see also:

• potassium physiology
• hypokalaemia
• rhabdomyolysis
• UK Newcastle Mx flow chart (pdf)
• Life in the fast lane - hyperkalaemia
• medications which may cause or contribute to hyperkalaemia

• hyperkalaemia¹⁾ is a potentially life-threatening emergency, but first one should ensure that the lab result is not a spuriously high result from post-venesection haemolysis of the blood specimen - if there is no ECG evidence, and no obvious reason for it, check the potassium level again ASAP.
• serum potassium may also appear to be elevated due to thrombocytosis or leukocytosis.

• impaired excretion of potassium:
  • acute kidney injury (AKI) / acute renal failure (ARF) / dehydration
  • chronic renal failure
  • potassium-sparing diuretics, especially with ACE inhibitors
  • decreased sodium delivery to distal tubule (contributory but rarely sole cause) eg. congestive cardiac failure, hyponatraemia
• release from cells through cell necrosis:
  • rhabdomyolysis
  • haemolysis
  • severe crush injuries / trauma
  • major burns
  • internal occult bleeding eg. retroperitoneal haemorrhage, GIT bleed
• transport of potassium out of cells into extracellular fluid:
  • digoxin toxicity
  • suxamethonium
  • severe metabolic acidosis (eg. diabetic ketoacidosis (DKA)
  • hyperosmolality
  • hypoaldosteronism (Addison's disease)
  • periodic hyperkalaemic paralysis
• excess potassium load:
  • potassium supplementation
  • blood transfusions
  • crystalline penicillin (1 million units = 1.7 mmol K⁺
• medications which may cause or contribute to hyperkalaemia

• decreased resting membrane potential → increased automaticity
• inactivation of the fast Na channels preventing action potential development
• hypocalcaemia tends to exacerbate the cardiac effects of hyperkalaemia
• NB. the anecdotal value of calcium in pulseless electrical activity (PEA) may be related to its electrophysiological antagonism of K, in a situation where there is intracardiac hyperkalaemia associated with an acidotic milieu

• see also basics of the ECG
• see ECG images at emedicine
• only 50-60% of patients with hyperkalaemia > 6.5mM have ECG changes suggestive of hyperkalaemia - do NOT rely on the ECG to diagnose it!
• actual ECG effects vary with patients but generally the effects as related to serum level are:

• narrow peaked T (V2-4) & shortening of QTc assoc. with early repolarisation
• decreased intraventricular conduction ⇒ LBBB usually
• if peaked T's → Rx immediately otherwise can usually treat over a few hrs;

• prolonged PR & QTc associated with slowing of Vmax

• absent P waves, wide QRS with LAD & merging S & T waves
• may look like “slow AF”
• see https://lifeinthefastlane.com/ecg-library/100-ecgs/quiz-ecg-003/

• sine waves/ slow idioventricular rhythm followed by ventricular fibrillation (VF) or classically choking / respiratory arrest / cardiac arrest / BLS / ALS / CPR

• neuromuscular symptoms most common complaints - esp. ascending weakness

• at risk of cardiac arrhythmias even if no ECG changes
• oxygen if hypoxic
• cardiac monitor if K+ > 5.6mM or ECG changes
• iv access
• if life-threatening cardiac arrhythmia or severe ECG changes of acute hyperkalaemia, then commence immediate Rx with IV calcium gluconate as per below
• determine cause and Rx
  • if dialysis patient who missed dialysis:
    • arrange emergent dialysis
    • if wide QRS or loss of p waves start insulin/dextrose as below whilst arranging dialysis and consider iv calcium
  • if in urinary retention, place IDC
  • if digoxin overdose then Mx with Fab Ab's +/- magnesium - see digoxin toxicity rather than Mx as below.
  • if Addisonian crisis Rx with corticosteroids

• 1g calcium gluconate 10% 10ml over 3-5min
  • effect only lasts 30-50min;
  • avoid if rhabdomyolysis as risk of increased necrosis
  • can repeat dose once if no resolution of hyperkalaemic ECG changes - are they really due to the hyperkalaemia?
  • controversial: perhaps infusion of calcium may provide longer lasting protection whilst waiting for other measures to work?
  • if digoxin toxicity, stat calcium is traditionally C/I (although detrimental effects may be more theoretical than actual) thus use:
    • slower iv infusion calcium gluconate:
      • add 10ml 10% calcium gluconate to 100mL 5% dextrose and infuse over 20-30 minutes to avoid transient hypercalcaemia and worsening digoxin toxicity
    • digoxin Fab Ab's is the preferred Rx if digoxin OD and K > 5.0 in adults or > 6.0 in children
• 3% hypertonic saline if also hyponatraemic:
  • don't use if not hyponatraemic

• insulin/dextrose infusion over 1hr:
  • only give insulin-dextrose if blood glucose > 4mMol/L
  • avoid insulin if hyperkalaemia is due to adrenal insufficiency, use corticosteroid replacement instead
  • dose:
    • 50% glucose 50ml with 10 units short acting insulin as a IV bolus, or,
    • 25% glucose 100ml & 10 units short acting insulin infusion over 5 minutes which is less irritant, or
    • 10% glucose 250mL IV with 10 units short acting insulin over 15 minutes
  • onset of action 10-30min, duration of hypokalaemic effect 4-6hr
  • lowers serum K⁺ by 0.5-1.2mM
  • watch for hypoglycaemia as 25g dextrose may not be sufficient to prevent hypoglycaemia at 1hr post 10 units regular insulin
    • if hypoglycaemia after initial insulin-dextrose Rx consider starting glucose 10% IV infusion at 75 to 100 mL/hour
  • if blood glucose > 15mM then either:
    • can use 10% dextrose rather than the more irritating 25% or 50% solutions, or,
    • no dextrose but monitor glucose level every 30min
  • avoid if heat stroke as potential liver damage creates risk of hypoglycaemia
• consider adjunctive sodium bicarbonate infusion if metabolic acidosis
  • avoid if cannot tolerate 1L fluid load
  • main utility is as an adjunct in the patient with metabolic acidosis as a prolonged infusion:
    • 150mEq NaHCO3 in 1L 5% dextrose infused over 2-4hrs
    • this may drop serum K by 0.6mM and raise serum bicarb by about 10mM at 4hrs
  • NB. the traditional 8.4% NaHCO3 1ml/kg over 5min may cause dangerous hypernatraemia and does not appear to be beneficial although traditionally said to have onset 5-10min and lasting 1-2hr
• NB. nebulised salbutamol is no longer a favored treatment²⁾
  • 10-20mg salbutamol in 4mls NSaline nebulised
  • onset of action 15-30min, peak at 90min, duration 2-6hrs
  • lowers serum K⁺ by 0.9-1.14mM
  • quicker initiation than insulin Rx and additive effects to insulin Rx
  • may cause tachycardia/tremor ⇒ avoid in those with acute coronary syndrome
  • never use as sole Rx for patients already taking beta adrenergic blockers
  • 20-40% of dialysis patients may be resistant to effects of beta 2 adrenergic agonists

• NB. above Rx will only be temporary unless measures are made to remove the excess K+ and stop further K+ administration
• diuresis of 1L
  • will remove 20-30mmol K within ~15min if patient has normal renal function and does not have impaired renal potassium secretion
  • eg. frusemide / furosemide / Lasix 20-80mg + consider IDC if concern of urinary retention
  • if not fluid overloaded, also give iv 0.9% saline to maintain fluid volume
• consider resonium although little to support its use
  • orally 15g tds or rectally
    • onset 1-2hr, effect lasts 4-6hr, each 1g is said to remove 1mEq K+ however recent studies failed to show benefit in [K+] levels at 4,8 and 12hrs
    • give with lactulose to reduce risk of constipation which will exacerbate the issue
  • avoid if sensitive to sodium administration - can use a calcium polystyrene sulfonate instead
  • may not be effective as unproven despite being used since 1961, and does have a small risk of colonic necrosis ³⁾
  • do not give once K+ levels fall below 5mmol/L
• consider dialysis if acute kidney injury (AKI) / acute renal failure (ARF), chronic renal failure or severe rhabdomyolysis
  • haemodialysis is preferred to peritoneal dialysis as the rate of potassium removal is many times faster
  • haemodialysis can remove 25-50 meq of potassium per hour as long as K+ has NOT been driven into cells before dialysis
  • may require dialysis in cases of large potassium loads such as severe rhabdomyolysis
  • all patients will have a post-dialysis rebound as K shifts back into serum
    • there is thus little point of measuring K+ immediately post dialysis, but one should wait a few hours at least
    • this can be severe if K+ had been driven into cells before dialysis and require a second dialysis session

• consider ceasing, with-holding and/or reducing dose of these medications (see medications which may cause or contribute to hyperkalaemia)
• ACE inhibitors
• potassium sparing diuretics such as spironolactone
• potassium supplements
• digoxin
• non-steroidal anti-inflammatory drugs (NSAIDs)
• non-selective beta adrenergic blockers such as propranolol
• avoid fasting as this can raise K+ by 0.6mM
• avoid foods high in potassium:
  • whole grains, beans
  • sports drinks
  • soy milk and dairy products
  • peanut butter, nuts, seeds, chocolate, molasses
  • many fruits such as bananas, apricots, avocados, coconut, melons, citrus, prunes, dates, etc
  • most vegetables - peel, then slice and soak in water overnight to reduce K content
  • fish, ground beef
  • “salt-free” soups
  • salt substitutes

• may be useful as adjunct to low potassium diet, particularly in those needing ACE inhibitors and who have reasonable renal function
• potassium losing diuretics
• potassium GIT excreting agents:
  • resonium - cation exchange resin
  • patiromer- a nonabsorbable organic polymer binds potassium in the colon in exchange for calcium
  • zirconium cyclosilicate - exchanges both sodium and hydrogen ions for potassium throughout its intestinal transit

• cardiac monitor until K+ below 5.6mM
• blood glucose hourly for 6hrs
• serum K levels at 1,2,6 and 12hrs post Rx
• repeat above steps if K levels not adequately returned to normal and call renal team for ? dialysis if Rx failing or C/I.