Electrophysiologic and Hemodynamic Effects of Sodium Bicarbonate in a Canine Model of Severe Cocaine Intoxication

Wilson, Lance D.; Shelat, Chandresh

doi:10.1081/clt-120025342

Cited by 17 publications

(16 citation statements)

References 37 publications

(52 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…However, at higher concentrations cocaine will begin to bind to sodium and potassium channels and thus cardiac effects will occur. Animal models of cocaine poisoning have consistently shown slowed intracardiac conduction with cocaine poisoning [72,74,82,93] and there are numerous human reports demonstrating cardiotoxicty due sodium channel antagonism following cocaine overdose [75,76]. Cocaine concentrations reported in most fatal cases will also saturate serum binding proteins and esterases, leading to a dramatic increase in free cocaine concentrations and a relative slowing of cocaine metabolism.…”

Section: Cocaine Toxicity: Tying Together Concentrations and Receptormentioning

confidence: 99%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

View full text Add to dashboard Cite

Abstract:Patients with acute cocaine poisoning present with life-threatening symptoms involving several organ systems. While the effects of cocaine are myriad, they are the result of a limited number of cocaine-protein interactions, including monoamine transporter, neurotransmitter receptor and voltage-gated ion channels. These primary interactions trigger a cascade of events that ultimately produce the clinical effects. The purpose of this article is to review the primary interactions of cocaine and the effects that these interactions trigger. We also describe the progression of symptoms observed in cocaine poisoning as they relate to serum cocaine concentrations.

show abstract

Section: Cocaine Toxicity: Tying Together Concentrations and Receptormentioning

confidence: 99%

Mechanisms of Acute Cocaine Toxicity

Heard¹,

Palmer²,

Zahniser³

2008

TOPHARMJ

View full text Add to dashboard Cite

show abstract

“…The study was insufficiently powered to detect differences in return of spontaneous circulation or eventual survival between groups, and future studies are planned with these outcomes as principal endpoints. The selection of hypertonic saline solution as study agent, as opposed to the frequently employed sodium bicarbonate [31] was based on earlier work conducted by the authors' investigative group [32], and with the intention of excluding substantive differences in induced pH as confounders. Given the absence of blood gas analysis in the present work, however, we are unable to comment on any effect of induced hyperchloraemic acidosis in the results of the group receiving hypertonic saline.…”

Section: Discussionmentioning

confidence: 99%

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

Cave

Harvey²,

Prince

et al. 2010

Anaesthesia

View full text Add to dashboard Cite

SummaryIntravenous lipid emulsion is established therapy for bupivacaine induced cardiotoxicity. The benefit of combined hypertonic saline and lipid treatment is unexplored. In this experiment, sedated rabbits were resuscitated from bupivacaine‐induced asystole with intravenous lipid according to the Association of Anaesthetists of Great Britain and Ireland’s guideline, or by identical lipid dosing with hypertonic saline: 6 mEq.kg−1 21% sodium chloride. Early electrocardiography QRS prolongation was less with lipid plus hypertonic saline (mean (SD) QRS 0.19 (0.07) s lipid only vs 0.09 (0.01) s lipid plus hypertonic saline; p = 0.003) at 9 min though not different from the lipid only group at 20 min. No difference was observed in rates of circulatory return (7/10 lipid only and 9/10 lipid plus hypertonic saline; p = 0.58) or survival (5/10 lipid only and 6/10 lipid plus hypertonic saline; p = 1.00). Some benefit to cardiac conduction may be afforded by hypertonic saline co‐administered with lipid emulsion in bupivacaine‐induced cardiotoxicity.

show abstract

“…The management of Naþ channel blocking agents consists of administration of sodium or creation of an alkalosis [26][27][28][29][30]. Infusion of sodium bicarbonate by intermittent bolus or by continuous infusion has been advocated.…”

Section: Managementmentioning

confidence: 99%

ECG Manifestations: The Poisoned Patient

Holstege

Eldridge

Rowden

2006

Emergency Medicine Clinics of North America

View full text Add to dashboard Cite

Emergency physicians routinely evaluate and manage poisoned patients. In 2003, more than 2 million human exposure cases were reported to poison centers throughout the United States [1]. Of those cases, 22% were treated in a health care facility with most of those cases evaluated in the emergency department. Cardiovascular drugs were listed as the fifteenth most frequently encountered human exposure (66,401) and the fifth leading cause of poisoning deaths.Drug-induced changes and abnormalities on the 12-lead electrocardiogram (ECG) are common. There are numerous drugs that can cause ECG changes and lead to cardiac dysrhythmias. The diagnoses and subsequent management of patients manifesting ECG changes following poisonings can challenge even the most experienced physician. Drugs that are advocated in Advanced Coronary Life Support protocols for cardiac dysrhythmias may not apply or may even worsen the condition of overdose patients [2].Despite that drugs have widely varying indications for therapeutic use, many unrelated drugs share a common cardiac pharmacologic effect if taken in overdose. The purpose of this article is to group together agents that cause similar electrocardiographic effects, review their pharmacologic actions, and discuss the electrocardiographic findings reported in the medical literature. The five main categories reviewed include potassium (Kþ) efflux blockers, sodium (Naþ) channel blockers, sodium-potassium adenosine-triphosphatase (Naþ/Kþ ATPase) blockers, calcium channel blockers (CCB), and beta-adrenergic blockers (BB). It is important to keep in mind, however, that many medications have actions that involve more than one of these

show abstract

Electrophysiologic and Hemodynamic Effects of Sodium Bicarbonate in a Canine Model of Severe Cocaine Intoxication

Abstract: NaHCO3 improved ECG changes secondary to cocaine toxicity and improved myocardial function.

Cited by 17 publications

References 37 publications

Mechanisms of Acute Cocaine Toxicity

Mechanisms of Acute Cocaine Toxicity

Effect of hypertonic saline on electrocardiography QRS duration in rabbit model of bupivacaine toxicity resuscitated by intravenous lipid

ECG Manifestations: The Poisoned Patient

Contact Info

Product

Resources

About