Metoprolol overdose

Abstract

We report the first two documented cases of the deliberate metoprolol overdose occurring in the United States, one of which eventually proved fatal. The potentially lethal cardiotoxic effects of this drug are illustrated and correlated with the blood and tissue levels of metoprolol. We emphasize the often sudden and rapid clinical deterioration which excessive ingestion of this drug may produce, and the need for close, careful supervision and monitoring of these patients.

Successful Treatment of Metoprolol-Induced Cardiac Arrest With High-Dose Insulin, Lipid Emulsion, and ECMO

“…Metoprolol, in particular, causes rapid deterioration, as supported by our case, consistent with previous reports demonstrating symptom development of immediaterelease formulations occurring within 2 hours post-ingestion time [4][5][6]. Although the patient's comprehensive toxicologic screening examination detected either atenolol or metoprolol, after discussion with toxicology laboratory staff, this was due to the similar molecular structure of the drugs, as quantitative send out measures of metoprolol were significantly elevated.…”

“…Overdose signs and symptoms include bradycardia; hypotension; bronchospasm; myocardial infarction; cardiac failure; and, eventually, death [2]. Metoprolol distributes rapidly between blood and extravascular sites, causing sudden and rapid deterioration [4,5]. A retrospective review of patients suffering from β-adrenergic antagonist toxicity found that all 39 patients developed symptoms within 6 hours, the majority developing symptoms 2 hours after ingestion [6].…”

The Management of Acute Poisoning Due to β-Adrenoceptor Antagonists

“…Following metoprolol overdosage (Moller 1976;Sire 1976), normal sinus rhythm is usually maintained despite hypotension, as in a case reported by Shore et al (1981) with a plasma concentration of 63 mg/L, Profound bradycardia has been reported in the near terminal stages of metoprolol poisoning (Shore et al 1981;Wallin & Hulting 1983), but then it was probably due to secondary factors such as hypoxia and acidosis. However, metoprolol does have a small degree of membrane depressant activity which may contribute to toxicity.…”

“…2.5 to 10~g/kg/min) is very limited and the few reports give conflicting accounts of its efficacy (Shore et al 1981 tried, but usually with little success (Weinstein 1984). Experience with dobutamine (e.g.…”

A Comparison of Vasopressin and Glucagon in Beta-Blocker Induced Toxicity

“…Glucagon is considered a first line vasopressor in this setting due to its ability to increase intracellular cyclic AMP via a non-catecholamine receptor on the cell wall (2,3). The ability of glucagon to reverse β-blocker toxicity is variable, however, and has failed as a single agent in several case reports (4)(5)(6).…”