Potassium

Question 1

Clinical features of hypokalaemia?

Answer 1

• Muscle weakness
  
  • Hypotonia (Flaccid paralysis)
  • Cramps
• Cardiac arrhythmia
• Polyuria & Polydipsia (Nephrogenic DI)

Question 2

ECG features of hypokalaemia?

Answer 2

1. Prolonged PR interval
2. Small/absent/inverted T wave
3. U wave
4. ST depression

Question 3

Causes of hypokalaemia in general?

Answer 3

Increased excretion
Increased cellular influx
Reduced intake

Question 4

Causes of increased potassium loss?

Answer 4

1. Redistribution into cells
2. GI loss
   
   • D+V
   • High output stoma
3. Renal loss
   
   • Loop + Thiazide Diuretics
     
     • Prevents Na+ resorption upstream of principle cells, so more Na+ influx into principle cells -> increased Na/K pump activity -> more K+ efflux into urine
     • Also more water in lumen, so lower K+ conc. in lumen -> more K+ efflux
   • Hyperaldosteronism - aldosterone increases K+ excretion in principle cells
     
     • Conn’s (Primary hyperaldosteronism)
     • Compensated HF
     • Cirrhosis
   • Congenital
     
     • ​Bartter and Gitelman syndromes -> deficiency of Na+ reuptake channels so prevents Na+ resorption upstream of principle cells -> more K+ excreted in exchange for Na+ influx

Rare causes: Renal tubular acidosis type 1&2, Hypomagnesaemia

Question 5

Causes of increased redistribution of K+ into cells?

Answer 5

• Stimulation of Na+/K+ ATPase pump (3Na+ OUT, 2K+ IN)
  
  • Insulin
  • Beta-2 agonists (salbutamol)
• Alpha antagonists
  
  • Alpha receptors stimulate Calcium-dependent K+ channels which pump K+ OUT of cells into blood
  • Blocking these will prevent efflux of K+, and hence increase intracellular K+
• Refeeding syndrome
• Metabolic alkalosis:
  
  • H+ ions leave cells to correct alkalosis
  • In exchange K+ enters cells, leading to less K+ in blood

Question 6

What happens to body in terms of acid-base?

Answer 6

In metabolic alkalosis, there’s not enough H+ in blood

So to reduce pH, H+ is pumped out of cells into blood, and in exchange K+ is pumped into cells

If acidotic, consider renal tubular acidosis or partially treated DKA

In resp. alkalosis (low CO2 in blood), CO2 is lipid soluble so they freely move out of cells. No need for K+ exchange, hence K+ levels not affected.

Question 7

Investigations for hypokalaemia?

Answer 7

• ECG
• U&Es
• ?Mg - Low Mg can cause hypokalaemia so correct this

HYPERTENSION + Hypokalaemia = do aldosterone:renin ratio -

If aldosterone:renin ratio is HIGH (i.e. excess aldosterone production): Primary hyperaldosteronism (Conn’s)

Question 8

Management of hypokalaemia?

Answer 8

Mild/moderate (3.0-3.5)

• Oral KCl (2 Sando-K tablets tds for 48hrs)

Severe (<3.0)

• IV KCl (max 10mmol/hr) + continuous ECG monitoring

Always treat underlying cause
Daily U&Es in ALL cases

Question 9

Normal K+ range?

Answer 9

3.5 - 5.0 mmol/L

Question 10

What is the main ECG feature of hyperkalaemia?

List other ECG changes

Answer 10

• Peaked ‘tall-tented’ T waves = FIRST/MAIN CHANGE (6-7mmol/L)

Other changes with higher levels of K+:

• Loss of P wave
• Broadened QRS
• Sinusoidal wave pattern -> Ventricular Fibrillation -> DEATH

NOTE: ECG changes do not correlate with SEVERITY of hyperkalaemia

Question 11

Main causes of hyperkalaemia?

Answer 11

Think in this order:

1. Renal impairment (reduced GFR - CKD, AKI)
2. Drugs (ACEi, ARBs, Spironolactone)
3. Low aldosterone (Addison’s, type 4 renal tubular acidosis)
4. Release from cells (rhabdomyolysis, metabolic acidosis)

Question 12

Causes of decreased redistribution of K+ into cells?

Answer 12

• Insulin deficiency
  
  • Reduced Na/K pump activity
• Beta blockers
  
  • B2 receptor normally stimulates Na/K pump (i.e. K+ influx into cells)
• Alpha agonists
  
  • Alpha adrenergic receptors stimulate calcium-dependent K+ channels -> leads to K+ release into blood
• Hyperosmolarity (e.g. HHS)
  
  • Increased osmolarity in ECF draws water out of cells
  • Less water inside cells = Higher conc. of intracellular K+
  • Hence K+ moves out into ECF
• Cell lysis
  
  • Severe burns
  • Rhabdomyolysis
  • Tumour lysis (chemo)
• Metabolic acidosis
  
  • H+ drawn into cells, in exchange K+ pumped out
  • Respiratory acidosis and metabolic acidosis caused by organic acids (lactic acid, ketoacid) doesn’t cause hyperkalaemia

Question 13

Causes of increased potassium intake/retention?

Answer 13

• Iatrogenic (rapid, excessive intake of K+ e.g. IV fluids)
• Reduced GFR
• Reduced effect of aldosterone
  
  • Low Renin
    
    • Type 4 renal tubular acidosis
    • NSAIDs (e.g. indomethacin)
  • Low Aldosterone
    
    • Addison’s (adrenal insufficiency)
  • Drugs which inhibit aldosterone
    
    • ACE inhibitors (e.g. ramipril, enalapril, perindopril)
    • ARBs (e.g. losartan, irbesartan, valsartan)
    • Spironolactone (Mineralocorticoid receptor antagonist - aldosterone is a mineralocorticoid)
    • Eplerenone (Selective Aldosterone Receptor Antagonist)

Question 14

Management of hyperkalaemia?

Answer 14

• 10ml 10% calcium gluconate
• 50ml 50% dextrose + 10 units Insulin
  
  • 50% is textbook dose
  • In reality you should give around 100ml of 20% dextrose
• Nebulized salbutamol
• Treat underlying cause