Hyperkalemia

Question 1

Definition

Answer 1

Serum potassium > 5.5.mmol/L

Question 2

Causes

Answer 2

• Excessive exogenous potassium load (Increased Intake e.g. bananas)
  
  • Redistribution (Shift from intracellular to extracellular fluid)
    
    • Diabetic ketoacidosis (to compensate for acidosis & increase blood pH, increased H+ in the blood are transported into cells via H+/K+ antiporter,K+ transported out of cells into blood. In T1DM there is absolute insulin deficiency so insulin is not available to transport K+ into cells via the Na+/K+ ATPase pump resulting in hyperkalemia. NOTE: DKA is a complication of T1DM not T2DM)
    • Metabolic acidosis e.g. lactic acidosis (to compensate for acidosis & increase blood pH, increased H+ in the blood are transported into cells via H+/K+ antiporter,K+ transported out of cells into blood. )
    • Tumour lysis syndrome (massive tumour cell lysis after starting hemotherpay resulting in release of K+ & other electrolytes)
    • Rhabdomyolysis (trauma causes death of muscle fibres & release of intracellular K+ into bloodstream)
  • Decreased renal potassium excretion e.g.
    
    • renal failure/CKD/AKI
    • Adrenal insufficiency (Addison’s disease= autoimmune primary adrenal insufficiency) (no aldosterone which is needed to excrete K+)
  • Drugs
    
    • Aldosterone antagonists/K+ sparing diuretics (Spironolactone, Eplerenone)
    • ACE-inhibitors (e.g. Ramipril- block angiotensin II production so no aldosterone to excrete K+)
    • Angiotensin II receptor blockers (Candesartan, Losartan)
    • NSAIDs. Combination of ACE-inhibitors with aldosterone anatagonists or NSAIDs is VERY dangerous.

Question 3

Pathophysiology

Answer 3

• The amount of K+ in the blood determines the resting membrane potential & thus excitability of nerve and muscle cells, including skeletal muscle, smooth muscle and cardiac muscle
• When K+ levels in the blood rise, the resting membrane potential becomes more positive (inside the cell is LESS negative relative to outside) in cardiac myocytes so the cell reaches threshold potential more easily resulting in increased depolarisations. This leads to abnormal heart rhythms (arrythmias) that can result in ventricular fibrillation and cardiac arrest
• In smooth muscle (of GI tract) it can cause intestinal cramping - due to depolarisation and contraction
• In skeletal muscle it can cause weakness and flaccid paralysis - resting potential is too high, which means muscle can’t repolarise and then contract again
• In cardiac muscle it can cause arrhythmias or even cardiac arrest

Question 4

Presentation

Answer 4

Symptoms

• **muscle weakness ** (muscles are more excitable & depolarise more readily but become weak due to refractory period - period following initiation of an action potential when another action potential can’t be propagated)
• muscle cramps
• paraesthesia (increased excitability of nerves results in numbness & tingling)
• **abdominal cramping & diarrhoea **
• hyperreflexia

Relating to heart problems:

• tachycardia
• palpitations (symptom)
• ventricular tachycardias → ventricular fibrillation (arrythmia)

Question 5

Investigations

Answer 5

• ECG changes
• U &E - serum K+ > 5.5 mmol/L
• ABG- check for metabolic acidosis (most commonly DKA) which may be causing the hyperkalemia

Question 6

ECG changes in hyperkalemia

Answer 6

• Small/absent P waves (GO)
• Prolonged PR interval (>200ms) (GO LONG)
• Tall, tented T waves (GO TALL)
• Wide QRS complex (>120ms or 3 small squares) (GO WIDE)
• Sine wave pattern (due to wide QRS complex & peaked T-waves, it mimics a sign wave pattern).

Question 7

Management

Answer 7

• If ECG changes- stabilise cardiac membrane by IV calcium gluconate/ calcium chloride (DOES NOT LOWER SERUM POTASSIUM LEVELS, reduces arrythmia risk)
• 1st line = If no hyperkalemic ECG changes shift potassium into cells (from ECF → ICF): by giving combined insulin/dextrose infusion + nebulised salbutamol - if hyperkalemia is severe (beta-2 agonist, beta-2 aadrenergic receptors shift K+ into cells)
• 2nd line = Remove potassium from body by giving Calcium resonium (potassium binder, binds K+ in gut to prevent absorption). Consider haemodialysis for refractory hyperkalemia.

All patients with severe hyperkalaemia (≥ 6.5 mmol/L) or with ECG changes should have emergency treatment

• IV calcium gluconate: to stabilise the myocardium
• insulin/dextrose infusion: short-term shift in potassium from ECF to ICF
• other treatments such as nebulised salbutamol may be given to temporarily lower the serum potassium

Further management includes:

• stop exacerbating drugs e.g. ACE inhibitors
• treat any underlying cause

Question 8

Complications

Answer 8

• arrythmias, particularly ventricular tachycardia leading to ventricular fibrillation
• cardiac arrest