hypokalaemia

see also:

• potassium physiology
• Life in the fast lane - Mx of hypokalaemia
• Western Health procedure: Potassium chloride infusion

• redistribution of K⁺ into cells:
  • beta 2 adrenergic receptor activation (eg. salbutamol)
  • aldosterone - lowers slope of linear relationship of [K⁺]serum vs total body K
  • periodic hypokalaemic¹⁾ paralysis
  • metabolic alkalosis - for each increase in pH by 0.1 ⇒ serum [K⁺] decreases by ~0.6 (artificially low)
  • insulin - rarely a cause in practice
• decreased total body potassium levels:
  • 24hr urine potassium excretion (when good urine output) can help determine whether it is renal loss or otherwise:
    • < 20mmol/day excreted in adults suggests inadequate potassium intake or GIT losses such as diarrhoea or vomiting
    • >20mmol/day excreted in adults suggests renal losses:
      • most commonly, potassium losing diuretics such as loop diuretics, thiazides or osmotic diuretics (including glycosuria in diabetic ketoacidosis (DKA))
      • rarely can be caused by aciclovir nephrotoxicity
      • other causes include:
        • renal tubular acidosis
        • hyperaldosteronism - primary or secondary
        • licorice
        • excessive glucocorticosteroids
        • Liddle's syndrome (extremely rare genetic disorder):
          • hyporeninaemic hypoaldosteronism, hypertension, hypokalaemia and enhanced erythrocyte sodium influx
        • toxic serum levels of lysozyme (LYZ) as in some cancers (also causes renal impairment)

• neuromuscular symptoms most common
  • may be masked by hypocalcaemia
• cardiac:
  • ECG effects:
    • rounded T ⇒ low voltage T ⇒ ST decreased & U increased ⇒ SV ectopics ⇒ ventricular tachycardia (VT)/ventricular fibrillation (VF);
    • NB. similar ECG to hypocalcaemia as flat T + U may look like prolonged QTc!!!
    • see also: https://lifeinthefastlane.com/ecg-library/100-ecgs/quiz-ecg-006/

• consider if it could be redistribution of K+ into cells which is caused by overactive Na-K ATPase pump, thus manage this rather than giving more K⁺ as this risks rebound hyperkalaemia.
  • examples of redistributive causes of hypokalaemia include:
    • salbutamol nebuliser therapy (or other beta 2 adrenergic agonists)
    • metabolic alkalosis - see potassium physiology for calculation to adjust [K⁺] for pH
    • if Asian male with weakness, consider thyrotoxic hypokalaemic periodic paralysis (TPP) 
      • Rx is beta blockers rather than K+ supplementation.
• Rx any coexisting hypocalcaemia while treating the hypokalaemia
• if decreased total body K rather than just redistributive:
  • ⇒ IV KCl < 0.5mEq/kg/hr to max. 20mEq/hr (usually 10mmol/hr in adults unless circumstances dictate higher rates and monitoring is used)
    • unless very high on-going K loss rates demands higher replacement rates & max. infusion concentration 40-60mEq/L;

• normal range for K+ is 3.5 to 5.5 mmol/L.
• in certain circumstances, the minimum level is raised to 4.0mmol/L, for the following reasons:
  • hypokalaemia promotes electro-physiological instability. Significant complications include neuromuscular and cardiac dysrhythmia dysfunction (especially in patients on digoxin).

• cardiac monitor if severely hypokalaemic, high risk patients or those requiring infusion rates of KCl > 10mmol/hr
• maintain K+ > 4.0 mmol/l
• 6 hourly Serum K+ levels minimum. (2 hourly in diabetic ketoacidosis (DKA), etc.)
• Western Health procedure: Potassium chloride infusion
  • KCl ampoules are NOT to be used except in ICU
  • the only pre-mixed high concentration KCl infusion solution in WH is 100ml 0.29% saline with 10mmol KCl (= 0.75% = 0.75g)
  • other pre-mixed solutions each with 30mmol KCl (= 0.224% = 2.24g) in 1L include:
    • 0.9% saline
    • 0.18% saline with 4% glucose
    • 5% glucose
    • Hartmann's solution (modified)

• other keywords: hypokalemia