What is the emergency management of a patient with suspected tricyclic antidepressant (TCA) overdose?

Emergency Management of Tricyclic Antidepressant Overdose

Immediately administer sodium bicarbonate 1-2 mEq/kg IV bolus if QRS duration exceeds 100 milliseconds on ECG, and repeat as needed to maintain arterial pH 7.45-7.55. 1

Immediate Assessment and Monitoring

• Obtain an ECG or rhythm strip during initial assessment; QRS duration >100 msec indicates severe toxicity requiring immediate intervention 1
• Establish continuous cardiac monitoring for early detection of arrhythmias, as ventricular dysrhythmias, heart block, bradyarrhythmias, or asystole are common 2, 3
• Assess airway patency and consider intubation for respiratory depression, as TCA overdose causes CNS and respiratory depression 1
• Maintain adequate oxygenation and ventilation; avoid respiratory acidosis during mechanical ventilation as this potentiates cardiotoxicity 1
• Check for hyperthermia, flushing, and intestinal ileus as anticholinergic signs 4

Gastrointestinal Decontamination

• Administer activated charcoal 30-50 g orally or by nasogastric tube if the patient presents within a reasonable timeframe and has a protected airway 3
• Do not induce emesis 5
• Do not delay transportation or definitive treatment to administer activated charcoal 5

Sodium Bicarbonate Therapy (First-Line for Cardiotoxicity)

Indications for sodium bicarbonate:

• QRS duration >100 milliseconds 1, 3, 5
• Terminal right-axis deviation >120 degrees in lead aVR 6
• Ventricular dysrhythmias 6
• Persistent hypotension despite fluid resuscitation 1

Dosing protocol:

• Initial bolus: 1-2 mEq/kg IV (1-2 mL/kg of 8.4% solution) 1, 6
• Repeat boluses every 5-10 minutes as needed until clinical stability is achieved 1
• Target arterial pH: 7.45-7.55 1, 6
• Target serum sodium: <150-155 mEq/L to avoid hypernatremia 1, 6

Mechanism: Sodium bicarbonate works through sodium loading and alkalinization, which overcome sodium channel blockade, improve cardiac conduction, and reduce cardiotoxicity 6

Management of Hypotension

• Administer IV fluid boluses (10 mL/kg) of normal saline for initial management of hypotension 1
• Continue sodium bicarbonate therapy for persistent hypotension despite fluid resuscitation 1
• Use standard vasopressors if hypotension persists after fluids and bicarbonate 5

Second-Line Therapy: Lidocaine for Refractory Wide-Complex Tachycardia

• If QRS duration remains ≥120 ms despite optimized sodium bicarbonate therapy (pH 7.45-7.55, sodium <150-155 mEq/L), administer lidocaine 1-1.5 mg/kg IV bolus slowly 1
• Lidocaine is a Class Ib antiarrhythmic that may narrow QRS complex and improve hemodynamics in refractory cases 1

Third-Line Therapy: Intravenous Lipid Emulsion (ILE)

• Consider 20% intravenous lipid emulsion for life-threatening toxicity refractory to sodium bicarbonate and lidocaine 1
• Standard ILE regimen: 1.5 mL/kg bolus of 20% lipid emulsion over 1 minute, followed by continuous infusion at 0.25 mL/kg/min 1
• The "lipid sink" effect sequesters lipophilic TCAs, reducing their free plasma concentration 1

Fourth-Line Therapy: VA-ECMO

• Consider venoarterial extracorporeal membrane oxygenation (VA-ECMO) for cardiac arrest or refractory cardiogenic shock unresponsive to high-dose vasopressors, sodium bicarbonate, lidocaine, and ILE 2, 1
• Early consultation with an ECMO team improves outcomes, especially when initiation occurs before prolonged cardiac arrest 1
• VA-ECMO provides mechanical circulatory support while allowing time for drug metabolism and elimination 1

Management of Seizures

• Administer benzodiazepines for TCA-associated seizures 5
• Seizures worsen acidosis and hyperthermia, which potentiate cardiotoxicity 1

Critical Contraindications and Pitfalls

Never use the following agents:

• Physostigmine for anticholinergic symptoms - absolutely contraindicated as it worsens cardiac toxicity and can cause asystole 1, 7
• Flumazenil - absolutely contraindicated even if benzodiazepine co-ingestion is suspected, as it may precipitate seizures or arrhythmias 2, 1, 5
• Class Ia antiarrhythmics (quinidine, procainamide) - exacerbate sodium channel blockade 1
• Class Ic antiarrhythmics (flecainide) - worsen conduction defects 1
• Class III antiarrhythmics (amiodarone) - further slow conduction and depress contractility 1
• Beta-blockers - may precipitate hypotension and cardiac arrest 1

Avoid respiratory acidosis:

• During mechanical ventilation, maintain mild hyperventilation to support alkalemia (pH 7.45-7.55) 1
• Respiratory acidosis potentiates cardiotoxicity by increasing the active, ionized form of the TCA 1

Monitoring Parameters

• Continuous ECG monitoring for QRS duration and dysrhythmias 6
• Serial arterial blood gases to maintain pH 7.45-7.55 1, 6
• Serum sodium levels to avoid hypernatremia (target <150-155 mEq/L) 1, 6
• Serum potassium levels, as hypokalemia may develop during sodium bicarbonate therapy 1
• Maintain normothermia, as hyperthermia worsens toxicity 2, 1

Observation Period

• Asymptomatic patients are unlikely to develop symptoms if the interval between ingestion and initial assessment is greater than 6 hours 5
• Symptomatic patients require continued cardiac monitoring after clinical recovery due to delayed absorption and prolonged half-life 4