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hyperkalaemia

hyperkalaemia

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

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 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

> 9.0mM

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
    • 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 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

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