Harvey's Garden

Hyperkalemia

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Epidemiology

Etiology

  • Potassium excess: due to altered K+ metabolism or intake
    • Reduced excretion: acute and chronic kidney disease
    • Endocrine causes: hypocortisolism, hypoaldosteronism
    • Drugs: potassium-sparing diuretics, ACE inhibitors, angiotensin receptor blockers, NSAIDs, and trimethoprim-sulfamethoxazole
      • Especially in HIV patients who are taking high-dose TMP-SMX
      • Similar to the actions of amiloride, trimethoprim blocks the epithelial sodium channel in the distal tubule and collecting duct. This reduces transepithelial voltage and impairs sodium-potassium exchange, leading to reduced potassium excretion and hyperkalemia.
    • Type IV renal tubular acidosis
    • Increased intake
      • High potassium diet, e.g., fresh fruits, dried fruits and legumes, vegetables, nuts, seeds, bran products, milk, and dairy products
      • K+ containing IV fluids
  • Extracellular shift
  • Extracellular release

Pathophysiology

Clinical features

Diagnostics

Treatment

  • Scenario A: “Unstable” (ECG changes, palpitations, or severe K+ > 6.5-7.0)
    1. Membrane Stabilization: IV Calcium Gluconate (or Calcium Chloride). c
      • Logic: Protects the heart from arrhythmia. Does NOT lower K+. Immediate onset.
    2. Intracellular Shift (Temporizing):
      • Insulin (Regular) + Dextrose (D50): Most reliable shifter.
      • Inhaled Beta-agonists (Albuterol): High dose required.
      • Sodium Bicarbonate: Only if acidosis is present.
  • Scenario B: “Stable” (No ECG changes, moderate elevation)
    • Eliminate K+ from the body (Definitive Management).
    • Loop Diuretics (Furosemide): If kidneys make urine.
    • K+ Binders (Patiromer, Zirconium Cyclosilicate, Sodium Polystyrene Sulfonate): Slow onset (hours/days).
  • Scenario C: Renal Failure/ESRD:
    • Hemodialysis: The definitive treatment for symptomatic hyperkalemia in dialysis patients.

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