The Effect of Sodium Bicarbonate on Propranolol-Induced Cardiovascular Toxicity in a Canine Model

Love, Jeffrey J.; Howell, John M.; Newsome, Joseph T.; Skibbie, D F; Dickerson, Linda W.; Henderson, Kristina

doi:10.1081/clt-100100952

Cited by 13 publications

(10 citation statements)

References 14 publications

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“…21 A study in a canine model found IV sodium bicarbonate ineffective in the reversal of QRS widening associated with propranolol toxicity. 22 It is clear from our experiment that we failed to demonstrate any narrowing of Taxus-induced QRS widening from sodium bicarbonate therapy. In fact, QRS duration was even wider in animals receiving sodium bicarbonate or receiving mannitol, a volume-expansion control.…”

Section: Discussionmentioning

confidence: 63%

Hypertonic Sodium Bicarbonate for Taxus media-induced Cardiac Toxicity in Swine

et al. 2002

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Abstract. Objective: To determine whether intravenous (IV) hypertonic sodium bicarbonate is effective in the reversal of QRS widening associated with severe Taxus intoxication. Methods: Seventeen anesthetized and instrumented swine were poisoned with an IV extract of Taxus media until doubling of the QRS interval on electrocardiography was achieved. After poisoning (time zero), the animals received either 4 mL/kg IV 8.4% sodium bicarbonate (experimental group; 6 animals), a similar volume of 0.7% NaCl in 10% mannitol (mannitol group; 6 animals), or nothing (control group; 5 animals). The main outcome parameter was QRS duration. Secondary outcome parameters were mean arterial pressure (MAP), heart rate (HR), and cardiac index (CI = cardiac output/kg). Additionally, arterial pH, partial pressure of carbon dioxide (pCO 2 ), and plasma-ionized calcium, sodium, and potassium were monitored. Results: Taxus toxicity, defined as a 100% increase in QRS duration, was produced in all animals. The an-

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Section: Discussionmentioning

confidence: 63%

Hypertonic Sodium Bicarbonate for Taxus media-induced Cardiac Toxicity in Swine

et al. 2002

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“…While the QRS did decrease, it was not statistically significant. In addition, the control dogs who received dextrose also had a narrowing QRS with time [77]. The clinical significance of this study in humans has not been determined.…”

Section: Antiarrhythmicsmentioning

confidence: 96%

“…Case report [71] In vitro data (references) Bupropion Case reports [72][73][74] Guinea pig hearts, rat neonatal myocytes, rat atria, canine ventricular tissue, crayfish axons [75,76] Human embryonic kidney cells [75] Propranolol Canine study [77] …”

Section: Propoxyphenementioning

confidence: 99%

A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening

Bruccoleri

Burns

2015

J. Med. Toxicol.

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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.

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“…Propranolol is unique because of its Naþ channel blocking activity in overdose that can result in a prolonged QRS interval (O0.10 seconds) [58,[61][62][63]. Propranolol overdose has been associated with a higher mortality rate compared with other BBs [66].…”

Section: Electrocardiographic Manifestationsmentioning

confidence: 99%

“…Some of these agents have equal affinity for b 1 and b 2 receptors (eg, propranolol), whereas others are selective and have greater b 1 than b 2 receptor blocking activity (eg, metoprolol). Some agents also block other receptors, such as a-adrenergic receptors (eg, labetalol), cardiac sodium channels (eg, propranolol, acebutolol), and cardiac potassium efflux channels (eg, sotalol) [58,59].…”

Section: Introductionmentioning

confidence: 99%

ECG Manifestations: The Poisoned Patient

Holstege

Eldridge

Rowden

2006

Emergency Medicine Clinics of North America

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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

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The Effect of Sodium Bicarbonate on Propranolol-Induced Cardiovascular Toxicity in a Canine Model

Abstract: In this canine model of propranolol toxicity, intravenous sodium bicarbonate appears to be an ineffective single therapy. Furthermore, these results may suggest a different mechanism of sodium channel blockade for propanolol than that of type IA antiarrhythmic agents.

Cited by 13 publications

References 14 publications

Hypertonic Sodium Bicarbonate for Taxus media-induced Cardiac Toxicity in Swine

Hypertonic Sodium Bicarbonate for Taxus media-induced Cardiac Toxicity in Swine

A Literature Review of the Use of Sodium Bicarbonate for the Treatment of QRS Widening

ECG Manifestations: The Poisoned Patient

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