Document Detail


Electrophysiologic and hemodynamic effects of sodium bicarbonate in a canine model of severe cocaine intoxication.
MedLine Citation:
PMID:  14677787     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Cocaine toxicity causes myocardial depression, malignant dysrhythmias, and sudden death, partially due to cocaine-related myocardial sodium channel blockade. Because of cocaine's ability to block cardiac sodium channels, sodium bicarbonate (NaHCO3) has been proposed as an antidote. The hypothesis of this study was that NaHCO3 would correct cocaine-induced conduction abnormalities and resultant hemodynamic compromise in an animal model simulating severe cocaine intoxication.
METHODS:
DESIGN: Prospective, controlled, experimental study in which 15 anesthetized dogs were given three successive boluses of cocaine (7 mg/kg) and then randomized to receive NaHCO3, 2 mEq/kg (n = 8) or placebo (n =7).
MEASUREMENTS: Arterial, left ventricular, and pulmonary artery pressures; cardiac output (CO); electrocardiogram (ECG); blood gases; and serum concentrations of cocaine were measured at baseline, at fixed time intervals after each bolus of cocaine, and then after administration of NaHCO3 or placebo. Statistical significance was determined by analysis of variance (ANOVA) for repeated measures.
RESULTS: Seven dogs experienced significant arrhythmias, including VT, pulseless electrical activity, and third-degree atrioventricular block; 2 of these dogs expired prior to receiving NaHCO3 and were excluded. Immediately after administering NaHCO3, QRS duration decreased by 30% (p < 0.001), returning to baseline more quickly than in the control group. This effect was associated with a brief 30% decrease in MAP (p = NS). After NaHCO3, CO increased 78% and remained increased for 5 min (p < 0.007). One dog converted from complete heart block to sinus rhythm shortly after NaHCO3 administration.
CONCLUSIONS: NaHCO3 improved ECG changes secondary to cocaine toxicity and improved myocardial function.
Authors:
Lance D Wilson; Chandresh Shelat
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of toxicology. Clinical toxicology     Volume:  41     ISSN:  0731-3810     ISO Abbreviation:  J. Toxicol. Clin. Toxicol.     Publication Date:  2003  
Date Detail:
Created Date:  2003-12-17     Completed Date:  2004-01-05     Revised Date:  2014-07-28    
Medline Journal Info:
Nlm Unique ID:  8213460     Medline TA:  J Toxicol Clin Toxicol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  777-88     Citation Subset:  AIM; IM    
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MeSH Terms
Descriptor/Qualifier:
Animals
Antidotes*
Arrhythmias, Cardiac / chemically induced,  drug therapy,  physiopathology
Blood Gas Analysis
Blood Pressure / drug effects
Cardiac Output / drug effects
Cocaine / antagonists & inhibitors*,  toxicity*
Dogs
Electrocardiography / drug effects
Electrophysiology
Heart Rate / drug effects
Hemodynamics / drug effects*
Sodium Bicarbonate / pharmacology*
Sodium Channel Blockers / toxicity*
Ventricular Function, Left / drug effects
Chemical
Reg. No./Substance:
0/Antidotes; 0/Sodium Channel Blockers; 8MDF5V39QO/Sodium Bicarbonate; I5Y540LHVR/Cocaine

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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