High Dose Insulin Euglycemia Therapy (HIET) Calculator

Addresses life-threatening calcium channel blocker (CCB) overdose and severe beta blocker (BB) poisoning.

Refer to the text below the tool for the current guidelines on the use of HIET to improve myocardial contractility and restore hemodynamic stability.


High-dose Insulin Euglycemic Therapy (HIET) is a first-line treatment for life-threatening calcium channel blocker (CCB) overdose and for severe beta blocker (BB) poisoning.

The target of HIET is to address the myocardial depression by restoring cardiac output and ameliorating associated symptoms. Compared to conventional therapies, such as atropine, glucagon, calcium boluses, and high-dose vasopressors, HIET improves hemodynamic stability quicker.


Step 1 - an initial insulin bolus (if blood glucose is greater than 250 mg/dL /16.7 mmol/L – not necessary) to rapidly saturate insulin receptors to speed the physiological response:

  • Intravenous bolus of regular insulin at a dose of 1 unit/kg.
  • If serum glucose <250 mg/dL, concurrently administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV.

Step 2 - continuous infusion:

  • Regular continuous insulin: start with 0.5–1 unit/kg/hr.
  • Dextrose: 0.5 g/kg/hr (titrate to maintain glucose 110–250 mg/dL).

To avoid fluid overload, insulin recommendation to be concentrated to 10 units/mL.


Body weight
Serum glucose
Dextrose replacement for infusion
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High Dose Insulin Euglycemia Therapy (HIET) Explained

High-dose Insulin Euglycemic Therapy (HIET) is a first-line treatment for life-threatening calcium channel blocker (CCB) overdose and for severe beta blocker (BB) poisoning.

The target of HIET is to address the myocardial depression by restoring cardiac output and ameliorating associated symptoms. Compared to conventional therapies, such as atropine, glucagon, calcium boluses, and high-dose vasopressors, HIET improves hemodynamic stability quicker and increases myocardial glucose uptake, resulting in improved contractility.

During HIET, glucose, potassium and ejection fraction should be monitored because most commonly met adverse effects include hypoglycemia and hypokalemia.

Step 1 is to administer an initial insulin bolus (if blood glucose is greater than 250 mg/dL /16.7 mmol/L – not necessary) to rapidly saturate insulin receptors to speed the physiological response:

  • Intravenous bolus of regular insulin at a dose of 1 unit/kg.
  • If serum glucose <250 mg/dL, concurrently administer a bolus of dextrose 25-50 g (or 0.5-1 g/kg) IV.

Step 2 is to administer the continuous infusion:

  • Regular continuous insulin: start with 0.5–1 unit/kg/hr.
  • Dextrose: 0.5 g/kg/hr (titrate to maintain glucose 110–250 mg/dL).

To avoid fluid overload, insulin recommendation to be concentrated to 10 units/mL.

  • In parallel with HIET, continuous monitoring of serum glucose every 30 minutes for 1-2 hours until stable and of potassium every 1 hour, must take place.

Calcium channel blocker overdoses usually result in:

  • hypoinsulinaemia, as insulin release is dependent on calcium influx into islet beta cells through L-type calcium channels;
  • calcium channel blocker-induced insulin resistance;
  • impaired uptake of glucose and free fatty acids by cardiac myocytes;
  • inhibition of calcium-dependent mitochondrial activity (which is needed in the glucose catabolism.

Please note than whilst the overall action of insulin may appear to improve myocardial contractility, it has no chronotropic effect and may cause vasodilation.

The below table summarizes the main possible adverse effects of HIET:

HIET Adverse Effect Notes
Hypoglycaemia (<3.3 mmol/L in about 16% of cases) May be more likely in milder cases without marked hypotension.
Hypokalaemia Noted in only two of seven in Greene et al’s small series, with a minimum potassium level of 2.8 mmol/L.
Caution should be exerted for excessive correction of hypokalaemia because it only mimics potassium-depleted state and reflects the intracellular shift of potassium from the extracellular compartment.
Hypophosphataemia -
Hypomagnesaemia -
 

References

Original reference

Kerns, W. Antidotes in Depth (A18): Insulin-Euglycemia Therapy. Goldfrank’s Toxicologic Emergencies 2015, 10th e. L. S. Nelson, N. A. Lewin, M. Howland et al. New York, NY, McGraw-Hill.

Other references

Holger JS, Stellpflug SJ, Cole JB, Harris CR, Engebretsen KM. High-dose insulin: a consecutive case series in toxin-induced cardiogenic shock. Clin Toxicol (Phila). 2011; 49(7):653-658.

Greene SL, Gawarammana I, Wood DM, Jones AL, Dargan PI. Relative safety of hyperinsulinaemia/euglycaemia therapy in the management of calcium channel blocker overdose: a prospective observational study. Intensive Care Med. 2007; 33(11):2019-2024.

Nickson CP, Little M. Early use of high-dose insulin euglycaemic therapy for verapamil toxicity. The Medical journal of Australia. 2009; 191 (6), 350-2.


Specialty: Endocrinology

System: Endocrine

Abbreviation: HIET

Article By: Denise Nedea

Published On: September 26, 2020

Last Checked: September 26, 2020

Next Review: September 26, 2025