hyperkalaemia
Table of Contents
hyperkalaemia
see also:
introduction
- 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.
aetiology of true hyperkalaemia
- impaired excretion of potassium:
- 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:
- haemolysis
- severe crush injuries / trauma
- major burns
- internal occult bleeding eg. retroperitoneal haemorrhage, GIT bleed
- transport of potassium out of cells into extracellular fluid:
- 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+
effects of hyperkalaemia
cardiac effects
- 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
ECG changes
- 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:
>5.6mM
- 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;
>6.5mM
- prolonged PR & QTc associated with slowing of Vmax
> 8.0mM
- absent P waves, wide QRS with LAD & merging S & T waves
- may look like “slow AF”
> 9.0mM
- sine waves/ slow idioventricular rhythm followed by ventricular fibrillation (VF) or classically choking / respiratory arrest / cardiac arrest / BLS / ALS / CPR
neurologic effects
- neuromuscular symptoms most common complaints - esp. ascending weakness
emergency Mx of hyperkalaemia
- 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
immediate reversal of membrane abnormalities if wide QRS or loss of P waves
- 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
restore transcellular gradient if ECG abnormalities
- in dialysis patients, immediate dialysis in a cardiac monitored area (ICU or ED) is preferable to driving K into cells as this then reduces the effectiveness of dialysis in removing K+ resulting in rebound hyperkalaemia after dialysis
- if K > 7mM or wide QRS or loss of P waves, it is probably worth starting insulin/dextrose whilst awaiting dialysis, particularly if there is delay
- 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
remove K from body if increased total body K:
- 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
with-hold drugs and foods which increase hyperkalaemia
- consider ceasing, with-holding and/or reducing dose of these medications (see medications which may cause or contribute to hyperkalaemia)
- potassium sparing diuretics such as spironolactone
- potassium supplements
- 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
consider long term potassium losing agents
- 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
monitor progress
- 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.
hyperkalaemia.txt · Last modified: 2023/02/12 02:11 by wh