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Antidysrhythmic Toxicity Medication

  • Author: Nidhish Sasi, MD; Chief Editor: Asim Tarabar, MD  more...
 
Updated: Jun 27, 2016
 

Medication Summary

Discontinuation of the precipitating drug is of paramount importance. Gastrointestinal decontamination is empirically used to minimize systemic absorption of the drug. Hemodialysis may be indicated in certain drug toxicities as well as targeted antitidotal therapies.

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Antidotes, Other

Class Summary

GI decontamination with oral activated charcoal is selectively used in the emergency treatment of poisoning caused by some drugs and chemicals.

Activated charcoal (Actidose-Aqua, EZ-Char, Kerr Insta-Char)

 

Activated charcoal is used in emergency treatment for poisoning caused by drugs and chemicals. A network of pores adsorbs 100-1000 mg of drug per gram. 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.

Activated charcoal achieves its maximum effect when administered within 30 minutes after ingestion of a drug or toxin. However, decontamination with activated charcoal may be considered in any patient who presents within 4 hours after the ingestion.

Repeated doses may help to lower systemic levels of ingested compounds, especially sustained-release preparations. Activated charcoal does not dissolve in water. Supply it as an aqueous mixture or in combination with a cathartic (usually sorbitol 70%).

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Electrolyte Supplements, Parenteral

Class Summary

Potassium and magnesium should be repleted in patients taking QTc-prolonging drugs. High doses of magnesium may decrease the risk of QTc prolongation during ibutilide infusions.

Calcium chloride

 

Calcium is given to reverse hypotension and improve cardiac conduction defects. Calcium chloride theoretically increases calcium's concentration gradient, overcoming the channel blockade and driving calcium into the cells. It moderates nerve and muscle-performance by regulating action potential excitation threshold.

Magnesium sulfate

 

Magnesium acts as an antidysrhythmic agent and diminishes the frequency of premature ventricular contractions (PVCs), particularly those resulting from acute ischemia. Deficiency in this electrolyte can precipitate refractory ventricular fibrillation (VF) and is associated with sudden cardiac death. Magnesium supplementation is used for treatment of torsade de pointes, known or suspected hypomagnesemia, or severe refractory VF.

Sodium bicarbonate (Neut)

 

Intravenous sodium bicarbonate can be life saving in patients presenting with cardiotoxicity from antidysrhythmics with sodium-channel blocking properties and QRS widening. Sodium bicarbonate can be given as 1-2 mEq/kg (typically 100 mEq) as a bolus, followed by continuous infusion if the QRS narrows after bolus infusion. A 12-lead EKG should be run while administering the sodium bicarbonate bolus to ensure that QRS narrowing isn't missed because of a delayed EKG. Serum pH should be monitored if a sodium bicarbonate infusion is used. 

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Alpha/Beta-Adrenergic Agonists

Class Summary

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

Norepinephrine (Levophed)

 

Norepinephrine has strong beta1- and alpha-adrenergic effects and moderate beta2 effects, which increase cardiac output, blood pressure, and heart rate, while decreasing renal perfusion and pulmonary vascular resistance

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Beta1/Beta2 Adrenergic Agonists

Class Summary

These agents may be used to treat symptomatic arrhythmia.

Isoproterenol (Isuprel)

 

Isoproterenol is used to treat torsade de pointes if magnesium supplementation fails to treat it. It is also used to treat ventricular tachycardia or fibrillation in the setting of Brugada syndrome.

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Anticonvulsants, Other

Class Summary

By increasing the action of gamma aminobenzoic acid (GABA), a major inhibitory neurotransmitter, benzodiazepines may depress all levels of the central nervous system (CNS), including the limbic system and the reticular formation.

Diazepam (Valium, Diastat)

 

Diazepam depresses all levels of the CNS (eg, limbic system and reticular formation), possibly by increasing the activity of GABA. It is a third-line agent for agitation or seizures because of its shorter duration of anticonvulsive effects and the accumulation of active metabolites that may prolong sedation.

Lorazepam (Ativan)

 

Lorazepam is the drug of choice for treatment of status epilepticus because persists in the CNS longer than diazepam. The rate of injection should not exceed 2 mg/min. This agent may be administered intramuscularly if vascular access cannot be obtained.

Midazolam

 

Midazolam is an alternative agent for termination of refractory status epilepticus. Compared with diazepam, midazolam has twice the affinity for benzodiazepine receptors; however, because it is water soluble, midazolam takes approximately 3 times longer than diazepam to achieve peak electroencephalographic effects. Thus, the clinician must wait 2-3 minutes to fully evaluate sedative effects before initiating a procedure or repeating the dose. This agent may be administered intramuscularly if vascular access cannot be obtained.

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Contributor Information and Disclosures
Author

Nidhish Sasi, MD Resident Physician, Department of Emergency Medicine, Kings County Hospital Center, State University of New York Downstate Medical Center

Nidhish Sasi, MD is a member of the following medical societies: American Medical Association, American College of Emergency Physicians

Disclosure: Nothing to disclose.

Coauthor(s)

Sage W Wiener, MD Assistant Professor, Department of Emergency Medicine, State University of New York Downstate Medical Center; Director of Medical Toxicology, Department of Emergency Medicine, Kings County Hospital Center

Sage W Wiener, MD is a member of the following medical societies: American Academy of Clinical Toxicology, American Academy of Emergency Medicine, American College of Medical Toxicology, 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

Jennifer L Martindale, MD Clinical Assistant Professor, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center

Disclosure: Nothing to disclose.

Denise Ammon, MD, MA Resident Physician, Department of Emergency Medicine, Kings County Hospital, State University of New York Downstate Medical Center

Denise Ammon, MD, MA is a member of the following medical societies: American College of Emergency Physicians, American Medical Association, American Medical Student Association/Foundation, American Society of Anesthesiologists, Emergency Medicine Residents' Association

Disclosure: Nothing to disclose.

Acknowledgements

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.

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.

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.

Eileen C Quintana, MD Assistant Professor, Departments of Pediatrics and Emergency Medicine, St Christopher's Hospital for Children; Adjunct Clinical Professor, Departments of Pediatrics and Emergency Medicine, Temple University Hospital

Eileen C Quintana, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Richard H Sinert, DO Professor of Emergency Medicine, Clinical Assistant Professor of Medicine, Research Director, State University of New York College of Medicine; Consulting Staff, Department of Emergency Medicine, Kings County Hospital Center

Richard H Sinert, DO is a member of the following medical societies: American College of Physicians and Society for Academic Emergency Medicine

Disclosure: Nothing to disclose.

Carin M Van Gelder, MD Assistant Professor, Department of Emergency Medicine, Yale University School of Medicine; 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.

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.

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ECG in a patient who ingested 4 of flecainide. QRS = 200 milliseconds; QTc = 585 milliseconds. Used with permission from Lippincott, Williams & Wilkins (in Martindale JL, Brown DFM. Rapid Interpretation of ECGs in Emergency Medicine: A Visual Guide. Lippincott Williams and Wilkins; 2012).
Schematic of the cardiac action potential. Phase 0 depicts the the influx of sodium ions. Phases 1 and 3 correspond to the sodium-channel inactivation and the repolarizing eflux of potassium ions, respectively. Phase 2 depicts the opening of voltage-sensitive calcium channels causing a plateau in voltage.
 
 
 
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