High Dose Insulin Euglycemia Therapy (HIET) Calculator

High Dose Insulin Euglycemia Therapy (HIET) Calculator for Endocrinology. The numbers define a fixed starting point, not a fixed dose. The bolus and 0.5 to 1 U/kg/hr start are the floor; clinical response drives escalation. Because inotropic benefit lags 15 to 60 minutes behind dose changes, do not judge failure prematurely, and continue conventional pressors during onset. Rising infusion rates toward 10 U/kg/hr signal severe toxicity and should prompt escalation of monitoring and early consideration of mechanical support (ECMO). Glucose must be checked every 20 to 30 minutes initially, and dextrose plus potassium supplementation continued for up to 12 to 24 hours after the insulin is stopped, because hypoglycemia can be delayed.

How this calculator works

This tool converts patient weight into the concrete regular-insulin volumes needed for high-dose insulin euglycemia therapy (also called hyperinsulinemic-euglycemic therapy, HIET) in calcium-channel-blocker or beta-blocker cardiotoxicity. It applies the standard weight-based scheme: a loading bolus of 1 U/kg regular insulin, an initial maintenance infusion typically started at 0.5 to 1 U/kg/hr and titrated upward in 1 to 2 U/kg/hr steps toward a maximum of about 10 U/kg/hr, plus a concurrent dextrose bolus (commonly 0.5 g/kg, unless the presenting glucose is already high) and a dextrose infusion of roughly 0.5 g/kg/hr to hold euglycemia. Outputs are the actual bolus units and the infusion rate in units per hour at each titration level.

When to use this calculator

Use for hemodynamically significant CCB or BB overdose: hypotension, bradycardia, or cardiogenic shock with reduced cardiac output that is refractory to fluids, atropine, calcium, and glucagon. HIET targets the toxin-induced myocardial insulin resistance and metabolic shift, so it is most valuable in verapamil, diltiazem, and lipophilic beta-blocker (propranolol, metoprolol) poisoning. It is not a first-line agent for pure vasodilatory shock from dihydropyridines without myocardial depression, and it is not indicated for stable overdoses, non-cardiotoxic ingestions, or as a substitute for airway, pacing, or ECMO decisions.

Inputs used

  • Weight
  • Insulin bolus or infusion rate
  • Dextrose concentration
  • Glucose monitoring
  • Potassium monitoring

Clinical interpretation

The numbers define a fixed starting point, not a fixed dose. The bolus and 0.5 to 1 U/kg/hr start are the floor; clinical response drives escalation. Because inotropic benefit lags 15 to 60 minutes behind dose changes, do not judge failure prematurely, and continue conventional pressors during onset. Rising infusion rates toward 10 U/kg/hr signal severe toxicity and should prompt escalation of monitoring and early consideration of mechanical support (ECMO). Glucose must be checked every 20 to 30 minutes initially, and dextrose plus potassium supplementation continued for up to 12 to 24 hours after the insulin is stopped, because hypoglycemia can be delayed.

Worked example

For an 80 kg patient: bolus = 1 U/kg x 80 = 80 units regular insulin IV, given with a dextrose bolus of 0.5 g/kg x 80 = 40 g (about 80 mL of D50). The infusion starts at 1 U/kg/hr = 80 U/hr and, if shock persists, is titrated in steps toward the 10 U/kg/hr ceiling, which for this patient is 800 U/hr. A dextrose infusion at 0.5 g/kg/hr = 40 g/hr runs alongside, adjusted to point-of-care glucose. At an infusion of 800 U/hr the pharmacy must prepare a concentrated insulin drip to keep fluid volume manageable.

Limitations and safety notes

The evidence base is animal studies, case reports, and case series, with no randomized human trials, so the 1 to 10 U/kg/hr range is expert-derived rather than validated. The two dose-limiting harms are hypoglycemia and hypokalemia (from intracellular potassium shift, not depletion), and both can appear after the drip ends. High infusion rates create large dextrose fluid loads and demand concentrated insulin drips and reliable central access. The tool assumes actual body weight and standard concentrations; it does not account for pediatric dosing nuances, coexisting sodium-channel or digoxin toxicity, or renal-failure glucose handling.

Frequently asked questions

Why insulin instead of just epinephrine or high-dose vasopressors?

In CCB and BB toxicity the stressed myocardium switches from fatty-acid to carbohydrate metabolism but cannot take up glucose because of drug-induced insulin resistance. HIET restores glucose uptake and provides positive inotropy without the added afterload and myocardial oxygen demand that catecholamines impose, which is why animal survival studies favored insulin over calcium, glucagon, epinephrine, and vasopressin.

Do I have to wait for hypoglycemia before giving dextrose?

No. Give a dextrose bolus with the insulin bolus unless the initial glucose is already elevated (roughly above 250 to 300 mg/dL), then run a concurrent dextrose infusion. The goal is euglycemia, not correction of an existing low, and demand is highest early.

How fast can I escalate the infusion?

Titrate in 1 to 2 U/kg/hr increments every 10 to 15 minutes if shock persists, up to about 10 U/kg/hr. Because inotropic effect is delayed, keep other supportive measures running during titration rather than assuming HIET has failed.

When should I stop and how do I wean?

Wean as hemodynamics recover and pressor requirements fall, then continue glucose monitoring and dextrose for 12 to 24 hours afterward because insulin-driven hypoglycemia can be delayed once the drug and its metabolites clear.

Does the same protocol apply to dihydropyridine (amlodipine) overdose?

HIET can still help, but amlodipine and other dihydropyridines cause predominantly vasodilatory shock with relatively preserved contractility, so vasopressors and vasopressin often matter more than inotropy. The greatest inotropic benefit is in verapamil, diltiazem, and beta-blocker poisoning.

References

  • Engebretsen KM, Kaczmarek KM, Morgan J, Holger JS. High-dose insulin therapy in beta-blocker and calcium channel-blocker poisoning. Clin Toxicol (Phila). 2011;49(4):277-83. PMID: 21563902.
  • Krenz JR, Kaakeh Y. An Overview of Hyperinsulinemic-Euglycemic Therapy in Calcium Channel Blocker and beta-blocker Overdose. Pharmacotherapy. 2018;38(11):1130-1142. PMID: 30141827.
  • Page C, Hackett LP, Isbister GK. The use of high-dose insulin-glucose euglycemia in beta-blocker overdose: a case report. J Med Toxicol. 2009;5(3):139-43. PMID: 19655287.

Editorial review and citation methodology

Reviewed by the Quick Medical Calculator Editorial Team. Last reviewed: May 30, 2026. The review checks calculator inputs, intended population, interpretation, limitations, and source alignment.

  • Prefer original validation studies for scoring systems and prediction tools.
  • Use current specialty society guidance, transplant allocation policy, public health guidance, or regulator resources when they govern clinical use.
  • Include limitations and safety notes when a calculator is population-specific, context-dependent, or unsuitable as a standalone decision tool.

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