Definition: A serum potassium level > 5.5 mEq/L


  • Common electrolyte disorder
  • 10% of hospitalized patients (Elliott 2010)


  • Pseudohyperkalemia: extravascular hemolysis
  • Renal failure (potassium is primarily eliminated by the kidneys)
  • Acidosis
  • Massive cell death (tumor lysis syndrome, rhabdomyolysis, burns, crush injuries, hemolysis)
  • Drugs: ACEI, ARBs, Spironalactone, NSAIDs, Succinycholine

Clinical Manifestations

  • Mild hyperkalemia often asymptomatic
  • Cardiac Effects
    • Increased potassium raises the resting membrane potential of cardiac myocytes
    • Slows ventricular conduction
    • Decreases length of action potential
    • Increases cardiac myocyte excitability
    • Cardiac effects can manifest in lethal dysrhythmias
  • Neuromuscular Effects
    • Paresthesias
    • Weakness
    • Flaccid paralysis
    • Depressed or absent deep tendon reflexes


  • Suspect hyperkalemia in ALL patients with renal impairment, especially end-stage renal disease (ESRD)
  • Serum potassium
    • Can be artificially elevated by extravascular hemolysis
    • Blood gas results may differ from standard metabolic panels by up to 0.5mmol/L
  • 12-Lead EKG
    • Screening test that can rapidly detect severe cardiac manifestations of hyperkalemia
    • A normal EKG with a significant serum potassium elevation should raise concerns for spurious results (extravascular hemolysis)
    • Sensitivity of EKG to detect hyperkalemia is poor (Wrenn 1991, Aslam 2002, Montague 2008)
    • Classic EKG Findings
      EKG Changes - LITFL

      EKG Changes – LITFLClassic EKG findings

      • PR prolongation
      • Peaked T waves
      • Loss of P waves
      • Widening of QRS complex
      • Sine wave
      • Ventricular Fibrillation
      • Asystole
    • Note: Hyperkalemia can present with a number of “non-classic” EKG findings including AV blocks and sinus bradycardia (Mattu 2000)
    • Note: Hyperkalemic EKG changes do not necessarily occur in order (i.e. patients can jump from peaked T waves to sine wave)


Basics: ABCs, IV, O2, Cardiac Monitor and, 12-lead EKG

  • Identify + treat underlying cause of hyperkalemia (i.e. rhabdomyolysis -> hydration)
  • Remove inciting factors (i.e. stop ACEI, NSAIDs etc)

Asymptomatic Patients without EKG Changes

  • Eliminate potassium from the body
    • Sodium Polystyrene (Kayexalate) no proven efficacy
    • Enhance renal elimination
      • Intravenous hydration if volume depleted
      • Consider potassium wasting loop diuretics (i.e. furosemide)
    • Dialysis for anuric patients (i.e. ESRD)

Symptomatic Patients or Significant EKG Changes

  • Stabilize cardiac myocytes with calcium salts
    • Mechanism: Recreates the electrical gradient leading to rapid reversal of cardiac effects and rapid stabilization
    • Two Options: CaGluconate, CaCl2
    • Onset of action: seconds to minutes
    • Duration: 20-30 minutes
  • Shift potassium into intracellular space (temporary)
    • Insulin
      • Mechanism: Activation of the Na-K-ATPase
      • Dose: 10 units IV (higher doses quoted but little literature to backup any dose)
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Give with dextrose (0.5 – 1 g/kg) unless hyperglycemia present
      • Caution: Duration of action of insulin may outlast administered dextrose. Be vigilant for hypoglycemia
    • Beta-adrenoreceptor agonists (i.e. albuterol)
      • Mechanism: Activation of beta receptors
      • Dose: 10-20 mg inhaled (4-8 standard ampules)
      • Onset of Action: < 15 min
      • Effect: Lowers potassium by about 0.6 mmol
      • Duration of action: 30-60 min
      • Additive effect with insulin (Allon 1990)
      • Note: Unlikely to have effect in patients taking beta-adrenoreceptor blocker medications
    • Sodium Bicarbonate (NaHCO3)
    • Eliminate potassium from the body (see above)

Asymptomatic Patients with Minor EKG Changes

  • Minimal recommendations on managing this clinical entity
  • Eliminate potassium from the body (see above)
  • Consider calcium salt administration: patients can rapidly progress through EKG changes and calcium administration may prevent this from occurring. However, the effects of calcium are temporary and offer no long-term protection
  • Consider medications to shift potassium intracellularly while waiting for elimination

Take Home Points

  • Always obtain an EKG in patients with ESRD upon presentation
  • Always obtain an EKG in patients with hyperkalemia as pseudohyperkalemia is the number one cause
  • If the patient with hyperkalemia is unstable or has significant EKG changes (wide QRS, sine wave) rapidly administer calcium salts
  • In patients who are anuric, early mobilization of dialysis resources is critical

Read More

EMCrit Podcast 32 – Treatment of Severe Hyperkalemia


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  • Wrenn K et al. The ability of physicians to predict hyperkalemia from the ECG. Ann Emerg Med 1991; 20(11): 1229-32. PMID: 1952310
  • Aslam S et al. Electrocardiography is unreliable in detecting potentially lethal hyperkalaemia in hemodialysis patients. Nephrol Dial Transplant 2002; 17: 1639-42. PMID: 12198216
  • Montague BT et al. Retrospective review of the frequency of ECG changes in hyperkalemia. Clin J Am Soc Nephrol 2008; 3:324–330. PMID: 18235147
  • Mattu A et al. Electrocardiographic manifestations of hyperkalemia. Am J Emerg Med 2000; 18: 721-9. PMID: 11043630
  • Allon M, Copkney C. Albuterol and insulin for treatment of hyperkalemia in hemodialysis patients. Kidney Int 1990; 38:869–872. PMID: 2266671
  • Weisberg LS. Management of hyperkalemia. Crit Care Med 2008; 36: 3246-51. PMID: 18936701