Hypokalemia and Hyperkalemia

Normal value: 3.5-5 mEq/L

Hypokalemia <3.5-5 mEq/L > Hyperkalemia
Hyperkalaemia
• Causes:
Causes
Increased k+ intake
Cellular death – by freeing the
intracellular potassium
Impaired renal K+ excretion
Shifting of potassium to
extracellular compartment
- Medication contaning K+
- High potassium foods
- Massive transfusion with packed red blood cells
- Haemolysis
- Rhabdomyolysis
- Burns
- Catabolic states = fasting
- Reduced GFR due to acute renal failure, chronic renal failure, obstructive
uropathy, reduced renal perfusion (shock, dehydration)
- Impaired tubular excretion of K+
- Diabetic ketoacidosis with compomised renal excretory mechanism
Hyperkalaemia
• ECG changes in
hyperkalemia
Hyperkalaemia
• COCKTAIL REGIME for hyperkalaemia:
1. I/V slow bolus 10ml of 10% Calcium Gluconate over 2-5 minutes
• The FIRST medication to be given immediately !
• Cardiac (ECG) monitoring
2. I/V bolus 50ml of Dextrose 50% over 30-60 min (Glucose not
required if HYPERGLYCEMIC/DKA)
3. I/V bolus insulin 10 IU

Ref: Sarawak Handbook of Medical Emergencies

 Hyperkalaemia
• Complication
• Cardiac arryhthmia
• Dysfunctional heart muscles leading to bradycardia and bundle branch blocks
• Muscle weakness and paralysis
• Life threatening - if involve respirator muscles
• Rebound hypokalemia and hypotension are seen with aggressive diuresis
Hypokalemia
Causes
I. Reduced K+ intake - Starvation
- Clay ingestion
II. Redistribution into cells (Intracellular shift - Acid base
of K+) - Metabolic alkalosis
A. Acid-base - Hormonal
B. Hormonal - Insulin
C. Anabolic state - Increased B2-adrenergic sympathetic activity: post-myocardial infarction, head injury
- B2-adrenergic agonists – bronchodilators, tocolytics
- Aa-Adrenergic antagonist
- thyrotoxic periodic paralysis
- Downstream stimulation of Na+/K+-ATPase: theophyllin, caffeine
- Anabolic state
- Vit b12/folic acid administration (rbc production)
- Total parenteral nutrition
III. Increased loss - Non renal
A. Non renal - Gastrointestinal loss – diarrhoea
B. Renal - Integumentary – loss – sweat
- Renal
- Increased distal flow and dital Na+ delivery: diuretics, osmotic diuresis, salt-wasting nephropathies
- Increased secretion of K+
- Mineralocorticoid excess: primary & secondary hyperaldosteronsm, Cushing’s syndrome, Bartter’s
syndrome, Gitelman's syndrome
- Apparent mineralocorticoid excess
- Distal delivery of nonreabsorbed anions: vomiting, nasogastric suction, proximal renal tubular acidosis,
diabetic ketoacidosis
- Magnesium deficiency
Hypokalemia
• Complication
• Cardiac arrhythmias
• dysfunctional heart muscles – tachycardia, ventricular fibrillation
• Paralysis
• Common
• Life-threatening
• Elevated thyroid function tests (thyrotoxic periodic paralysis)
• Rebound hyperkalemia is also seen with aggressive replacement.