**See The Poison Control Center’s Tip Sheets for high-dose insulin therapy and lipid emulsion therapy. * Combined cardiac pump failure and vasoplegia are most typical of calcium channel blocker toxicity and multiple therapeutic pathways may need to be considered concurrently again, the choice of therapies is best based upon the underlying physiology of shock. A suggested dosing regimen includes utilizing a loading dose (0.6 ml kg 1 of 10 calcium gluconate) and infusion (0.61.6 ml kg 1 h 1) titrated to haemodynamic parameters and a serum ionized calcium up to two times the upper limit of the reference.
#Beta blocker antidote calcium gluconate trial
Some advocate a trial of lipid emulsion** therapy when standard therapies seem to be failing. Calcium can be used as a temporizing measure while preparing other inotropic agents.If standard therapies prove insufficient, high-dose insulin** therapy might be added to increase cardiac output.
Standard pharmacological inotropes and vasopressors, such as norepinephrine, may be titrated in goal-directed fashion to achieve optimal cardiac output and tissue perfusion. Goal = to effect peripheral vasoconstriction to maintain cerebral and coronary perfusion. Treatment of distributive shock due to calcium channel blockade Extracorporeal life support (such as “ECMO”) may be used to support cardiovascular function when all other therapies have failed, until the calcium channel blocker has been eliminated.ī. Some advocate a trial of lipid emulsion** therapy (not FDA-approved for indication) when insulin and other therapies seem to be failing. For cases of CCB poisoning where cardiotoxicity is evident, a combination of calcium and epinephrine should be used initially, reserving HDIDK for refractory cases. Some have also suggested a role for glucagon, but its benefit beyond that of standard inotropes and vasopressors is unclear. For cases of beta-blocker poisoning where symptomatic bradycardia and hypotension are present, high-dose glucagon is considered the first-line antidote. Standard goal-directed pharmacological inotropes and vasopressors, such as epinephrine, may be used if insulin therapy is insufficient. Cardiac contractility assessed by ultrasonography. Success of therapy may be measured by assessment of perfusion. Not a vasoconstrictor, so improvements in blood pressure may be modest. Appears most effective if initiated early in course of poisoning illness. High-dose insulin** therapy can increase cardiac output without increasing myocardial oxygen demand. Goal = to improve cardiac output to maintain sufficient perfusion of vital organs. Treatment of cardiogenic shock due to calcium channel blockade*
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