01Approach to the Critical Patient/attcp74

Immediate threats

›Airway and respiratory priorities

›Rapidly declining GCS mandates early intubation

›Abrupt deterioration can occur without warning

›Do not delay for GI decontamination if airway unsafe

›Respiratory depression from CNS sedation

›Apnea risk with severe toxicity

›Ventilatory support may be required

›RSI preferred; avoid succinylcholine if hyperkalemia suspected

›Ketamine acceptable induction agent

›Rocuronium 1.2 mg/kg alternative

›Cardiovascular collapse threats

›Wide-complex tachycardia or ventricular fibrillation

›Sodium channel blockade mechanism

›QRS >= 100 ms predicts arrhythmia and seizures

›Refractory hypotension

›Alpha-adrenergic blockade and myocardial depression combined

›SBP < 90 mmHg or MAP < 65 mmHg triggers immediate action

›Most deaths occur prehospital or within first few hours

›Rapid clinical trajectory possible

›Continuous cardiac monitoring mandatory

›Seizure threat

›Risk highest with QRS >= 100 ms

›Seizures may precipitate cardiovascular collapse

›Benzodiazepines first-line

›Prophylactic alkalinization for ECG-confirmed toxicity

›Target pH 7.45 to 7.55

›Do not await seizure before treating QRS widening

Monitoring and targets

›Continuous monitoring bundle

›Continuous cardiac monitor with rhythm strip

›QRS duration trend every 15 to 30 minutes

›R wave in aVR amplitude monitoring

›Pulse oximetry continuous

›SpO2 target >= 95%

›Prepare for rapid desaturation

›Frequent vital signs

›Blood pressure every 5 to 15 minutes in unstable patient

›Temperature for hyperthermia from anticholinergic effects

›pH and sodium monitoring during bicarbonate therapy

›Target arterial pH 7.45 to 7.55

›Do not exceed pH 7.55 to 7.60

›Repeat ABG every 30 to 60 minutes

›Serum sodium monitoring

›Do not exceed 155 mmol/l during therapy

›Potassium falls with alkalinization; replace aggressively

Immediate interventions

›Resuscitation priorities

›Large bore IV access bilateral

›IO access if IV unobtainable

›Fluid bolus for hypotension: 20 mL/kg isotonic crystalloid

›12-lead ECG immediately

›QRS duration and terminal R wave in aVR are key prognostic markers

›Brugada-like pattern may be unmasked

›Poison Control Center consultation

›All TCA overdoses regardless of initial clinical appearance

›Expert guidance on decontamination and antidote dosing

›GI decontamination

›Activated charcoal 1 g/kg if within 1 to 2 hours and airway protected

›Contraindicated if mental status impaired without secured airway

›Emesis absolutely contraindicated

›Gastric lavage rarely indicated; charcoal preferred

›Only consider if large dose with protected airway within 1 hour

›Procedure risk vs benefit assessment required

Consult triggers

›Immediate consultation requirements

›Poison Control Center for all cases

›1-800-222-1222 North America

›Management guidance and antidote advice

›Critical care or toxicology for ICU-level toxicity

›QRS >= 100 ms

›Seizures or arrhythmias

›Cardiac surgery or ECMO team for refractory shock

›When VA-ECMO may be required

›Early activation improves survival

›Psychiatry consultation once medically stable

›Intentional overdose is a psychiatric emergency

›Suicide risk assessment and safety planning required

02History/hx61

Ingestion details

›TCA agent identification

›Amitriptyline, nortriptyline, desipramine, imipramine, doxepin, clomipramine

›Desipramine associated with higher death rate in overdose

›Agent affects expected clinical course

›Dose ingested

›Toxic range approximately 5 to 20 mg/kg

›Reported dose unreliable and poor predictor of outcome

›Time of ingestion

›Critical for activated charcoal eligibility

›Anticipates clinical trajectory timing

›Formulation

›Immediate-release vs sustained-release

›Pill count if available for dose estimation

Symptom timeline

›Presenting symptoms

›Neurological

›Drowsiness, confusion, agitation, delirium

›Seizures may occur within hours of ingestion

›Cardiovascular

›Palpitations, chest pain, syncope

›Rapid progression possible

›Anticholinergic symptoms

›Dry mouth, blurred vision, urinary retention

›Hot flushed dry skin

›Vomiting history

›Spontaneous emesis may have occurred

›Does not eliminate ongoing absorption risk

03Physical Exam/exam57

Vitals and general appearance

›Hemodynamic snapshot

›Heart rate

›Sinus tachycardia typical from anticholinergic effects

›Rate often > 120 beats per minute

›Blood pressure

›Hypotension from alpha blockade and myocardial depression

›SBP < 90 mmHg signals hemodynamic toxicity

›Temperature

›Hyperthermia from anticholinergic impairment of sweating

›Significant hyperthermia can worsen cardiac toxicity

›Respiratory rate

›Depression signals CNS compromise

›Tachypnea with acidosis may indicate compensatory breathing

Anticholinergic toxidrome findings

›Classic anticholinergic signs

›Pupils

›Mydriasis, dilated and poorly reactive

›Bilateral symmetric

›Skin

›Dry, flushed, and warm

›Absence of diaphoresis distinguishes from serotonin syndrome

›Mucous membranes

›Dry oral mucosa

›Diminished salivation

›Bladder

›Urinary retention

›Distended bladder on palpation

04Differential Diagnosis/ddx47

Life-threatening mimics

›Other sodium channel blocker toxicity

›Cocaine toxicity

›ICD-10 T40.5

›Sympathomimetic features with diaphoresis

›Class Ia antiarrhythmics: quinidine, procainamide

›ICD-10 T46.2

›QRS widening without anticholinergic toxidrome typical

›Class Ic antiarrhythmics: flecainide, propafenone

›ICD-10 T46.2

›Sine wave morphology in severe toxicity

›Carbamazepine overdose

›ICD-10 T42.1

›Can cause false positive TCA urine screen

›Other cardiotoxic poisonings

›Propranolol overdose

›ICD-10 T44.7

›Bradycardia rather than tachycardia

›Diphenhydramine overdose

›ICD-10 T45.0

›Anticholinergic toxidrome; false positive TCA urine screen

Toxidromes that overlap

›Anticholinergic toxidrome from other agents

›Antihistamines: diphenhydramine, hydroxyzine

›ICD-10 T45.0

›No QRS widening distinguishes from TCA

›Antipsychotics: quetiapine, chlorpromazine

›ICD-10 T43.5

05Laboratory Tests/lt53

Core toxicology labs

›Urine drug screen

›Qualitative TCA screen

›Sensitivity varies by assay

›False positives: carbamazepine, cyclobenzaprine, quetiapine, diphenhydramine

›Serum TCA levels not useful for guiding management

›ECG findings are more predictive than serum concentrations

›Do not delay treatment awaiting serum level

›Co-ingestant screen

›Serum acetaminophen level

›Common co-ingestant in deliberate overdose

›Treatment with N-acetylcysteine if elevated

›Serum salicylate level

›Rule out aspirin co-ingestion

›Both cause altered mental status

Metabolic and electrolyte panel

›Basic metabolic panel

›Serum sodium

›Baseline before sodium bicarbonate therapy

›Do not exceed 155 mmol/l during treatment

›Serum potassium

›Hypokalemia worsens arrhythmia risk

›Falls with alkalinization; aggressive replacement required

›Glucose

›Hypoglycemia can mimic altered mental status

›Point of care glucose on arrival

›Renal function

›Creatinine and urea for drug clearance assessment

06Diagnostic Tests/dt63

Scoring Systems

›ECG-based risk stratification

›QRS duration thresholds

›< 100 ms: lower risk for seizures and arrhythmias

›>= 100 ms: high risk for seizures; sodium bicarbonate indicated

›>= 160 ms: high risk for ventricular arrhythmias

›R wave in aVR

›> 3 mm: predictive of seizures and arrhythmias

›Combined with QRS duration for risk stratification

›Terminal 40 ms axis

›Rightward deviation > 120 degrees

›Reflects sodium channel blockade in right bundle branch

›Clinical severity assessment

›Grades of TCA toxicity

›Mild: anticholinergic symptoms only, QRS < 100 ms

›Moderate: QRS 100 to 160 ms, hypotension, altered mental status

›Severe: QRS > 160 ms, seizures, ventricular arrhythmias, coma

›ACEP Level B recommendation for ECG-guided management

›Serial ECGs required

›QRS trend guides bicarbonate dosing

MRI

›MRI role in TCA toxicity

›Limited utility in acute poisoning management

›Not a primary diagnostic tool for TCA toxicity

›Availability and monitoring constraints in acute setting

›Potential indications for neurological complications

›Hypoxic-ischemic injury after cardiac arrest

›Persistent neurological deficits after toxicity resolves

07Disposition/dispo46

Admission criteria

›All TCA overdoses require hospital admission

›Mandatory minimum 6-hour cardiac monitoring observation period

›Monitor for CNS depression, hypotension, arrhythmias, seizures

›Late fatal dysrhythmias reported after inadequate monitoring

›Any symptom development during observation mandates extended admission

›ICU-level care for any clinical toxicity

›Do not discharge within 6 hours regardless of appearance

ICU admission indications

›High-acuity admission triggers

›QRS >= 100 ms on any ECG

›Sodium bicarbonate therapy required

›Continuous cardiac monitoring in monitored bed

›Seizures

›Risk of recurrence and cardiovascular collapse

›Ongoing anticonvulsant therapy required

›Ventricular arrhythmias

›Immediate resuscitation capability required

›Defibrillation and antiarrhythmic access

›Hemodynamic instability

›Vasopressor requirement

›Fluid-refractory hypotension

›Altered mental status or GCS < 13

›Airway protection concern

›Aspiration risk management

›Need for intubation or ventilatory support

›ICU-level ventilator management

›Alkalinization strategy requires ventilator target PCO2

08Treatment/t121

Sodium bicarbonate therapy

›Sodium bicarbonate indications

›Indications for therapy

›QRS >= 100 ms on ECG

›Hypotension refractory to initial fluids

›Ventricular arrhythmias

›Seizures secondary to TCA toxicity

›Mechanism

›Reverses sodium channel blockade via pH-mediated effect

›High sodium concentration directly competes for sodium channel

›Alkalinization reduces free drug fraction

›Dosing protocol

›Initial bolus

›1 to 2 mmol/kg IV push

›May repeat every 3 to 5 minutes until QRS narrows

›Maximum cumulative dose 6 mmol/kg

›Maintenance infusion

›150 mEq in 1 L D5W at 200 to 250 mL/hour

›Titrate to maintain arterial pH 7.45 to 7.55

›Monitoring targets during therapy

›Arterial pH not to exceed 7.55 to 7.60

›Serum sodium not to exceed 155 mmol/l

›Correct hypokalemia aggressively during therapy

›Monitor for hypocalcemia with prolonged therapy

Seizure management

›First-line anticonvulsants

›Lorazepam IV

›0.05 to 0.1 mg/kg IV

›Maximum 4 mg per dose

›Repeat every 5 to 10 minutes if seizures continue

›Diazepam IV alternative

›5 to 10 mg IV

›May repeat every 5 minutes

›Maximum 30 mg

›Second-line anticonvulsants

›Phenobarbital IV

›15 to 20 mg/kg IV at 50 to 100 mg/minute

›Respiratory depression risk; airway management required

›Phenytoin or fosphenytoin

›15 to 20 mg/kg IV

›Rate limit to reduce cardiac risk

›Less preferred than phenobarbital for TCA-induced seizures

›Sodium bicarbonate should also be given for all TCA seizures

›Alkalinization reduces seizure threshold

›Treat concurrently with anticonvulsants

Vasopressor and hemodynamic support

›Hypotension management

›Initial fluid resuscitation

›Normal saline or Ringer's lactate 20 mL/kg IV bolus

›Reassess after each bolus

›Vasopressor therapy for fluid-refractory hypotension

›Norepinephrine first-line

›0.05 to 0.5 mcg/kg/minute IV infusion

›Titrate to MAP >= 65 mmHg

›Direct-acting vasopressors preferred over indirect-acting

›TCA depletes norepinephrine stores

›Epinephrine as alternative if norepinephrine insufficient

›Avoid vasopressors with adrenergic agonism that may worsen arrhythmias

›Dopamine less preferred; norepinephrine superior

›Class IIa recommendation per AHA 2023 guideline

›Titrate to clinical response

Antiarrhythmic therapy

›For wide-complex tachycardia refractory to sodium bicarbonate

›Lidocaine IV

›1 to 1.5 mg/kg IV bolus

›Class Ib sodium channel antagonist competes for binding

›Follow with 1 to 4 mg/minute infusion

›Sodium bicarbonate remains first-line before lidocaine

›Alkalinization should precede antiarrhythmic trials

›AHA 2023 guideline recommendation

›Absolutely contraindicated antiarrhythmics

›Class Ia antiarrhythmics: quinidine, procainamide, disopyramide

›Worsen sodium channel blockade

›Associated with fatal outcomes

›Class Ic antiarrhythmics: flecainide, propafenone

›Same mechanism; absolutely contraindicated

›FDA and AHA strongly recommend avoidance

Rescue therapies

›Intravenous lipid emulsion

›Indications

›Life-threatening toxicity refractory to standard therapies

›When VA-ECMO not available or as bridge to ECMO

›Dosing protocol

›20% lipid emulsion 1.5 mL/kg IV bolus over 1 minute

›Follow with 0.25 mL/kg/minute infusion for 30 to 60 minutes

›May repeat bolus once if no response

›Mechanism

›Lipid sink sequestration of lipophilic TCA

›AHA 2023 Circulation guideline evidence

›Veno-arterial ECMO

›Refractory cardiogenic shock or cardiac arrest

›When conventional resuscitation fails

›Early activation improves survival outcomes

›Indications

›Persistent hemodynamic instability despite vasopressors and bicarbonate

›Cardiac arrest with suspected TCA toxicity

›Bridge to hepatic clearance of drug

›AHA 2023 and 2025 CPR guidelines support ECMO for refractory toxicologic arrest

›Class IIa recommendation

›Requires specialized center capability

Mechanical ventilation strategy

›Intubated patient alkalinization

›Target PCO2 30 to 35 mmHg

›Synergistic with sodium bicarbonate for alkalinization

›Mechanical hyperventilation narrows QRS

›Arterial pH target 7.45 to 7.55 maintained with combined strategies

›Adjust ventilator rate to achieve PCO2 target

›Coordinate with bicarbonate infusion rate

›Avoid respiratory acidosis

›PCO2 > 45 mmHg worsens TCA toxicity

›Increases free drug fraction

›Aggravates sodium channel blockade

Contraindicated treatments

›Physostigmine

›Avoid unless specifically recommended by toxicologist

›Risk of worsening cardiac conduction and seizures

›Only for life-threatening anticholinergic symptoms unresponsive to all other therapy

›If used, only in consultation with Poison Control Center

›Never use with QRS widening or conduction abnormalities

›Bradycardia and asystole risk

›Flumazenil

›Absolutely contraindicated if benzodiazepine co-ingestion possible

›May precipitate seizures

›Cannot determine co-ingestion safely

›Induced emesis

›Absolutely contraindicated

›Aspiration risk with deteriorating mental status

›FDA contraindication for all TCA overdoses

09Special Populations/sp78

Pregnancy

›Pregnancy-specific considerations

›Pharmacokinetic changes in pregnancy

›Increased volume of distribution affects drug levels

›Altered hepatic metabolism may increase or decrease clearance

›TCA teratogenicity concern

›Category D risk classification historically

›Limb reduction defects reported with first-trimester exposure

›Fetal cardiac effects

›TCA crosses placenta

›Fetal arrhythmia risk in severe maternal toxicity

›Maternal management priorities

›Sodium bicarbonate is not contraindicated in pregnancy

›Maternal hemodynamic stability protects fetal perfusion

›Treat maternal toxicity aggressively

›Activated charcoal can be used if airway protected

›Aspiration risk higher in pregnancy due to delayed gastric emptying

›RSI with cricoid pressure if intubation needed

›Vasopressors for refractory hypotension

›Norepinephrine acceptable in pregnancy for life-threatening hypotension

›Phenylephrine may reduce uterine blood flow; use cautiously

›Fetal monitoring

›Continuous fetal monitoring when fetus viable

›Obstetric consultation immediately

›Discuss delivery timing based on gestational age and maternal stability

›Neonatal assessment at delivery

›Neonatal TCA toxicity may manifest postpartum

›Neonatology team involvement

Geriatric

›Pharmacokinetic and pharmacodynamic changes

›Increased sensitivity to anticholinergic effects

›Lower doses may produce significant toxicity

›Urinary retention and ileus more prominent

›Reduced cardiac reserve

›Less tolerance for hypotension and arrhythmias

›Baseline conduction disease increases arrhythmia risk

›Polypharmacy interactions

›Multiple QRS-prolonging agents common in elderly

›Drug-drug interactions amplify toxicity

›Clinical presentation differences

›May present with fall or confusion as chief complaint

›High index of suspicion required

›Medication reconciliation critical

›Atypical anticholinergic presentation

›Delirium may be primary manifestation

›Delirium workup should include medication review

›Management modifications

›Aggressive hemodynamic support

›Lower MAP targets may be acceptable given baseline

›Assess baseline blood pressure from records

›Careful volume resuscitation

›Diastolic dysfunction common; pulmonary edema risk

›Smaller fluid boluses with reassessment

›Higher admission threshold

›Frailty and limited physiologic reserve

›Extended monitoring even with mild initial presentation

Pediatrics

›Pediatric sensitivity to TCA toxicity

›Higher sensitivity than adults at comparable doses

›Any amount must be considered potentially serious

›Life-threatening toxicity reported with small doses in young children

›Accidental ingestion most common mechanism

›Identify prescription holder in household

›Childproof storage counseling after recovery

›Weight-based dosing

›Sodium bicarbonate

›1 to 2 mmol/kg IV bolus same as adult on per-kg basis

›Repeat dosing guided by serial ECG and pH monitoring

›Lorazepam for seizures

›0.05 to 0.1 mg/kg IV

›Maximum 4 mg per dose

›Activated charcoal

›0.5 to 1 g/kg (younger child) to 1 g/kg (older child)

›Only if airway protected and child cooperative

›Pediatric intravenous lipid emulsion

›20% lipid emulsion 1.5 mL/kg bolus

›Evidence from case series and narrative reviews

›Lee et al Pediatric Emergency Care 2023 review

›Reserve for life-threatening toxicity refractory to standard care

›Same indications as adult

›Pediatric toxicology consultation strongly recommended

10Background/b79

Epidemiology

›Incidence and clinical burden

›TCA overdose remains a leading cause of prescription drug fatality

›High case fatality rate compared to newer antidepressants

›SSRIs and SNRIs have largely replaced TCAs for depression

›Most common remaining indications for TCA prescribing

›Chronic pain syndromes

›Neuropathic pain

›Migraine prophylaxis

›Enuresis in children

›Deliberate self-harm accounts for majority of ED presentations

›Often in context of psychiatric illness and social crisis

›Pediatric cases typically accidental

›Mortality patterns

›Most deaths occur prehospital or within first few hours

›Rapid cardiovascular collapse primary mechanism

›Desipramine associated with higher mortality than other TCAs

›Survivors who reach ICU care with appropriate treatment have good outcomes

›Hepatic metabolism clears drug over 24 to 48 hours

›Cardiac toxicity generally resolves within 24 to 48 hours

Pathophysiology

›Primary toxicity mechanisms

›Sodium channel blockade

›Fast sodium channel (INa) inhibition in His-Purkinje system and myocardium

›QRS prolongation, decreased contractility, ventricular arrhythmias

›Muscarinic (M1) receptor antagonism

›Anticholinergic toxidrome: tachycardia, mydriasis, dry skin, ileus, urinary retention

›Central anticholinergic syndrome: delirium, coma

›Alpha-1 adrenergic blockade

›Vasodilation and hypotension

›Postural hypotension and reflex tachycardia

›GABA-A receptor antagonism

›Seizure predisposition

›Lowers seizure threshold

›Histamine H1 receptor antagonism

›CNS sedation contribution

›Additive to muscarinic CNS effects

›Effect of acidosis on toxicity

›Decreased pH increases non-ionized free drug fraction

›More drug crosses blood-brain barrier

›More drug available to bind sodium channels

›Acidosis worsens cardiac sodium channel blockade

›Vicious cycle: arrhythmia leads to hypotension leads to acidosis leads to worse arrhythmia

›Breaking this cycle is the rationale for alkalinization

›ECG changes and mechanism

›QRS prolongation from His-Purkinje sodium channel blockade

›Rightward shift of terminal 40 ms QRS axis

›Produces large R wave in aVR and S waves in I and aVL

›QTc prolongation from potassium channel blockade

›Torsades de pointes risk though less common than VT from sodium channel effect

›Brugada pattern unmasked in susceptible individuals

Therapeutic Considerations

›Alkalinization rationale

›Dual mechanism of benefit

›High pH increases ionized fraction reducing free drug

›High sodium directly competes for sodium channel binding site

›Both pH and sodium contribution important

›Hypertonic saline alone has some efficacy in refractory cases

›Combination approach standard of care

›Chan and Buckley Clinical Toxicology 2024 on optimizing bicarbonate use

›Common pitfalls include inadequate bolus dosing

›Maintenance infusion after bolus response

›Decontamination considerations

›Activated charcoal efficacy window

›Greatest benefit within 1 hour of ingestion

›May be extended to 2 hours for large ingestions

›Anticholinergic effects delay gastric emptying

›May extend decontamination window

›Caution: altered mental status increases aspiration risk

›Gastric lavage rarely indicated

›Benefits generally do not outweigh risks

›Only if within 1 hour with protected airway

›Pharmacokinetics and clearance

›High volume of distribution: 10 to 50 L/kg

›Extensive protein binding and tissue distribution

›Extracorporeal removal not effective: EXTRIP workgroup conclusion

›Hepatic metabolism primary clearance pathway

›CYP2D6 and CYP3A4 mediated

›Polymorphism in CYP2D6 affects individual toxicity risk

›Clinical toxicity typically resolves within 24 to 48 hours

›With appropriate supportive care

›Monitor for late dysrhythmias in high initial severity

11Patient Discharge Instructions/pdi45

copy discharge instructions

›Tricyclic antidepressant poisoning: going home

›You were treated for a poisoning from a tricyclic antidepressant medication

›Your heart rhythm was monitored and is now normal

›Your doctors have confirmed it is medically safe to go home

›Medication safety at home

›Store all medications in a locked or secure location

›Return to your prescriber to discuss alternative medications if TCAs were prescribed for you

›Do not take any TCA medications without direct prescriber guidance

›Psychiatric care

›A referral to mental health support has been arranged if this was an intentional overdose

›Please attend all follow-up appointments

›If you are having thoughts of harming yourself, go to the nearest emergency room immediately or call a crisis line

›Return to the emergency room immediately if you have

›Heart pounding, racing, or skipping beats

›Any new irregular heart rhythm

›Chest pain or pressure

›Fainting or loss of consciousness

›Even brief blackouts

›Dizziness when standing

›Seizures or convulsions

›Call 911 immediately

›Do not drive yourself

›Confusion, agitation, or extreme drowsiness

›Not able to be woken normally

›Markedly confused or disoriented

›Difficulty passing urine

›Severe lower abdominal pain and inability to urinate

12References/r32

Guidelines and key sources

›American Heart Association guidelines

›AHA 2025 Circulation: Part 10 Adult and Pediatric Special Circumstances of Resuscitation

›Cao D, Arens AM, Chow SL, et al

›Specific guidance on TCA toxicity management and ECMO indications

›AHA 2023 Focused Update on Cardiac Arrest or Life-Threatening Toxicity Due to Poisoning

›Lavonas EJ, Akpunonu PD, Arens AM, et al. Circulation 2023

›Class IIa recommendations for sodium bicarbonate, norepinephrine, ILE, ECMO

›Toxicology-specific evidence

›EXTRIP Workgroup: Extracorporeal Treatment for TCA Poisoning

›Yates C, Galvao T, Sowinski KM et al. Seminars in Dialysis 2014

›Concluded extracorporeal removal not effective given high volume of distribution

›Chan BS, Buckley NA. Common Pitfalls in Hypertonic Sodium Bicarbonate for Cardiac Toxic Drug Poisonings

›Clinical Toxicology 2024

›Optimization of alkalinization strategy

›Pai K, Buckley NA, Isoardi KZ et al. Optimising Alkalinisation and QRS Narrowing in TCA Poisoning

›British Journal of Clinical Pharmacology 2022

›Mechanical hyperventilation synergy with bicarbonate

›Pediatric evidence

›Lee SH, Kim S, Sohn JT. Lipid Emulsion Treatment for Drug Toxicity in Pediatric Patients

›Pediatric Emergency Care 2023

›Narrative review supporting ILE use in pediatric TCA toxicity

›Regulatory and prescribing information

›FDA drug labels for tricyclic antidepressants

›Nortriptyline, amitriptyline, imipramine, doxepin, desipramine prescribing information

›Toxicity management and contraindicated medications guidance

›Coding reference

›ICD-10 T43.011 poisoning by amitriptyline, accidental

Evidence & Review