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Although the mechanism of this beneficial action is not fully explained, HIET should be considered in patients with CBB-induced cardiovascular compromise. There is growing experimental and clinical evidence of the value and the safety of HIET in the management of CCB poisoning. By targeting this insulin-mediated pathway, hyperinsulinemia/euglycemia therapy (HIET) appears to have a distinct role, and its clinical potential is underrecognized in the management of severe CCB toxicity. Blockade of the L-type calcium channels that mediate the antihypertensive effect of CCBs also decreases the release of insulin from pancreatic β-islet cells and reduces glucose uptake by tissues (insulin resistance). However, the conventional therapies are unsuccessful in reversing the cardiovascular toxicity of CCB, so they commonly fail to improve the hemodynamic condition of the patient. Most of these therapies are intended to increase transmembrane calcium flow (calcium salts) or increase cyclic adenosine monophosphate (cAMP) concentration by stimulating production of adenylate cyclase (with norepinephrine and glucagon) or by inhibiting production of phosphodiesterase (with amrinone and milrinone). Conventional treatments for CCB overdose include intravenous (IV) fluids, calcium salts, dopamine, dobutamine, norepinephrine, phosphodiesterase inhibitors, and glucagon. Keywords: Calcium channel blocker toxicity Hyperinsulinemia/euglycemia therapy Shock IntroductionĬalcium channel blocker (CCB) overdose, whether intentional or accidental, is a common clinical scenario and can be very lethal. We present a case of young man with amlodipine toxicity successfully managed with high dose of IV insulin therapy. Calcium channel blocker (CCB ) overdose, whether intentional or accidental, is a common clinical scenario and can be very lethal.