrhythmias not responsible to sodium bicarb therapy

(AKA your first backup option)

Question 27

TCA OD management: arrhythmia control- magnesium sulfate indication

Answer 27

Consider after alkalization, sodium loading, and a trial of lidocaine fails

Question 28

TCA OD management: arrhythmia control- which drugs are CI’ed?

Answer 28

Class 1A, 1C, and III antiarrhythmics

Question 29

Why are Class 1A and 1C antiarrhythmics CI’ed?

Answer 29

Their chemical structures are similar to TCAs

Question 30

Why are Class III antiarrhythmics CI’ed?

Answer 30

They prolong the QT interval…when the QT interval is already prolonged

Question 31

TCA OD management: hypotension- what treatments can you consider for this?

Answer 31

NS, sodium bicarb

Also extracorporeal membrane oxygenation

Question 32

TCA OD management: hypotension- what to do if you administered fluids and the patient is still hypotensive

Answer 32

NE, vasopressin can be added PRN

Question 33

TCA OD management: seizures- what’s first line treatment?

Answer 33

BZDs, like lorazepam 4mg IV push in adults; can repeat q3-5mins if they continue

Question 34

TCA OD management: seizures- what’s second line treatment if BZDs don’t work?

Answer 34

Propofol or a barbiturate

Question 35

TCA OD management: seizures- what drugs are CI’ed?

Answer 35

Phenytoin
Flumazenil
Physostigmine

Question 36

TCA OD management: seizures- why is phenytoin CI’ed?

Answer 36

Fails to terminate seizures, enhances CV toxicity

Question 37

TCA OD management: seizures- why are flumazeil and physostigmine CI’ed?

Answer 37

They both induce seizures

Question 38

TCA OD management: seizures- seizures can do what to serum lactate levels?

Answer 38

Cause an acute increase, which decreases serum pH, increases risk of cardiac toxicity, bradycardia, and systole

Question 39

TCA OD management: an decrease in serum pH leads to what?

Answer 39

TCAs becoming ionized and binding more to sodium channels

Question 40

TCA OD management: ILE

Answer 40

Salvage therapy used when CV therapy is refractory to standard therapies

Question 41

TCA OD management: ILE is only effective for what kinds of TCAs?

Answer 41

Lipophilic drugs (amitriptyline, clomipramine)

Question 42

ADEs of ILE

Answer 42

ARDS, pancreatitis