Description

• An electrolyte disorder defined as a plasma potassium (K) concentration >5.5 mEq/L (>5 mmol/L)
• Hyperkalemia depresses cardiac conduction and can lead to fatal arrhythmias.
• Normal K regulation involves tightly coordinated mechanisms:
  • After ingestion, K enters the portal circulation, stimulating pancreatic insulin release, which promotes entry of K into cells.
  • In the kidneys, K stimulates renin release from juxtaglomerular cells, activating the renin-angiotensin-aldosterone system (RAAS). Angiotensin II in the lungs stimulates aldosterone secretion from the adrenal zona glomerulosa. Aldosterone acts on the renal collecting ducts to enhance K excretion and sodium reabsorption.
• Four major causes
  • Increased load: either endogenous from tissue breakdown (i.e., rhabdomyolysis or hemolysis) or exogenous (dietary or iatrogenic), usually in association with impaired renal function due to chronic kidney disease (CKD)
  • Decreased excretion (most common): due to reduced glomerular filtration rate or impaired aldosterone secretion
  • Cellular redistribution: shifts from intracellular space (majority of K is intracellular) to extracellular space (as in metabolic acidosis, tissue injury)
  • Pseudohyperkalemia: artificial elevation of K due to hemolysis of blood sample, thrombocytosis, or leukocytosis

Geriatric Considerations
Increased risk for hyperkalemia because of decline in renin and aldosterone production with age, which impairs renal K excretion, especially in the setting of comorbid conditions

Epidemiology

Etiology and Pathophysiology

• Impaired K excretion (most common)
  • Renal insufficiency/failure, obstructive uropathy
  • Addison disease
  • Mineralocorticoid deficiency
  • Type IV renal tubular acidosis
  • Cirrhosis
  • Congestive heart failure
  • Sickle cell disease
  • Amyloidosis
  • Systemic lupus erythematosus
• Increased K intake (2)
  • Bananas, potatoes, melons, citrus juice, avocados, red meat, nuts, and dried fruits
  • Salt substitutes given to CKD patients
• Transcellular shift (redistribution)
  • Metabolic acidosis
  • Insulin deficiency
  • Hyperglycemia (diabetic ketoacidosis or hyperosmolar hyperglycemic state)
  • Tissue damage (rhabdomyolysis, tumor lysis syndrome, burns, trauma)
• Medication-induced (3)
  • RAAS inhibitors
  • K-sparing diuretics
  • NSAIDs
  • Heparin
  • Trimethoprim
  • β-Blockers
• Pseudohyperkalemia
  • Hemolysis of blood sample (artifactual)
  • Thrombolysis, thrombocytosis, leukocytosis
  • Hereditary spherocytosis
  • Infectious mononucleosis
  • Familial pseudohyperkalemia

Risk Factors

• Impaired renal excretion of K
• Acidemia
• Massive cell breakdown (rhabdomyolysis, burns, trauma)
• Use of K-sparing diuretics
• Excess K supplementation
• Comorbid conditions: CKD, diabetes, heart failure, liver disease

General Prevention

Low K diet and oral supplement compliance in those at risk

Commonly Associated Conditions

• Acute kidney injury (AKI) or CKD, typically with GFR <30 mL/min
• Congestive heart failure; myocardial infarction
• Rhabdomyolysis
• Liver disease
• Use of offending medications