Pharmacology · 16 min read

Insulin Types, Peaks & Hypoglycemia

Onset, peak and duration drive every insulin question. Hypoglycemia risk lives at the peak.

The four families

Rapid-acting analogs (lispro, aspart, glulisine) start working in 10–15 minutes, peak at 1–2 hours and are done by 3–5 hours. Because onset is so quick, the meal must already be in front of the client.

Short-acting regular insulin begins in 30–60 minutes, peaks at 2–4 hours and lasts 5–8 hours. It is the only insulin routinely infused intravenously, which is why it appears in every diabetic ketoacidosis question.

Intermediate NPH begins in 1–2 hours, peaks broadly at 4–12 hours and lasts 12–18 hours. That long, blunt peak is why nocturnal hypoglycemia questions almost always involve NPH given in the evening.

Long-acting glargine and detemir are essentially peakless over 20–24 hours. They provide basal coverage and are never mixed in a syringe with another insulin.

Recognizing hypoglycemia

Early hypoglycemia is adrenergic: diaphoresis, tremor, tachycardia, hunger, anxiety. As glucose continues to fall the picture becomes neuroglycopenic — confusion, slurred speech, seizure, coma.

Beta-blockers mask the adrenergic warning signs. A client on both a beta-blocker and insulin may present with diaphoresis alone, or with nothing until confusion appears.

  • Conscious and able to swallow → 15 g oral carbohydrate, recheck in 15 minutes
  • Unconscious with IV access → 25 g dextrose 50% IV push
  • Unconscious without IV access → glucagon 1 mg IM or subcutaneous
  • Once glucose is above 70 mg/dL → give a protein-plus-carbohydrate snack to prevent rebound

Test pattern

A client who is confused and diaphoretic at 0300 after evening NPH is hypoglycemic until proven otherwise. Check the glucose — do not give more insulin, and do not attribute it to sundowning.

Sick-day and DKA logic

Clients with type 1 diabetes never stop their basal insulin during illness, even when they are not eating. Stress hormones drive glucose up, and stopping insulin is the fastest route to ketoacidosis.

In DKA management, potassium is the trap. Total-body potassium is depleted even when the serum level reads normal or high, because acidosis pushes potassium out of cells. Insulin drives it straight back in. Confirm the potassium is above 3.3 mEq/L before starting the insulin infusion.

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