Etiology

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Clinical Manifestations

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

• 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)

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

Other

• Orthostatic Hypotension (see Orthostatic Hypotension)

Neurologic Manifestations

• Fatigue (see Fatigue)
• Generalized Weakness (see Weakness)
• Hyporeflexia (see Hyporeflexia)
• Muscle Cramps (see Myalgias)
• Paralysis
• Parasthesias (see Parasthesias)
• Restless Legs
• Rhabdomyolysis (see Rhabdomyolysis)
• Tetany (see Tetany)

Metabolic Manifestations

• Worsened Hepatic Encephalopathy (see Hepatic Encephalopathy)
• Glucose Intolerance (see Hyperglycemia)

Gastroenterologic Manifestations

• Ileus (see Ileus)

Renal Manifestations

• Metabolic Alkalosis (see Metabolic Alkalosis)
• Polyuria (see Polyuria)
• Decreased Glomerular Filtration Rate (GFR)

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Treatment

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

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References

• A patient with severe hyponatremia and hypokalemia: osmotic demyelination following potassium repletion. Am J Kidney Dis. 2010 Apr;55(4):742-8 [MEDLINE]