Antidysrhythmic Toxicity Medication

  • Author: Joshua B Gaither, MD; Chief Editor: Asim Tarabar, MD   more...
 
Updated: Nov 21, 2011
 

Medication Summary

Discontinuation of the precipitating drug is of paramount importance.

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GI decontaminants

Class Summary

Empirically used to minimize systemic absorption of the toxin.

Activated charcoal (Liqui-Char)

 

Prevents absorption by adsorbing drug in intestine. Multidose charcoal may interrupt enterohepatic recirculation and enhance elimination by enterocapillary exsorption. Theoretically, by constantly bathing the GI tract with charcoal, the intestinal lumen serves as a dialysis membrane for reverse absorption of drug from intestinal villous capillary blood into intestine. Supply as an aqueous mixture or in combination with a cathartic (usually sorbitol 70%).

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Cardiovascular agents

Class Summary

Alter the electrophysiologic mechanisms responsible for arrhythmia.

Calcium chloride

 

Moderates nerve and muscle-performance by regulating action potential excitation threshold.

Magnesium sulfate

 

Acts as antiarrhythmic agent and diminishes frequency of PVCs, particularly when secondary to acute ischemia.

Deficiency in this electrolyte is associated with sudden cardiac death and can precipitate refractory VF. Magnesium supplementation is used for treatment of torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Norepinephrine (Levophed)

 

DOC. Vasopressors are indicated for persistent hypotension not responsive to judicious fluid loading and sodium bicarbonate.

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Benzodiazepines

Class Summary

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

Diazepam (Valium)

 

Depresses all levels of CNS (eg, limbic and reticular formation), possibly by increasing activity of GABA. Third-line agent for agitation or seizures because of shorter duration of anticonvulsive effects and accumulation of active metabolites that may prolong sedation.

Lorazepam (Ativan)

 

DOC for treatment of status epilepticus because persists in the CNS longer than diazepam. Rate of injection should not exceed 2 mg/min. May administer IM if unable to obtain vascular access.

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. Has twice the affinity for benzodiazepine receptors than diazepam. May be administered IM if unable to obtain vascular access.

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Contributor Information and Disclosures
Author

Joshua B Gaither, MD  Fellow in Emergency Medicine Services, Prehospital and Disaster Care, Denver Health-University of Colorado

Joshua B Gaither, MD is a member of the following medical societies: American College of Emergency Physicians, Society for Academic Emergency Medicine, and Wilderness Medical Society

Disclosure: Nothing to disclose.

Coauthor(s)

Carin M Van Gelder, MD  Assistant Professor, Department of Emergency Medicine, Yale University; EMS Medical Director, NHSHP and EMS Physician, SHARP Team; Attending Physician, Emergency Medicine, Yale-New Haven Medical Center

Carin M Van Gelder, MD is a member of the following medical societies: American Academy of Emergency Medicine, American College of Emergency Physicians, Massachusetts Medical Society, National Association of EMS Physicians, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

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 Clinical Toxicologists, American College of Emergency Physicians, American College of Medical Toxicology, American College of Occupational and Environmental Medicine, Society for Academic Emergency Medicine, and Texas Medical Association

Disclosure: Nothing to disclose.

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.

Michael J Burns, MD  Instructor, Department of Emergency Medicine, Harvard University Medical School, Beth Israel Deaconess Medical Center

Michael J Burns, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American College of Emergency Physicians, American College of Medical Toxicology, and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

John D Halamka, MD, MS  Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center

John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency 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

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Eileen C Quintana, MD, and Richard Sinert, DO, to the development and writing of this article.

References
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