Toxin-Induced Cardiovascular Failure - 25/11/13

Doi : 10.1016/j.emc.2013.10.003

David H. Jang, MD, MSc ^a,^⁎ , Meghan B. Spyres, MD ^b, Lindsay Fox, MD ^c, Alex F. Manini, MD, MS ^d
^a Division of Medical Toxicology, Department of Emergency Medicine, School of Medicine, New York University, 462 First Avenue, 27th Street, Room A340, New York, NY 10016, USA
^b Emergency Medicine Residency, School of Medicine, New York University, 462 First Avenue, 27th Street, Room A340, New York, NY 10016, USA
^c Emergency Medicine Residency, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029-657, USA
^d Division of Medical Toxicology, Department of Emergency Medicine, Elmhurst Hospital Center, Icahn School of Medicine at Mount Sinai, One Gustave L. Levy Place, New York, NY 10029-657, USA

^∗Corresponding author.

Résumé

Adverse cardiovascular events comprise a large portion of the morbidity and mortality in drug overdose emergencies. Adverse cardiovascular events encountered by emergency physicians treating poisoned patients include myocardial injury, hemodynamic compromise with shock, tachydysrhythmias, and cardiac arrest. Early signs of toxin-induced cardiovascular failure include bradycardia, tachycardia, and specific ECG findings. Treatment of toxicologic tachycardia relies on rapid supportive care along with proper use of benzodiazepines for sedation. Treatment of toxicologic bradycardia consists of the use of isotonic fluids, atropine, calcium salts, and glucagon. High-dose insulin euglycemia should be used early in the course of suspected severe poisoning and intravenous lipid emulsion given to patients who suffer cardiac arrest.

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Keywords : β-blocker, Cardiac arrest, Cardiac injury, Calcium channel blocker, Digoxin, Dysrhythmia, Overdose