IV calcium doesn’t lower potassium — it stabilizes the myocardium within minutes so you can buy time for potassium-shifting and removal therapies. The pearls below distill what clinicians need at the bedside, with referral links to the full clinical explainer by Gyath Shammha.
When serum potassium is dangerously high (often K⁺ ≥ 6.0–6.5 mmol/L or any K⁺ with ECG changes), lethal dysrhythmias are a real risk. IV calcium raises the myocardial threshold potential, counteracting conduction changes (peaked T waves, QRS widening, sine wave, bradyarrhythmias). It stabilizes the heart; it does not reduce K⁺.
Re-check the ECG in ~5 minutes and redose if the QRS stays wide or instability persists.
10% calcium chloride (CaCl₂) contains more elemental calcium per mL than 10% calcium gluconate. Many protocols that target ~6.8 mmol elemental calcium use either 10 mL CaCl₂ 10% or 30 mL Ca gluconate 10% over ~2–5 minutes, with ECG reassessment. Others start with 1 g (10 mL) Ca gluconate 10% and repeat if needed. Follow your local algorithm and line considerations (gluconate is preferred peripherally; chloride is caustic and best via central access unless in true peri-arrest).
If severe digoxin toxicity is strongly suspected, many references advise avoiding IV calcium and prioritizing digoxin immune Fab alongside standard hyperkalemia care. Defer to your toxicology/cardiology guidance.
No. It stabilizes cardiac membranes while other therapies shift or remove K⁺.
Onset within minutes; effect about 30–60 minutes. Monitor and redose if ECG changes persist.
Calcium gluconate is safe via peripheral IV; calcium chloride is tissue-injury–prone and usually given via central line (except true peri-arrest situations).
