Relative Toxicity of Beta Blockers in Overdose

Reith, David; Dawson, Andrew; Whyte, Ian M; Buckley, Nicholas A; Sayer, Geoffrey P.

doi:10.3109/15563659609013789

Cited by 90 publications

(59 citation statements)

References 17 publications

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“…In addition to its lipophicity, the sodium channel blocking effect of propranolol-when compared to other beta blockers-is thought to contribute to increased mortality [1][2][3]. The magnitude of sodium channel blockade can be measured experimentally as a blockade of fast inward sodium channels results in a QRS prolongation on the surface ECG (4).…”

Section: Introductionmentioning

confidence: 99%

The role of fat emulsion therapy in a rodent model of propranolol toxicity: A preliminary study

2006

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Introduction: In animal models, lipid emulsion therapy has been shown to ameliorate toxicity from a number of lipid soluble agents. This preliminary study addresses the hypothesis that pretreatment with lipid emulsion protects against propranolol toxicity in rodents.Methods: Ten spontaneously ventilating Rattus norvegicus rats were pretreated with either lipid emulsion or 0.9% normal saline before undergoing a constant infusion of propranolol until death. An electrocardiogram (ECG) sampling of heart rate and a QRS duration was performed at two-minute intervals until demise.Results: There was no significant difference in lethal doses of propranolol between groups. Comparison of percent change in QRS prolongation and heart rate reduction was performed at 60% of the mean lethal dose in control animals. The percent change in QRS duration was reduced (from −0.9 to 17.3, p = 0.016) in the intralipid pretreatment group. Attenuation of propranolol-induced bradycardia observed in the lipid emulsion group approached statistical significance (0% vs. 10.3%, p = 0.06).Interpretation: The results suggest that lipid emulsion may be effective in ameliorating propranolol toxicity in rats. Previous work gives reason to postulate a pharmacokinetic mechanism for this effect. The results represent encouraging exploratory work, and further work is planned to evaluate the role of lipid emulsion therapy in propranolol toxicity.

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Section: Introductionmentioning

confidence: 99%

The role of fat emulsion therapy in a rodent model of propranolol toxicity: A preliminary study

2006

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“…The common feature is excessive blockade of the β-receptors resulting in bradycardia and hypotension. 10 When β-receptors are blocked, the G protein responsible for converting adenosine triphosphate to cyclic adenosine monophosphate is disabled, which results in less cytosolic calcium being available for muscular contraction (Figure 1). Because β-selectivity is lost in overdose, even "β 1 -selective" agents can block β 2 -and β 3 -receptors and bring about bronchospasm and a reduction in inotropy, respectively.…”

Section: Comparison Of Pharmacologic Properties Of Various β-Blockersmentioning

confidence: 99%

“…7,8 In general, β-blockers with low lipid solubility that lack membrane-stabilizing effects are much safer than agents that have these effects. [9][10][11] Among CCBs, the newer agents are generally safer than diltiazem or verapamil.…”

Section: Comparison Of Pharmacologic Properties Of Various β-Blockersmentioning

confidence: 99%

Treatment of poisoning caused by β-adrenergic and calcium-channel blockers

Shepherd

2006

American Journal of Health-System Pharmacy

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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%

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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Relative Toxicity of Beta Blockers in Overdose

Abstract: Propranolol should be avoided in patients at risk of self-poisoning. Propranolol poisonings should be observed closely for the first six hours post ingestion. Syrup of ipecac should not be used to decontaminate the gastrointestinal tract after beta blocker overdose.

Cited by 90 publications

References 17 publications

The role of fat emulsion therapy in a rodent model of propranolol toxicity: A preliminary study

The role of fat emulsion therapy in a rodent model of propranolol toxicity: A preliminary study

Treatment of poisoning caused by β-adrenergic and calcium-channel blockers

ECG Manifestations: The Poisoned Patient

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