Hormone · Hyperkalemia treatment
Insulin
Indications
- DKA and HHS, as a continuous IV infusion
- ICU or perioperative hyperglycemia in diabetes, by IV protocol to 140–180 mg/dL
- Stress hyperglycemia without known diabetes, same protocols (off-label)
- Hyperkalemia, with dextrose, to shift potassium into cells (off-label)
- Beta-blocker or calcium channel blocker poisoning, as high-dose insulin (off-label)
- Hypertriglyceridemia-induced acute pancreatitis (off-label)
Dosing
Insulin (regular) drip card and mL/h converterStart: DKA: 0.1 units/kg/h once K is above 3.5 (2024 consensus; older sources 3.3, or 0.14 with no bolus); bolus 0.1 units/kg only if IV access is delayed. ICU hyperglycemia: per protocol, target 140–180
| Where | Dose |
|---|---|
| Metabolic and electrolyte boluses | Insulin regular + dextrose: 5–10 units IV with 25 g dextrose (50 mL D50); check glucose hourly for 4–6 h |
| Other ICU drugs | Insulin: Needs fall as kidney function falls (less insulin clearance) |
On the quick cards
Mechanism of action
Insulin binds the α subunits of its receptor, a receptor tyrosine kinase, and the β subunits then phosphorylate each other and insulin receptor substrate (IRS) proteins. Through PI3-kinase and Akt, GLUT4 moves to the surface of muscle and fat cells, glycogen synthesis rises, and hepatic glucose output, lipolysis and ketogenesis stop. The same signals activate the Na⁺/K⁺-ATPase, fed sodium by Na⁺/H⁺ exchange, so potassium moves into cells: the basis for treating hyperkalemia and for insulin-induced hypokalemia.
Pharmacology
- Metabolic: lowers glucose through muscle and fat uptake and less hepatic output; brain glucose uptake does not need insulin
- Metabolic: stops lipolysis and ketogenesis, so only insulin clears DKA; as glucose falls, add dextrose rather than stop the drip
- Metabolic: drives K⁺, phosphate and Mg²⁺ into cells; after 10 units IV, potassium falls within about 15 min, is lowest at 30–60 min, and the effect fades over 4–6 h
- Cardiovascular: high doses act as an inotrope in beta-blocker and CCB poisoning (AHA 2023)
Pharmacokinetics
| Onset | IV 10–15 min (Humulin R label); SC about 30 min |
|---|---|
| Peak | SC 1.5–3.5 h (Novolin R label) |
| Duration | SC about 8 h; one IV dose about 4 h (2–6) in clamp studies (label) |
| Half-life | 4–6 min in plasma (Duckworth 1998); labels report 20–23 min after IV doses; SC 1.5 h, set by absorption |
| Distribution | Vd 0.32–0.67 L/kg (Humulin R label) |
| Protein binding | Negligible, apart from anti-insulin antibodies |
| Metabolism | Receptor uptake, then insulin-degrading enzyme, mainly in the liver (label) |
| Elimination | The kidney filters and degrades much systemic insulin, so needs fall with GFR; liver failure also prolongs action |
| Drip transition | Levels fall within minutes after a drip stops, so give SC basal insulin 1–2 h before (2024 consensus) |
Chemistry
- A 51-amino-acid peptide: A chain (21) and B chain (30) joined by two disulfide bonds (A7–B7, A20–B19), with a third inside the A chain (A6–A11); MW 5,808 Da (label)
- Recombinant human insulin from E. coli (Humulin R) or yeast (Novolin R, Myxredlin); clear at pH 7.0–7.8, above its isoelectric point of about 5.4
- Zinc (two ions per hexamer, on B10 histidines) and metacresol stabilize hexamers, which must dissociate before SC absorption, delaying onset; IV insulin is diluted to monomers at once
- Binds plastic tubing: prime about 20 mL through new lines (Goldberg 2006); premixed Myxredlin keeps 30 days at room temperature (label)
Adverse effects and cautions
In the one-pagers
- Electrolyte ImbalancesHyperkalemia: stabilize, shift, remove: Shift: regular insulin 10 units IV with dextrose 25–50 g. K falls within 15 min, lowest at 30–60 min.
- Medical Emergencies: Neuro, Endocrine, Blood and InfectionDiabetes: meters, pumps, look-alikes: Pump failure: Pump (no long-acting insulin) kinked for hours: No waiting for a set change: NS bolus, go: ED
- Toxidromes and AntidotesCardiotoxic drugs: Beta-blockers, CCBs: High-dose insulin 1 unit/kg, then 1–10 units/kg/h: Give dextrose; check glucose, K
- BurnsBurn shock and the systemic response: From about day 3 the flow phase takes over: catecholamines rise up to 50-fold, with cortisol and glucagon (Williams 2009), driving tachycardia, fever, high cardiac output, low SVR, insulin resistance and muscle wasting, so fever and tachycardia no longer prove infection. In children with burns over 30% TBSA the response was still measurable 3 years later (Jesc
- EMT By-Complaint Quick PagesSeizure, confusion, diabetes, stroke: Low glucose: 60 mg/dL or less with symptoms (ADA: under 70): Oral glucose per protocol (NASEMSO 25 g; ADA 15 g; child 0.5-1 g/kg) only if awake and swallowing; cannot swallow: airway, ALS; stop the insulin pump if ALS is not available
- ACLS Algorithms in BriefReversible causes: bedside clues and ultrasound: Potassium: Dialysis, missed session, peaked T or wide QRS: High: calcium, bicarbonate, insulin; low: K⁺
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In the algorithms
Other hormone drugs
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Sources
- FDA label: Humulin R U-100 (2023)
- FDA label: Myxredlin (2025)
- Duckworth 1998 (insulin degradation)
- ADA hyperglycemic crises consensus (2024)
For education and exam preparation only. Follow your institution’s protocols. Typical adult values for study. Follow your local protocols and medical direction.