statszuloo.blogg.se - Beta blocker antidote

Insulin bolus infusion can take 20-30 minutes to induce clinical inotropic/chronotropic effect.

Serum glucose every 30 minutes for 1-2 hours until stable.

If hypoglycemia does occur, bolus with dextrose and/or increase dextrose infusion first before considering a decrease or cessation of insulin infusion.

If the fluid overload is a concern, the insulin can be concentrated to 10 U/mL.

Dextrose: 0.5 g/kg/hr (titrate to maintain glucose 110 – 150 mg/dL.

Regular insulin: start 0.5 – 1 unit/kg/hr.

If serum glucose <250 mg/dL, concurrently administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV.

Intravenous bolus of regular insulin at a dose of 1 unit/kg.

Hyperinsulinemia Euglycemia Therapy (HIET) Initiation:.

Using Hyperinsulinemia Euglycemia Therapy(Lugassy 2015)

Even in a CCB poisoned animal model insulin increases myocardial glucose uptake resulting in improved contractility.

In vitro and in vivo evidence has shown insulin’s positive inotropic and chronotropic effects( Reikeras 1985, Kline 1995).

In a stressed state the heart turns to prefer carbohydrate and insulin appears to facilitate this preference.Under normal physiologic conditions the heart prefers to use free fatty acids as its primary energy source.CCB inhibits lactate oxidation resulting in lactic acidosis.As a result of lower insulin levels, glucose cannot move into the myocardial cells at a rate sufficient to respond to demand. CCB inhibits insulin secretion from the beta-islet cells of the pancreas.Blockade of calcium channels leads to effects outside the cardiovascular system as well.The liver responds to this increased demand by releasing glucose via gluconeogenesis, ultimately resulting in hyperglycemia. As the myocardium becomes stressed, it switches from catabolizing free fatty acids to catabolizing carbohydrates.This can lead to vasodilation, decreased systemic vascular resistance, bradycardia, conduction delay, decreased contractility, hypotension and cardiogenic shock. BBs and CCBs lead to decreased intracellular calcium within the myocardial cells.Calcium channel blocker overdose is less frequent than that of beta-blockers, but has been associated with the highest mortality rates among the cardiovascular drug overdoses( Woodward 2014).In 2012 alone, there were 24,465 beta-blocker exposures (Mowry 2013). The most common cause of poison-induced cardiogenic shock is beta-blocker toxicity.

Cardiogenic shock due to beta-blocker (BB) or calcium channel blocker (CCB) toxicity is frequent and potentially lethal.