Pseudohypokalemia

• Lab Error

Intracellular Shift of Potasssium

• Albuterol (see Albuterol)
• During Course of Treatment in Diabetic Ketoacidosis (DKA) (see Diabetic Ketoacidosis and Hyperosmolar Hyperglycemic State): intracellular shift of potassium occurs with insulin therapy
• Hypothermia (see Hypothermia)
• Refeeding Syndrome (see Refeeding Syndrome)
  • Physiology: glucose causes insulin release, resulting in increased cellular uptake of magnesium and potassium

Renal Potassium Loss

• Corticosteroids (see Corticosteroids)
• Hyperaldosteronism (see Hyperaldosteronism)
  • Abiraterone (Zytiga) (see Abiraterone): due to mineralocorticoid excess
• Diuretics
  • Bumetanide (Bumex) (see Bumetanide)
  • Ethacrynic Acid (Edecrin) (see Ethacrynic Acid)
  • Furosemide (Lasix) (see Furosemide)
• Leptospirosis (see Leptospirosis)
  • Physiology: outer membrane protein of Leptospira inhibits the Na/K/Cl cotransporter in the thick ascending limb of Henle, causing hypokalemia and renal sodium wasting

Extra-Renal Potassium Loss

• Diarrhea (see Diarrhea)
  • Physiology: xxx

Other

• Afatinib (Gilotrif) (see Afatinib)
• Barium Intoxication (see Barium): in the setting of ingestion, inhalation, or burns
• Ceftaroline (Teflaro, Zinfloro) (see Ceftaroline)
• Hydroxychloroquine Intoxication (see Hydroxychloroquine)
• Sorafenib (Nexavar) (see Sorafenib)

Cardiovascular Manifestations

Arrhythmias

• Prolonged Q-T with Increased Risk of Torsade (see Torsade)
  • Epidemiology
    • Risk of Torsade is Highest in the Setting of Antiarrhythmic Administration

Atrioventricular Heart Blocks

• Clinical
  • First Degree Atrioventricular Block (see First Degree Atrioventricular Block)
  • Second Degree Atrioventricular Block-Mobitz Type I (Wenckebach) (see Second Degree Atrioventricular Block-Mobitz Type I)
  • Second Degree Atrioventricular Block-Mobitz Type II (see Second Degree Atrioventricular Block-Mobitz Type II)
  • Third Degree Atrioventricular Block (see Third Degree Atrioventricular Block)

Electrocardiographic Changes (see Electrocardiogram)

• Clinical
  • Flattened T-Waves
  • S-T Depression
  • U-Waves

Orthostatic Hypotension (see Orthostatic Hypotension)

• Epidemiology
  • XXXXX

Neurologic/Neuromuscular Manifestations

Fatigue (see Fatigue)

• Epidemiology
  • XXXXX

Generalized Weakness (see Weakness)

• Epidemiology
  • XXXXX

Hyporeflexia (see Hyporeflexia)

• Epidemiology
  • XXXXX

Muscle Cramps (see Myalgias)

• Epidemiology
  • XXXXX

Paralysis

• Epidemiology
  • XXXXX

Paresthesias (see Paresthesias)

• Epidemiology
  • XXXXX

Restless Legs

• Epidemiology
  • XXXXX

Rhabdomyolysis (see Rhabdomyolysis)

• Epidemiology
  • XXXXX

Tetany (see Tetany)

• Epidemiology
  • XXXXX

Worsened Hepatic Encephalopathy (see Hepatic Encephalopathy)

• Epidemiology
  • XXXXX

Metabolic Manifestations

Glucose Intolerance (see Hyperglycemia)

• Epidemiology
  • XXXXX

Gastroenterologic Manifestations

Ileus (see Ileus)

• Epidemiology
  • XXXXX

Renal Manifestations

Decreased Glomerular Filtration Rate (GFR)

• Epidemiology
  • XXXX

Metabolic Alkalosis (see Metabolic Alkalosis)

• Epidemiology
  • XXXX

Polyuria (see Polyuria)

• Epidemiology
  • XXXX

Potassium Replacement in Specific Clinical Scenarios

Potassium Replacement in the Setting of Alkalosis/Normal Acid-Base Status

• Preferred Agents(s)
  • Potassium Chloride (KCL) (see Potassium Chloride): max rate of 10 mEq/hr IV through CVC (on monitor)

Potassium Replacement in the Setting of Metabolic Acidosis

• Preferred Agent(s)
  • Potassium Citrate (see Potassium Citrate)
  • Potassium Bicarbonate (see Potassium Bicarbonate)

Potassium Replacement in the Setting of Hyponatremia

• Potassium Replacement is Critical in This Setting, Due to the Role of Potassium in Increasing the Serum Sodium Back Toward Normal
  • See “Complications of Treatment of Hypokalemia” Section Below
  • While Potassium Replacement is a Critical Component of Correcting Hyponatremia, Care Must Be Taken to Correct the Serum Sodium <8 mEq/L Per Day to Avoid the Complication of Osmotic Demyelination Syndrome (ODS) (see Osmotic Demyelination Syndrome)

Complications of Treatment of Hypokalemia

Renal Complications

• Hyponatremia (see Hyponatremia)
  • Potassium is as Osmotically Active as Potassium and Replacing Potassium in the Setting of Hypokalemia Will Increase Serum Osmolality (Am J Kidney Dis, 2010) [MEDLINE]
  • Potassium Movement Intracellularly Increases the Serum Sodium by the Following Mechanisms
    • Intracellular Movement of Potassium Will Result in an Exchange of Sodium into the Extracellular Fluid (to Maintain Intracellular Electroneutrality)
    • Intracellular Movement of Potassium Will Result in an Exchange of Hydrogen Ions into the Extracellular Fluid
      • Hydrogen Ions are Buffered by Extracellular Bicarbonate (and Plasma Proteins), Creating Carbon Dioxide and Water (Bicarbonate is Replaced by Chloride Which was Administered with the Potassium)
    • Intracellular Movement of Potassium Drags Drags Chloride into the Cells, Increasing the Intracellular Osmolality, Which Results in Free Water Movement into Cells
  • Intracellular Movement of Potassium Increases the Intracellular Osmolality, Which Results in Free Water Movement into Cells