In cases of severe cardiogenic shock and/or cardiac arrest post-poisoning, extracorporeal cardiac assist devices have resulted in successful recovery.
Phosphodiesterase inhibitors and levosimendan have positive inotropic effects but also produce peripheral vasodilation, which can limit blood pressure improvement. High-dose glucagon infusions have provided moderate chronotropic and inotropic benefits in BB poisoning. Optimizing serum calcium concentration can confer some benefit to improving myocardial function and vascular tone after CCB poisoning. Catecholamine vasopressors and vasopressin are used in the treatment of vasodilatory shock. Catecholamine infusions are complementary to this therapy for both inotropic and chronotropic support. High-dose insulin euglycaemia is commonly recommended as a first-line treatment in these poisonings, to improve myocardial contractility, and should be instituted early when myocardial dysfunction is suspected. Treatment of shock requires a multimodal approach to inotropic therapy that can be guided by echocardiographic or invasive haemodynamic assessment of myocardial function. Provision of early gastrointestinal decontamination with activated charcoal and whole-bowel irrigation might mitigate this. Peak toxicity can be delayed by several hours. Additionally, CCBs, such as verapamil and diltiazem, are commonly ingested in sustained-release formulations. CCBs can also produce vasodilatory shock. Significant myocardial depression, bradycardia and hypotension result in both cases. Management of cardiovascular instability resulting from calcium channel antagonist (CCB) or beta-adrenergic receptor antagonist (BB) poisoning follows similar principles. Monash Medical Centre, Clayton, VIC, 3168, Australia Health, Dandenong Hospital, David Street, Dandenong, VIC, 3175, Australia and 3School of Clinical Sciences at Monash Health, Faculty of Medicine, Nursing and Health Sciences, Monash University, Hospital, David Street, Dandenong, VIC, 3175, Australia, 2Monash Emergency Program, Monash Keywords antidote, beta-receptor antagonist, calcium channel antagonist, overdose, poisoning. Monash Health Clinical Toxicology and Addiction Medicine Service, Monash Health, DandenongĬorrespondence Professor Andis Graudins, Department of Emergency Medicine, Dandenong Hospital, David Street, Dandenong, VIC, 3175, Australia. The high cost and limited availability of glucagon may be the only factors precluding its future clinical acceptance.Calcium channel antagonist and beta-blocker overdose: antidotes and adjunct therapies Andis Graudins,1,2,3 Hwee Min Lee1,2,3 & Dino Druda1,2 1 Glucagon-treated patients should be monitored for side effects of nausea, vomiting, hypokalemia, and hyperglycemia. The doses of glucagon required to reverse severe beta-blockade are 50 micrograms/kg iv loading dose, followed by a continuous infusion of 1-15 mg/h, titrated to patient response. Because it may bypass the beta-receptor site, glucagon can be considered as an alternative therapy for profound beta-blocker intoxications. This suggests that glucagon's mechanism of action may bypass the beta-adrenergic receptor site. These effects are unchanged by the presence of beta-receptor blocking drugs. Glucagon increases heart rate and myocardial contractility, and improves atrioventricular conduction. Atropine and isoproterenol have been inconsistent in reversing the bradycardia and hypotension of beta-blocker overdose.
Medical complications of beta-blocker overdose include hypotension, bradycardia, heart failure, impaired atrioventricular conduction, bronchospasm and, occasionally, seizures. The effects of glucagon in reversing the cardiovascular depression of profound beta-blockade, including its mechanism of action, onset and duration of action, dosage and administration, cost and availability, and side effects are reviewed. Two cases of severe beta-blocker overdose are presented that were treated successfully with glucagon therapy.
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