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Hyperkalaemia Hypomagnesaemia Hypophosphataemia Hypernatraemia Hypokalaemia Hyponatraemia Hypocalcaemia Hypercalcaemia
Home | Articles | Electrolyte Disturbances | Hyperkalaemia

Hyperkalaemia

Last updated 19th March 2024

Causes

  1. Most important are acute kidney injury and chronic renal failure.
  2. Most of the others begin with A – Addisons, Acidosis, Artefact (haemolysis), ACEI, ARB, Aldosterone Antagonist (Spironolactone), Anti-inflammatory drug (NSAID)
  3. Other drugs that may cause hyperkalaemia are beta-blockers and digoxin (by transcellular shift), Trimethoprim, Heparin (rarely) and some laxatives e.g. Laxido
  4. Consider spurious hyperkalaemia e.g. prolonged tourniquet time, cell lysis, raised platelets/WBC

Hyperkalaemia and the Heart

  1. Serious dysrhythmia unlikely if serum K <6.0mmol/l though risk depends not only on blood level of K but also on the ECG changes and the likelihood K will rise further
  2. All patients with serum K ≥6.0mmol/l should have urgent ECG
  3. Sequence of ECG changes is peaking of T wave then loss of P wave then broadening of QRS complex then bradycardia then asystole
  4. Other dysrhythmias reported in hyperkalaemia include AF, VT, VF
  5. Asystole or VF may be the first manifestation of severe hyperkalaemia and can occur without warning ECG signs
  6. NB Suspect life threatening hyperkalaemia if called to resus for patient with bradycardia, broad complexes & no obvious P waves (absence of P waves distinguishes from complete heart block).

Measuring Potassium

  1. Point of care analysers give results in 2 minutes and are precise enough to justify their use in emergencies while waiting for a laboratory result
  2. Serum K is around 0.4mmol/l higher than plasma K because K leaks out of red cells and platelets during clotting – so plasma K recommended

5 Point Treatment Strategy

  1. Protect the heart – with Calcium Gluconate
  2. Push K into cells – Insulin/dextrose, Salbutamol, Bicarbonate.
  3. Remove K from body – establish diuresis, relieve obstruction, dialysis, sodium zirconium cyclocilicate.
  4. Monitor K and Glucose – check K at 1, 2, 4, 6 and 24 hours after treatment to cover possibility of rebound hyperkalaemia; check glucose every 30 mins for up to 6 hours after insulin-dextrose, because of risk of hypoglycaemia
  5. Prevent recurrence – stop all potentially offending drugs immediately and review need for their reintroduction eg if restarting ACEI tell patient to stop these drugs temporarily in event of further diarrhoea

Click here to access and download the Hyperkalaemia Bundle and Guide to using Hyperkalaemia Bundle (update pending)

Calcium Gluconate

  1. Renal Association (RA) recommend Calcium Gluconate 30ml 10% IV over 10 minutes when hyperkalaemia associated with ECG changes (see above), repeating after 5-10 mins until rate increases and QRS narrows
  2. Gluconate preferred to Chloride because it is safer – Calcium Chloride contains 3 x more Calcium and will cause tissue necrosis if extravasates.
  3. Calcium protects heart but doesn’t lower serum K
  4. Effective within minutes, duration of action 30-60 mins
  5. May precipitate if given in same line as bicarbonate
  6. Use cautiously in patients on Digoxin as rapid calcium administration can precipitate myocardial Digoxin toxicity.

Insulin/Dextrose

  1. RA recommend insulin-dextrose to treat serum K ≥6.5 mmol/l and suggest insulin-dextrose for patients with serum K 6.0-6.4mmol/l.
  2. Check patient’s blood glucose. Add 8 units Actrapid insulin to 100ml of dextrose 20% and infuse over 30 minutes
  3. If pre treatment BG <7.0mmol/l, follow step 2 with dextrose 10% at 50ml/hour for 5 hours (total 250ml) in order to prevent hypoglycaemia.
  4. For oligo-anuric or pulmonary oedema patients when fluid is being restricted, run dextrose 20% at 25ml/hr for 5 hours (total 125ml) instead.  Avoid 50% dextrose which carries risk of tissue necrosis if extravasates.
  5. This amount of insulin will lower serum K by around 1-2mmol/l for 1-2 hours which means that further infusions may be required unless or until steps have been taken to eliminate K from the body eg by dialysis, resonium or by re-establishing a urine output.
  6. Note that RA recommend glucose monitoring for up to 12 hours after insulin-dextrose infusion.

Salbutamol

  1. RA recommend nebulised salbutamol 10-20 mg in addition to dextrose-insulin when serum K ≥6.5 mmol/L and suggest salbutamol as adjunctive therapy when serum K 6.0-6.4mmol/l
  2. 20mg Salbutamol by nebuliser or 500 micrograms IV over 10min will lower K by around 1mmol/l – note dose is higher than that used for asthma/COPD, and should be limited to 10mg in IHD
  3. Onset of action 30-60 min, duration 4-6 hours.
  4. Salbutamol should not be given as monotherapy as up to 40% do not respond.
  5. Ideal in addition to insulin/dextrose for patient who is bradycardic. Reduce dose or avoid with tachycardia.

Sodium Bicarbonate

  1. RA suggest that intravenous sodium bicarbonate infusion is not used routinely for the acute treatment of hyperkalaemia.
  2. We generally give IV bicarbonate only in context of hyperkalaemia with AKI/CKD when serum bicarbonate <10mmol/l, & then give 500ml 1.26% over 4 hours.
  3. Sodium bicarbonate may lower K by around 0.5mmol/l
  4. Onset of action 30 to 60 minutes, duration 3-4 hours.
  5. Oral bicarbonate may be useful for diabetic Type 4 renal tubular acidosis patients:  1g tds if serum bicarbonate <20mmol/l.

Zirconium (Lokelma) in Life Threatening Hyperkalaemia

  1. Recommended for acute life-threatening hyperkalaemia (potassium > 6.5mmol/l) after giving insulin/dextrose and salbutamol as above.
  2. Inorganic powder that preferentially captures potassium in exchange for hydrogen and sodium cations throughout the gastrointestinal tract.
  3. Starts to reduce potassium 1 hour after ingestion
  4. Prescribe as 10g three times a day until normokalaemia or for a maximum of 72 hours in acute, life-threatening hyperkalaemia. 
  5. If hyperkalaemia is not controlled by this time, it should be discontinued.   There is no evidence for maintenance therapy in the acute setting at present.

Zirconium (Lokelma) as Maintenance Therapy in CKD and HF to allow RAAS Inhibition

  1. NICE guidelines state that RAAS inhibitors should not be routinely started in people with serum potassium ≥5mmol/l and should be stopped in people with levels ≥6mmol/l
  2. Zirconium may be indicated as maintenance therapy in patients with CKD and HF who are taking ACEI or ARBs and whose serum K ≥6mmol/l, in order to allow RAAS inhibition to continue to be prescribed
  3. The recommended dose for this indication is 5-10mg once daily
  4. This will normally only be prescribed by the renal physicians or the heart failure team.

Dialysis

  1. Definitive treatment for hyperkalaemia – will lower K by 1mmol/l in first hour & by further 1mmol/l in next 2 hrs.

Hyperkalaemia Discovered During Cardiac Arrest

  1. Adrenaline 1mg IV if not already given
  2. Calcium Chloride 10ml 10% IV into large forearm vein – otherwise use Calcium Gluconate 30ml 10% IV as above
  3. 10 units soluble insulin with 50ml 50% Dextrose IV into large forearm vein.  If vascular access is not secure then use 250ml 10% dextrose as above
  4. Sodium bicarbonate 50ml 8.4% solution over 5 min
  5. Salbutamol 20mg by nebuliser if hyperkalaemia discovered periarrest or post ROSC
  6. Consider emergency dialysis

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Content by Dr Nadeeka Rathnamalala, Dr Michael Kelly and Alison Crooks