Initial Management of Acute Hyperkalaemia

(District)
Introduction
Acute hyperkalaemia is associated with cardiac arrhythmias and cardiac arrest. The risk is highest
in patients with:
 K+ ≥7.0 mmol/l
 A rapid and/or large rise from baseline K+ (some patients have a baseline K+ of 6-6.5 for
example
 Pre-existing cardiac conduction disorders.
Life-threatening hyperkalaemia may also be heralded by ECG changes and symptoms (generalised
muscle weakness).

Assessment
1. Repeat the K+ level to confirm genuine hyperkalaemia. If initial K+ level is severe (≥7.0
mmol/l), the repeat blood test should be on an urgent venous blood gas sample (VBG).
2. Perform an immediate ECG: changes may or may not be present, and a normal ECG does
not guarantee patient safety. Abnormalities include (those in bold are highest risk for
progression to cardiac arrest):
a. T waves – narrow base, peaked
b. Wide QRS, long PR
c. Absent P waves, junctional rhythm
d. Broad bizarre QRS, “sine wave”
e. Variety of arrhythmias including sinus bradycardia, sinus tachycardia, AVN blocks,
asystole

3. Determine the underlying cause

The most common cause for isolate hyperkalaemia is a spurious – e.g. haemolysed sample, K+
containing iv fluid. Must recheck with VBG immediately for rapid confirmation

The majority will be related to acute or chronic kidney disease

Aggravated by dehydration (e.g. gastroenteritis)
Aggravated by potassium sparing drugs (e.g. ACE inhibitor, Angiotensin Blocker,
spironolactone).
Aggravated by high dietary potassium, potassium supplements

Other causes include:

a. Transcellular shift – e.g. acidosis (eg DKA), Digoxin toxicity
b. Tissue destruction – e.g. GI bleed, rhabdomyolysis, tumour lysis
c. Rare renal causes – e.g. renal tubular acidosis, hyperaldosteronism

Initial Management of Acute Hyperkalaemia Pharmacy (District)

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Indications for emergency treatment of acute hyperkalaemia (any of):
 K+ ≥7.0 mmol/l
 K+ >6.0 mmol/l with generalised muscle weakness (e.g. unable to sit up, difficulty
breathing)
 K+ >6.0 mmol/l with ECG changes – esp. wide QRS, junctional rhythm, bradycardia

Management Priorities in Emergency Treatment

NB: All initial treatment is temporising until the underlying cause is managed.
1. Stabilisation of myocardium
a. Calcium Gluconate 10% x 10ml iv bolus over 2-3 min. Provides cardio-protection
with onset 1-3 minutes and duration 30-60 min
i. Calcium Gluconate may be ineffective in liver failure
ii. Calcium Gluconate has 1/3 the elemental Ca as Calcium Chloride
b. Calcium Chloride 10% is alternative if Gluconate unavailable/unsuitable, very
irritating to peripheral veins
c. Calcium dose can be repeated 1-2x at 30 min intervals
2. Temporizing measures – shift potassium intracellularly
a. Insulin Actrapid (alternatives Novorapid, Humalog, Humulin R) 10 units iv bolus,
with 50mL 50% Dextrose iv bolus (can omit Dextrose if already hyperglycaemic,
>15 mmol/l). Shifts Potassium intracellularly, onset 10-20 min, duration 2-4 hours
b. Salbutamol 5mg nebuliser, 20mg initially (4 doses). Shifts potassium intracellularly,
onset 15 min, duration 1-2 hours.
3. Potassium removal
a. Haemodialysis. The only definitive way to remove potassium from the body.
Indicated if above measures fail, or severe hyperkalaemia that is unlikely to resolve
quickly, especially in anuric renal failure (eg dialysis patients). Discuss with senior
clinicians early.
b. Frusemide will enhance renal excretion of potassium. Only use if volume overloaded
and not in ESRF.

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Notes:

1. Discuss with a senior clinician as soon as possible.

2. Monitor serum potassium and glucose frequently (1-2 hourly initially). Monitor blood
glucose for up to 24 hours in those with CKD as insulin effects will last longer than
glucose.)
3. Ensure adequate hydration and blood pressure for optimal renal perfusion Monitor urine
output (must avoid IDC if possible).
4. Determine cause of hyperkalaemia, and treat, including withholding exacerbating drugs
(esp. ACEI/ARB, spironolactone, potassium sparing diuretics, digoxin, NSAID).
5. Insulin and Salbutamol both produce reduce serum K+ 0.5-1.0 mmol/l, and are synergistic.
Both can be repeated as/when the potassium begins to rise again. Salbutamol is less
effective in the face of Beta Blockade.
6. Other therapies:
a. Sodium Bicarbonate is not recommended except in cases of severe acidosis. Discuss
with Critical Care.
b. Resonium (Sodium Polystyrene Sulfonate) is designed to absorb potassium in the gut
and promote excretion. Its effect is small, variable, very slow (days) and associated
with bowel necrosis. It is not recommended in the acute setting.
7. Digoxin toxicity can increase serum potassium, and intracellular calcium. Avoid iv Calcium,
or use with caution by slow infusion (20 min in bag of 5% Dextrose). Consider Digoxin Fab
antidote (Digibind) after d/w Medical Team.

Bibliography
1. Hyperkalemia Revisited, Parham WA, Tex Heart Inst J. 2006; 33(1): 40–47.
2. Guidelines for the treatment of hyperkalaemia in adults. Guidelines and Audit
Implementation Network, Dept of Health Social Services and Public Safety. Northern
Ireland 2014.
3. Up to Date.

Dr Chris Johnstone, Clinical Director Emergency Medicine. August 2018

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