Related topics:
ACE inhibitors, ARBs, aldosterone antagonists (spironolactone)
Pseudohypoaldosteronism or true hypoaldosteronism
Congenital adrenal hyperplasia
Kidney failure
Generally occurs in setting of comorbid disorder (e.g., kidney insufficiency) as kidney can usually handle large potassium load
IV fluids
Hyperalimentation
PRBC transfusions
High-potassium foods, drugs, nutritional supplements
Acidosis
Hemolysis, tumor lysis, rhabdomyolysis (e.g., burn injury)
Hypoinsulinemia, diabetic ketoacidosis
β-blockers
Hemolysis
Capillary stick (finger/heel stick) technique
Specimen sitting for too long before testing
Shaking test tube, transporting in pneumatic tube
Usually asymptomatic
Muscle weakness, paralysis
EKG changes
Shortened QT interval
Widened PR interval
Widened QRS
Cardiac arrhythmia (ventricular fibrillation, asystole)
Ensure quality specimen (ideally venipuncture)
EKG to evaluate for electrocardiographic changes
Transtubular potassium gradient (TTKG) if concern for kidney potassium retention
Should be >7 if hyperkalemic; low value suggests hypoaldosteronism
Treat underlying cause
Stabilize:
Calcium
Insulin + glucose: shift potassium intracellularly by stimulating Na⁺/K⁺-ATPase
β-agonists (e.g., albuterol, epinephrine): shift potassium intracellularly by stimulating Na⁺/K⁺-ATPase
Sodium bicarbonate (NaHCO₃): stimulates release of H⁺ from cells in exchange for K⁺ via H⁺-K⁺ exchanger to maintain electroneutrality
Remove excess potassium (definitive therapy):
Diuretics
Thiazide diuretics
Loop diuretics
Sodium polystyrene sulfonate (SPS, Kayexalate®)
Ion exchange resin - exchanges Na⁺ for K⁺
Large sodium load, can cause hypernatremia
In vivo, 1 g of SPS delivers ~33 mg (1.4 mEq) Na⁺ and binds ~1 mEq of K⁺
Given orally or rectally
Risk of bowel obstruction, perforation or necrosis
Dialysis
Treatment of choice for severe, life-threatening hyperkalemia
[AMA formatted citations]
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