Hyperkalaemia

Serum potassium level >5.2mmol/L, classified by magnitude into:

Epidemiology and Risk Factors

Pathophysiology

Aetiology

Causes include:

  • ↑ Potassium intake
    • Oral supplementation
    • IV solutions
  • Redistribution
    • Cellular injury
      • Rhabdomyolysis
      • Tumour lysis syndrome
      • Burns
      • Haemolysis
      • Hyperthermia
    • Acidosis
      Intracellular buffering via H+/K+ exchange.
    • Drugs
      • Suxamethonium
      • β-blockade
  • ↓ Potassium elimination
    • Renal failure
    • Hypoaldosteronism
      • Addison’s disease
    • Drugs
      • Aldosterone inhibition
        • A2RB/
        • Spironolactone
        • β-blockade
  • Factitious
    • Haemolysed sample
      • Long tourniquet time
      • Delay to testing
      • Aggressive aspiration
    • Leucocytosis

Clinical Features

Assessment

History

Exam

Investigations

Bedside:

Laboratory:

Imaging:

Other:

  • ECG
    • Bradyarrhythmias
    • P wave flattening
    • AV nodal blockade
      • PR prolongation
      • CHB with ventricular escape rhythms
    • Bundle branch/fascicular blocks
    • QRS widening
      Progressively, trending towards a “sinusoidal” trace.
    • Peaked T waves
ECG Changes by Potassium level
Potassium level (mmol/L) Abnormality
5.5-6.5
  • Peaked T waves
6.5-7.0
  • P wave changes
  • 1st degree heart block
7.0-9.0
  • Sinus bradycardia
  • CHB with escape rhythms

9.0
  • Arrest

These ECG changes are a guide, patients do not always progress through all stages - a hyperkalaemic arrest can occur from a reasonably normal ECG. Conversely, patients with chronic hyperkalaemia (e.g. ESRD) may display a normal ECG despite a high serum potassium level.

Diagnostic Approach and DDx

Management

Goals of management

Resuscitation:

Specific therapy:

  • Pharmacological
  • Procedural
  • Physical

Supportive care:

Disposition:

Preventative:

Marginal and Ineffective Therapies

Anaesthetic Considerations

Complications

Prognosis

Key Studies

References