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Tricyclic Antidepressant Toxicity Medication

  • Author: Vivian Tsai, MD, MPH, FACEP; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jul 13, 2016
 

Medication Summary

Treatment of cyclic antidepressant (CA) toxicity focuses on airway management, dysrhythmias, seizures, and hypotension. Sodium bicarbonate, benzodiazepines, and norepinephrine are the drugs of choice for these complications.

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GI decontaminant

Class Summary

This agent prevents further absorption of drug and other co-ingestants from the GI tract.

Activated charcoal (Liqui-Char)

 

Emergency treatment in poisoning caused by drugs and chemicals. Network of pores present in activated charcoal adsorbs 100-1000 mg of drug per gram of charcoal. May be administered with or without cathartic (eg, Sorbitol 70%), except in young pediatric patients, where electrolyte imbalance may be of concern. Does not dissolve in water.

For maximum effect, administer within 30 min of ingesting poison.

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Cardiovascular agents

Class Summary

Sodium bicarbonate is indicated for QRS intervals greater than 100 milliseconds, seizures, acidosis (pH level < 7), hypotension, cardiac arrest, or dysrhythmia. Antidysrhythmic agents may be helpful. However, avoid certain drugs that exacerbate the cardiac effects of CAs, such as quinidine and procainamide (class IA), flecainide (class IC), and bretylium and amiodarone (class III). Vasopressors are used for the treatment of hypotension not corrected by intravenous fluids.

Sodium bicarbonate (Neut)

 

First-line therapy for QRS interval >100 milliseconds or if dysrhythmias are present. Correction of acidosis promotes protein binding of CA and improves myocardial contractility. Doses or IV drip may be administered with a pH goal of 7.5-7.55. Monitor and replace potassium as needed to prevent hypokalemia.

Lidocaine (Xylocaine)

 

Class IB antiarrhythmic that increases electrical stimulation threshold of ventricle, suppressing automaticity of conduction through tissue. Second DOC for CA dysrhythmias.

Norepinephrine (Levophed)

 

Stimulates beta1- and alpha-adrenergic receptors, which, in turn, increases cardiac muscle contractility, heart rate, and vasoconstriction. As a result, systemic blood pressure and coronary blood-flow increases. DOC to treat hypotension refractory to fluid resuscitation in CA toxicity. Dopamine is second-line and less effective.

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Anticonvulsants

Class Summary

Benzodiazepines are preferred for treatment of seizures. Do not use barbiturates in patients with hypotension. Do not use phenytoin in patients with dysrhythmias.

Lorazepam (Ativan)

 

Sedative hypnotic with short onset of effects and relatively long half-life (longer than diazepam).

By increasing the action of GABA, which is a major inhibitory neurotransmitter in the brain, may depress all levels of CNS, including limbic and reticular formation.

Monitoring patient's blood pressure after administering dose is important. Adjust prn.

Diazepam (Valium)

 

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Shorter acting than lorazepam.

Midazolam (Versed)

 

Used as alternative in termination of refractory status epilepticus. Because water soluble, takes approximately 3 times longer than diazepam to peak EEG effects. Thus, clinician must wait 2-3 min to fully evaluate sedative effects before initiating procedure or repeating dose.

Phenobarbital (Barbita, Luminal)

 

Used for seizures not responding to benzodiazepines. Significant respiratory depression; patient may require endotracheal intubation.

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Miscellaneous

Class Summary

Magnesium sulfate has been successfully used in an overdose with refractory ventricular fibrillation.[18] Animal studies have shown that magnesium sulphate converted ventricular tachycardia to sinus rhythm in 9 of 10 rats.[19]

Magnesium sulfate

 

Given parenterally, magnesium decreases acetylcholine in motor nerve terminals and acts on myocardium by slowing rate of S-A node impulse formation and prolonging conduction time. May be helpful in treating ventricular fibrillation in TCA toxicity, but further study is needed.

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Contributor Information and Disclosures
Author

Vivian Tsai, MD, MPH, FACEP Assistant Professor of Emergency Medicine, Mount Sinai School of Medicine, Queens Hospital Center

Vivian Tsai, MD, MPH, FACEP is a member of the following medical societies: Alpha Omega Alpha, American College of Emergency Physicians, Phi Beta Kappa

Disclosure: Nothing to disclose.

Coauthor(s)

Mark A Silverberg, MD, MMB, FACEP Assistant Professor, Associate Residency Director, Department of Emergency Medicine, State University of New York Downstate College of Medicine; Consulting Staff, Department of Emergency Medicine, Staten Island University Hospital, Kings County Hospital, University Hospital, State University of New York Downstate Medical Center

Mark A Silverberg, MD, MMB, FACEP is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, Council of Emergency Medicine Residency Directors, Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

John T VanDeVoort, PharmD Regional Director of Pharmacy, Sacred Heart and St Joseph's Hospitals

John T VanDeVoort, PharmD is a member of the following medical societies: American Society of Health-System Pharmacists

Disclosure: Nothing to disclose.

John G Benitez, MD, MPH Associate Professor, Department of Medicine, Medical Toxicology, Vanderbilt University Medical Center; Managing Director, Tennessee Poison Center

John G Benitez, MD, MPH is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, American College of Preventive Medicine, Undersea and Hyperbaric Medical Society, Wilderness Medical Society, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Chief Editor

Asim Tarabar, MD Assistant Professor, Director, Medical Toxicology, Department of Emergency Medicine, Yale University School of Medicine; Consulting Staff, Department of Emergency Medicine, Yale-New Haven Hospital

Disclosure: Nothing to disclose.

Additional Contributors

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT Associate Clinical Professor, Department of Surgery/Emergency Medicine and Toxicology, University of Texas School of Medicine at San Antonio; Medical and Managing Director, South Texas Poison Center

Miguel C Fernandez, MD, FAAEM, FACEP, FACMT, FACCT is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, American College of Medical Toxicology, Society for Academic Emergency Medicine, Texas Medical Association, American College of Occupational and Environmental Medicine

Disclosure: Nothing to disclose.

Acknowledgements

Mark Biittner, MD Consulting Staff, Department of Emergency Medicine, Sutter Roseville Medical Center

Mark Biittner, MD is a member of the following medical societies: American College of Emergency Physicians

Disclosure: Nothing to disclose.

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