Created on Fri, 03/25/2016 - 20:15
Last updated on Tue, 12/19/2017 - 14:20

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Hyperkalemia in the CICM SAQs has never appeared as a stand-alone question; rather it has been asked about in the context of characteristic ECG changes, with the "how would you manage" as a part 2 of an already low-yield question. A good example of these is Question 15.2  from the second paper of 2017, where identifying the ECG abnormality earned the candidate a pitiful 1.0 marks (10% of a 10-mark SAQ).

Oh's Manual offers a bare minimum of information on this topic. For those willing to dig deeper, Lawrence S. Weisberg's 2008 article ("Management of severe hyperkalemia") offers the desirable balance of brevity and detail. It was the most important resource used in the making of this summary, and unless otherwise stated is the reference for everything stated therein.

Diagnosis of hyperkalemia

Oh's Box 93.6 (page 956) sorts the causes of hyperkalemia according to their underlying physiological disturbance.

Causes of Hyperkalemia

Artifactual and spurious

  • Delay in separating RBCs
  • Haemolysis
  • High platelet count

Excessive potassium intake

  • Blood transfusion
  • Iatrogenic (eg. infusion)

Uncontrolled release of intracellular stores

  • Burns
  • Trauma
  • Rhabdomyolysis
  • Tumour lysis

Decreased excretion

  • Mineralocorticoid-blocking drugs
    • Spironolactone
    • Amiloride
    • ACE-inhibitors
    • NSAIDs
  • Hypoadrenalism
  • Renal failure

Compartment shift

  • Acidosis
  • Insulin deficiency
  • Digoxin overdose
  • Suxamethonium used for induction
  • Arginine hydrochloride
  • Hyperkalemic periodic paralysis
  • Fluoride toxicity

Clinical Features of Hyperkalemia

History and examination findings

Neurological effects

  • Paraesthesia
  • Weakness and flaccid paralysis (diaphragm is usually spared)
  • Loss of reflexes
  • Normal cranial nerves
  • Normal sensory function

Cardiovascular effects

  • Hypotension
  • Bradycardia

Biochemical abnormalities

  • Normal anion gap metabolic acidosis (due to decreased renal ammoniagenesis)

ECG changes

  • "Peaked" T-waves
  • Flattened P-waves
  • Widened QRS complex
  • Deep S-waves
  • Eventually, merging of S and T waves
  • Trend towards sine-wave at K+ over 7mmol/L

Management of hyperkalemia

The recommendations offered in Oh's Manual resemble the updated 2015 AHA guidelines. There are slightly different recommendations made in the Weisberg article. These have been blended into the list offered below:

Stabilize myocardial cell membrane:

  • Calcium chloride (10%): 6.8 mmol (10ml) over 2-5 minutes
  • Hypertonic saline (3%): apparently, this has been show to reverse the ECG changes of hyperkalemia, only when there is concurrent hyponatremia.

 Shift potassium into cells:

  • Sodium bicarbonate: 50-100mmol/L, over 5 minutes
  • 50ml of 50% dextrose with 10 units of Actrapid insulin
  • Salbutamol: 2-4 ×salbutamol nebs (5mg each)

Promote potassium excretion:

  • Frusemide 40 to 80 mg IV
  • Cation-exchange resin: AHA recommend "kayexelate", which is the same sodium polystyrene sulfonate which is marketed as "Resonium" in Australia.
    "15 to 50 g per oral or per rectum" is recommended in the AHA text, along with sorbitol (to promote rapid transit, one assumes). Oh's Manual suggests a flat dose of 50g, and does not mention sorbitol.
  • Dialysis is ultimately the most effective clearance mechanism



Lavonas, Eric J., et al. "Part 10: Special Circumstances of Resuscitation 2015 American Heart Association Guidelines Update for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care." Circulation 132.18 suppl 2 (2015): S501-S518.

Weisberg, Lawrence S. "Management of severe hyperkalemia." Critical care medicine 36.12 (2008): 3246-3251.