Acute Hyperkalaemia Protocol

Stabilise, shift, eliminate: what buys time, and what actually removes potassium · v1.2

  • Enter the potassium, the ECG findings, the current GRBS and the renal and volume status.
  • You get a stepwise emergency protocol covering membrane stabilisation, intracellular shift, elimination and the indications for dialysis.
  • The GRBS tailors the insulin and dextrose step, so enter it before you read the plan.
  • Check the sample before you act on it. A haemolysed sample, or one drawn after a long tourniquet, has started emergency treatment in a patient who never needed it.

  • Children and adolescents under 18.
  • The cause of the hyperkalaemia, and the treatment of the rhabdomyolysis, the tumour lysis or the acute kidney injury underneath it.
  • The dialysis prescription. It names the indication and stops there.
  • When a held ACE inhibitor, ARB or mineralocorticoid antagonist goes back on, which is measured in weeks and belongs with whoever owns the heart failure or the kidney.
  • The long-term binder therapy that keeps a CKD patient out of this situation altogether.
1. Biochemical & Electrical Status
2. Glycaemic & Renal Status
3. Clinical Modifiers
4. Concurrent K-Elevating Medications

Mechanisms, Doses and the Differential

1. Why Calcium Goes First

Calcium does not lower serum potassium. It antagonises the membrane effects of hyperkalaemia. A high potassium raises the resting membrane potential, making it less negative and bringing it closer to the threshold potential, which causes initial hyper-excitability and then inexcitability: conduction blocks, asystole. Calcium raises the threshold potential and restores the normal voltage gap. The potassium is still high; the heart is temporarily protected.

2. Gluconate and Chloride Are Not Interchangeable by Volume

  • Calcium Gluconate 10% carries 93 mg of elemental calcium, 2.3 mmol, in each 10 mL ampoule. Calcium Chloride 10% carries 272 mg, 6.8 mmol, in the same volume, which is three times as much.
  • That is the whole reason the gluconate dose is 30 mL and the chloride dose is 10 mL: both deliver 6.8 mmol, and they are equimolar rather than equivalent by millilitre.
  • Gluconate goes peripherally, because it causes less tissue injury on extravasation. Chloride goes through a central line only, and is preferred in cardiac arrest and peri-arrest where the smaller volume and shorter infusion matter. In Indian ICUs both are stocked, and the choice turns on the access you have and how fast you need it.
  • A note on the 10 mL figure. This page gave 10 mL of gluconate until 24 August 2026, and so does a great deal of teaching material. Ten millilitres delivers 2.2 mmol and is an underdose. The UK Kidney Association guideline of December 2023 and a national patient safety alert issued in June 2023, which followed a death, both put the dose at 30 mL over 10 minutes. If a colleague is working from the older figure, this is the sentence to show them.

3. What Each Intervention Does, and How Fast

Only dialysis and the binders take potassium out of the body. Everything above them either moves it into cells or protects the heart while the potassium is still there.

Intervention Mechanism Expected K+ Drop Onset Duration
Calcium Gluconate 10% IV Membrane stabilisation (no K+ change) 0 mEq/L (protects heart only) 1 - 3 min 30 - 60 min
Insulin 10U + Dextrose 25g IV Intracellular shift via Na+/K+-ATPase 0.5 - 1.2 mEq/L 15 - 30 min 4 - 6 h
Salbutamol 10-20 mg nebulised Intracellular shift via Beta-2 stimulation 0.5 - 1.5 mEq/L 15 - 30 min 2 - 4 h
NaHCO3 (if acidotic) Shift via pH correction 0.3 - 0.5 mEq/L 15 - 30 min 1 - 2 h
Furosemide 40-80 mg IV Renal elimination (kaliuresis) Variable (requires renal function) 15 - 30 min 4 - 6 h
SZC (Lokelma) 10g PO GI potassium binding 0.4 - 0.7 mEq/L 1 - 2 h Ongoing
CPS / K-Bind 30g PO/PR GI cation exchange 0.5 - 1.0 mEq/L (over hours-days) 2 - 6 h Variable
Haemodialysis Extracorporeal elimination 1.0 - 2.0 mEq/L per hour Immediate Duration of session
  • Insulin-dextrose. Insulin drives potassium into cells by stimulating the Na+/K+-ATPase pump; the dextrose is purely to prevent hypoglycaemia. The standard is 10 Units Actrapid with 25g Dextrose (100 mL of 25% Dextrose). Then the part that gets missed: delayed hypoglycaemia peaks at 2 to 3 hours, and it is the commonest complication of treating hyperkalaemia. Check GRBS every 30 minutes for 2 hours, then hourly for a further 4 hours.
  • Salbutamol, the underused adjunct. Nebulised at 10 to 20 mg, which is 4 to 8 times the bronchodilator dose, and additive to insulin-dextrose. Approximately 20 to 40% of ESRD patients are resistant to the potassium-lowering effect, which is the reason it cannot be the whole answer in a dialysis patient. Tachycardia and tremor are expected, with a heart rate rise of 15 to 25 bpm. Use with extreme caution in ischaemic heart disease or an existing tachyarrhythmia.
  • Sodium bicarbonate works only in acidosis. It shifts potassium intracellularly by correcting extracellular pH, and is effective only when significant metabolic acidosis is present (pH < 7.2). In the absence of acidosis it does not meaningfully lower potassium and should NOT be relied upon; when indicated, administer 50 to 100 mL of 8.4% NaHCO3 IV over 5 minutes. Each 50 mL ampoule delivers approximately 50 mEq of sodium, which is significant in heart failure.
Clinical Caution: Resins Are Too Slow for an Emergency
Cation-exchange resins (Calcium Polystyrene Sulphonate / K-Bind, Sodium Polystyrene Sulphonate / Kayexalate) take hours to days to meaningfully reduce serum potassium. Relying on them for acute emergency management delays the treatment that works. They are elimination adjuncts, not emergency interventions. Sodium Zirconium Cyclosilicate (SZC/Lokelma) acts faster (onset 1 to 2 hours) and is now available in Indian formularies.
Calcium and Bicarbonate Precipitate in the Line
Never administer IV Calcium Gluconate and IV Sodium Bicarbonate through the same intravenous line without thorough flushing. They precipitate instantly into insoluble Calcium Carbonate crystals, blocking the line and delivering no therapy.

4. The ECG Progression

The changes follow a predictable but not always sequential progression. Some patients go directly from peaked T waves to cardiac arrest. They do not correlate perfectly with the serum level either: a patient with K 7.0 may have a normal ECG, while one with K 5.8 on digoxin may have advanced changes.

Stage ECG Finding Typical K+ Range Clinical Significance
Early Tall, peaked, narrow-based T waves (best seen in V2-V4) 5.5 - 6.5 mEq/L First ECG change. Often subtle. May be confused with hyperacute T waves of STEMI.
Moderate PR prolongation, P wave flattening, ST depression 6.5 - 7.5 mEq/L Atrial conduction delay. P waves may become imperceptible.
Advanced QRS widening (> 120 ms), bizarre QRS morphology 7.0 - 8.0 mEq/L Ventricular conduction delay. May mimic bundle branch block or ventricular tachycardia.
Pre-arrest Sine wave pattern (fusion of widened QRS with T wave) > 8.0 mEq/L Imminent VF or asystole. This is a peri-arrest rhythm. Treat as cardiac arrest.

5. Check the Sample, Then Work Through the Differential

Pseudohyperkalaemia: Check the Sample First
Before initiating emergency treatment for unexpected hyperkalaemia in a clinically stable patient, always consider: Was there prolonged tourniquet time? Was the sample haemolysed? Is there extreme leukocytosis or thrombocytosis? A repeat sample from a fresh, atraumatic draw can prevent unnecessary treatment.
Pseudohyperkalaemia Transcellular Shift Impaired Excretion Increased Intake / Load
Prolonged tourniquet / fist clenching Metabolic acidosis (DKA, lactic acidosis, RTA) Acute Kidney Injury Excessive IV KCl supplementation
In vitro haemolysis (traumatic draw) Insulin deficiency / DKA CKD Stage 4-5 / ESRD Massive blood transfusion (stored blood)
Severe leukocytosis (> 70,000) Non-selective beta-blockers ACEi / ARBs / MRAs Tumour lysis syndrome
Severe thrombocytosis (> 500,000) Succinylcholine NSAIDs / Calcineurin inhibitors Rhabdomyolysis / crush injury
Delayed sample processing Digoxin toxicity TMP-SMX / Heparin Major burns / haemolysis
Hypertonicity (mannitol, hyperglycaemia) Hypoaldosteronism (Type 4 RTA) High-K diet in CKD patients

6. Indications for Emergent Dialysis

Dialysis is the definitive elimination therapy for hyperkalaemia. Haemodialysis removes 25 to 50 mEq of potassium per hour.

  • ESRD / Anuric patients: Loop diuretics and renal elimination are ineffective.
  • Refractory hyperkalaemia: K remains ≥ 6.0 mEq/L after two cycles of full medical therapy (calcium + insulin-dextrose + salbutamol + diuretics).
  • Persistent ECG changes: Life-threatening ECG changes (QRS widening, sine wave) unresponsive to calcium gluconate.
  • Massive tissue breakdown: Rhabdomyolysis, tumour lysis syndrome, major burns, or crush injury where ongoing potassium release will exceed medical elimination capacity.
  • Severe AKI with oliguria: When diuretic response is absent and K is rising despite shift therapies.

7. Common Drug Causes: An Indian Formulary Perspective

Drug Class Common Indian Brands Mechanism Action
ACE Inhibitors Enalapril (Envas), Ramipril (Cardace, Ramistar) Decreased aldosterone secretion Hold / dose-reduce
ARBs Losartan (Losar), Telmisartan (Telma, Telmikind) Decreased aldosterone secretion Hold / dose-reduce
MRAs Spironolactone (Aldactone), Eplerenone (Epleheart) Blocks aldosterone at collecting duct Hold until K normalises
NSAIDs Ibuprofen (Brufen), Diclofenac (Voveran) Decreased renal blood flow and renin Discontinue
TMP-SMX Cotrimoxazole (Bactrim, Septran) Blocks ENaC (amiloride-like effect) Discontinue / substitute
Heparin UFH, Enoxaparin (Clexane, Lonopin) Suppresses aldosterone synthesis Monitor; switch if possible
Potassium supplements K-Lor, Potklor, IV KCl Direct K+ load Discontinue immediately
Abbreviations: ACE (Angiotensin-Converting Enzyme) · ACEi (Angiotensin-Converting Enzyme Inhibitor) · ACS (Acute Coronary Syndrome) · AKI (Acute Kidney Injury) · ARB (Angiotensin Receptor Blocker) · ATPase (Adenosine Triphosphatase) · Ca2+ (Calcium) · CKD (Chronic Kidney Disease) · CNI (Calcineurin Inhibitor) · CPS (Calcium Polystyrene Sulphonate) · D50 (50% Dextrose) · DKA (Diabetic Ketoacidosis) · ECG (Electrocardiogram) · ENaC (Epithelial Sodium Channel) · ESRD (End-Stage Renal Disease) · Fab (Fragment Antigen-Binding) · GI (Gastrointestinal) · GRBS (Glucometer Random Blood Sugar) · HCO3 (Bicarbonate) · HHS (Hyperosmolar Hyperglycaemic State) · HR (Heart Rate) · ICU (Intensive Care Unit) · IHD (Ischaemic Heart Disease) · IV (Intravenous) · K+ (Potassium) · KCl (Potassium Chloride) · LMWH (Low Molecular Weight Heparin) · Mg2+ (Magnesium) · MRA (Mineralocorticoid Receptor Antagonist) · Na+ (Sodium) · NaHCO3 (Sodium Bicarbonate) · NSAID (Non-Steroidal Anti-Inflammatory Drug) · PO (Per Os) · PR (Per Rectum) · RAAS (Renin-Angiotensin-Aldosterone System) · RTA (Renal Tubular Acidosis) · STEMI (ST-Elevation Myocardial Infarction) · SZC (Sodium Zirconium Cyclosilicate) · TMP-SMX (Trimethoprim-Sulfamethoxazole) · UFH (Unfractionated Heparin) · VF (Ventricular Fibrillation)
References
  1. Weisberg LS. Management of severe hyperkalemia. Crit Care Med. 2008;36(12):3246-3251.
  2. Rossignol P, Legrand M, Kosiborod M, et al. Emergency management of severe hyperkalemia: Guideline for best practice and opportunities for the future. Pharmacol Res. 2016;113(Pt A):585-591.
  3. Indian Council of Medical Research (ICMR). Standard Treatment Workflows - Acute Kidney Injury and Hyperkalaemia. 2019.
  4. Maxwell AP, Linden K, O'Donnell S, et al. Management of hyperkalaemia. J R Coll Physicians Edinb. 2013;43(3):246-251.
  5. Lindner G, Burdmann EA, Clase CM, et al. Acute hyperkalemia in the emergency department: a summary from a Kidney Disease: Improving Global Outcomes conference. Eur J Emerg Med. 2020;27(5):329-337.
  6. UK Kidney Association. Clinical Practice Guidelines: Treatment of Acute Hyperkalaemia in Adults. December 2023.
  7. Packham DK, Rasmussen HS, Lavin PT, et al. Sodium zirconium cyclosilicate in hyperkalemia. N Engl J Med. 2015;372(3):222-231.
  8. Batterink J, Cessford TA, Taylor RAI. Pharmacological interventions for the acute management of hyperkalaemia in adults. Cochrane Database Syst Rev. 2015;(10):CD010344.
How to Cite This Tool

DOIhttps://doi.org/10.5281/zenodo.22401526

AMA Style:Umakanth S. Acute Hyperkalaemia Protocol. Version 1.2. MEDiscuss Clinical Decision Support System. Published 2026. Accessed . https://mediscuss.org/cdss/acute-hyperkalaemia. doi:10.5281/zenodo.22401526

Vancouver Style:Umakanth S. Acute Hyperkalaemia Protocol [Internet]. Version 1.2. MEDiscuss.org; 2026 [cited ]. Available from: https://mediscuss.org/cdss/acute-hyperkalaemia. doi:10.5281/zenodo.22401526

Disclaimer and scope
Disclaimer: This decision-support system is written for healthcare professionals. It does not substitute clinical judgment, and the treating physician retains absolute responsibility for every diagnostic, dosing and therapeutic decision. The algorithms are built on the evidence as it stands, and the evidence moves. Verify the output against your current institutional protocol, and against the patient in front of you.
© 2026 MEDiscuss.org. All rights reserved. Provided free of charge for clinical use. Unauthorised reproduction or redistribution is strictly prohibited.
Category Acute ResuscitationProtocol
Specialties Internal Medicine, Nephrology, Critical Care

Written and maintained by

Dr Shashikiran Umakanth

Last revised 24 August 2026

How these tools are written and reviewed

Related Clinical Tools
AKI & CKD Staging PathwayCombined Electrolyte PanelDKA & HHS ProtocolABG & Acid-Base Pathway