CCBs also inhibit L‐type calcium channels in pancreatic Islet cells, reducing insulin secretion 4 and resulting in hyperglycaemia and reduced cardiac glucose utilization 4. Calcium influx initiates excitation–contraction coupling, sino‐atrial node depolarization in the myocardium and the maintenance of vascular and gastrointestinal (GI) smooth muscle tone. Some agents, such as propranolol and labetalol, also antagonize voltage‐gated sodium channels in overdose and might be associated with a higher risk of mortality than other BBs 3.ĬCBs directly inhibit voltage‐gated L‐type calcium channel opening and calcium influx into myocardial and vascular smooth muscle cells. The resultant effect is a direct depressant action on the myocardium, resulting in conduction delays, bradycardia and reduced contractility with little or no effect on peripheral vasculature. Thus, BBs reduce the facilitation of calcium entry into cardiomyocytes produced by increased cAMP, resulting in negative chronotropic and inotropic effects. Poisoning with these agents has the potential for significant systemic toxicity and high rates of mortality 2.īBs competitively antagonize myocardial beta‐1 adrenoceptors, which normally activate adenyl cyclase to increase cyclic AMP (cAMP) production and phosphorylation and opening of L‐type calcium channels. Other treatments used in refractory hypotension include intravenous lipid emulsion for lipophilic CCB and BB poisoning and methylene blue for refractory vasodilatory shock.Ĭardiovascular system (CVS) poisoning with calcium channel antagonists (CCBs) or beta‐receptor antagonists (BBs) comprises a small percentage of all poisoning presentations 1. 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.
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