| Autor: |
Bruccoleri RE; Harvard Medical Toxicology Fellowship, Division of Emergency Medicine, Program in Medical Toxicology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA. Rebecca.Bruccoleri@childrens.harvard.edu., Burns MM; Harvard Medical Toxicology Fellowship, Division of Emergency Medicine, Program in Medical Toxicology, Boston Children's Hospital, 300 Longwood Avenue, Boston, MA, 02115, USA. |
| Jazyk: |
angličtina |
| Zdroj: |
Journal of medical toxicology : official journal of the American College of Medical Toxicology [J Med Toxicol] 2016 Mar; Vol. 12 (1), pp. 121-9. |
| DOI: |
10.1007/s13181-015-0483-y |
| Abstrakt: |
Sodium bicarbonate is a well-known antidote for tricyclic antidepressant (TCA) poisoning. It has been used for over half a century to treat toxin-induced sodium channel blockade as evidenced by QRS widening on the electrocardiogram (ECG). The purpose of this review is to describe the literature regarding electrophysiological mechanisms and clinical use of this antidote after poisoning by tricyclic antidepressants and other agents. This article will also address the literature supporting an increased serum sodium concentration, alkalemia, or the combination of both as the responsible mechanism(s) for sodium bicarbonate's antidotal properties. While sodium bicarbonate has been used as a treatment for cardiac sodium channel blockade for multiple other agents including citalopram, cocaine, flecainide, diphenhydramine, propoxyphene, and lamotrigine, it has uncertain efficacy with bupropion, propranolol, and taxine-containing plants. |
| Databáze: |
MEDLINE |
| Externí odkaz: |
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