Hyperkalaemia CCC
Clinical Cases
Causes of HYPERkalaemia
- Serum potassium levels above the normal range (3.5-5.0 mmol/L)
1) Increased potassium intake (rare)
- Oral (potassium supplements)
- IV (transfusion of stored blood, supplement infusions)
2) Increased production
- Tissue injury
- Rhabdomyolysis, tumour lysis syndrome
- Burns, ischaemia, haemolysis
- Intense physical activity
3) Decreased renal excretion
- Renal failure (ARF and CRF)
- Aldosterone (Mineralocorticoid acting on collecting duct to reabsorb Na and excrete K and maintain intravascular volume)
- Hypoaldosteronism, Addison’s, Chronic active hepatitis
- Obstructive uropathy
4) Transcellular shift
- Acidosis:
- Metabolic acidosis (DKA, mineral acid overdose)
- HYPERglycaemia
- Respiratory acidosis
5) Fictitious (Pseudohyperkalaemia)
- Laboratory error
- Haemolysis of sample, clenched fist, ischaemic tourniquet
- Leucocytosis, thrombocytosis
6) Drugs causing hyperkalaemia
- Transcellular
- Suxamethonium, Beta blockers, phenylephrine
- Aldosterone inhibition
- ACE inhibitors, Angiotensin II blockers
- Heparin, spironolactone, Beta blockers
- Increased aldosterone resistance (Trimethoprim, amiloride)
- Inhibition Na/K/ATPase (Digoxin)
- Potassium supplements and IV additives (Increase exogenous potassium)
Clinical
- Muscle weakness
- Lethargy
- Ascending paralysis
- Respiratory failure
Complications
Cardiac Arrhythmia
Correction
- Membrane stabilization
- Calcium chloride/gluconate
- ECF – ICF shift
- Sodium bicarbonate
- Insulin/dextrose
- Beta agonists (Salbutamol)
- Removal of K from body
- Urine – Frusemide
- Faeces – Resonium
- Blood – Dialysis
Correction principles for hyperkalaemia
MILD (5-6mEq/L)
- Diuretic-Frusemide
- Calcium resonium- sodium polystyrene sulphate 100/gram.
- PO or PR 6 hourly
- Exchange resin with 1mmol K for every gram used.
MODERATE (6-7)
- Glucose-insulin (10U insulin 50G dextrose)
- IV over 20-30 mins
- Decrease K 0.6-1.0
- Onset 15mins duration 60 mins
- Sodium bicarbonate (50ml 8.4% (50mEq/L) over 5 mins)
- Increase alkalinity so reduce K
- HCO3 increase causes extrusion of H from cells in return for K
- Onset 5 mins duration 2 hrs
- Especially in ARF with metabolic acidosis
- Salbutamol (nebulised 20mg) (iv 500mcg or 5 mcg/kg NOT if IHD)
- Additive effect in combination with insulin
- Binds to B receptors and activate Na-K-ATPase to increase intracellular K
SEVERE (>7) (Toxic ECG changes)
- Calcium
- Calcium chloride (10%) 10ml iv 5 mins
- Calcium Gluconate (10%) 20ml iv 5 mins
- Antagonise toxic effects of K on the myocardium and lower the risk of VF
- Immediate onset , duration 5 mins, but transient effect (30 minutes)
- ALL patients with severe ECG changes
- NOTE may potentiate digoxin toxicity
- Dialysis most rapid and effective method
Critical Care
Compendium
Associate Professor Curtin Medical School, Curtin University. Emergency physician MA (Oxon) MBChB (Edin) FACEM FFSEM Sir Charles Gairdner Hospital. Passion for rugby; medical history; medical education; and asynchronous learning #FOAMed evangelist. Co-founder and CTO of Life in the Fast lane | Eponyms | Books | Twitter |