REBEL Core Cast 125.0 – Hyperkalemia

REBEL Core Cast 125.0 – Hyperkalemia

Definition: A serum potassium level > 5.5 mmol/L

Epidemiology

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

Causes

• 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

Diagnosis

• 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
    • 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)

Management

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
  • Binding agents (SPS, Sodium zirconium cyclosilicate etc)
  • 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
    • No difference in time to onset (1^st pass metabolism is a myth)
    • Dose: 1 ampule CaCl₂ (270 mg Ca²⁺) = 3 ampules CaGluconate (90 mg Ca^2+/ampule)
  • Onset of action: seconds to minutes
  • Duration: 20-30 minutes
• Shift potassium into intracellular space (temporary)
  • Insulin (Moussavi 2021)
    • Mechanism: Activation of the Na-K-ATPase
    • Dose: 5-10 units IV
    • 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)
    • Evidence for the efficacy of NaHCO3 to lower serum potassium is scant and contradictory (Elliott 2010, Weisberg 2008)
• 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

References

Elliott MJ et al. Management of patients with acute hyperkalemia. CMAJ 2010; 182(15): 1631-5. PMID: 20855477

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

Moussavi K et al. Reduced alternative insulin dosing in hyperkalemia: a meta-analysis of effects on hypoglycemia and potassium reduction. Pharmacotherapy 2021; 41(7): 598-607. PMID: 33993515

Post Peer Reviewed By: Salim R. Rezaie, MD (Twitter/X: @srrezaie)