Hypokalaemia -

Hypokalaemia

Normal Potassium Physiology

Distribution of Potassium

Normal serum potassium: 3.5 – 5.0 mEq/L

Classification of Hypokalaemia

⚠ Severe hypokalaemia is strongly associated with cardiac arrhythmias and muscle paralysis.

Causes of Hypokalaemia –

1️⃣ Reduced Intake

Cause	Mechanism
Malnutrition	Low dietary potassium intake leading to gradual total body potassium depletion
Alcoholism	Poor intake + renal and GI potassium losses
Prolonged fasting / starvation	Reduced intake + intracellular redistribution during refeeding
TPN without potassium supplementation	Absence of potassium replacement despite ongoing renal and cellular losses

2️⃣ Transcellular Shift (Redistribution) – Total Body Potassium Normal

Cause	Mechanism
Insulin therapy	Stimulates Na⁺/K⁺ ATPase → shifts potassium intracellularly
Beta-2 agonists (salbutamol, terbutaline)	Beta receptor stimulation increases cellular potassium uptake
Metabolic or respiratory alkalosis	Hydrogen ions move out of cells → potassium moves into cells
Refeeding syndrome	Insulin surge promotes intracellular potassium uptake
Hypothermia	Cellular shift of potassium
Familial periodic paralysis	Genetic ion channel defect causing intracellular potassium sequestration
Thyrotoxic periodic paralysis	Increased Na-K ATPase activity from thyroid hormone excess
Acute catecholamine surge	Beta-adrenergic stimulation

3️⃣ Increased Potassium Loss

A. Renal Potassium Loss (Most Common in ICU)

Cause	Mechanism
Loop diuretics (furosemide)	Increased distal sodium delivery → increased potassium secretion
Thiazide diuretics	Increased distal tubular potassium excretion
Hyperaldosteronism (primary or secondary)	Increased sodium reabsorption and potassium secretion in collecting duct
Magnesium deficiency	Loss of ROMK channel inhibition → increased renal potassium wasting
Renal tubular disorders (Bartter syndrome)	Defective Na-K-2Cl transport in loop → potassium wasting
Renal tubular disorders (Gitelman syndrome)	Defective Na-Cl transport in distal tubule → potassium wasting
Renal tubular acidosis (Type I and II)	Increased potassium loss with bicarbonate wasting
Post-obstructive diuresis	Increased urinary flow causing potassium washout
Osmotic diuresis	Increased urinary solute load increases potassium excretion
Drug-induced renal loss (Amphotericin B)	Tubular membrane damage
Cisplatin	Direct tubular toxicity causing potassium wasting
Aminoglycosides	Tubular injury
High-dose steroids	Mineralocorticoid activity increasing potassium excretion
High urinary flow states	Increased distal potassium secretion

B. Gastrointestinal Potassium Loss

Cause	Mechanism
Vomiting	Indirect renal potassium loss due to metabolic alkalosis and secondary hyperaldosteronism
Diarrhea	Direct potassium loss in stool
Laxative abuse	Chronic GI potassium depletion
Intestinal fistulas	Continuous potassium-rich fluid loss
Nasogastric suction	Gastric potassium loss + metabolic alkalosis leading to renal potassium wasting
Villous adenoma of colon	Potassium-rich secretory diarrhea
Chronic intestinal pseudo-obstruction	Malabsorption and chronic GI loss
High-output ileostomy / jejunostomy	Large volume electrolyte-rich losses

Clinical Features

Neuromuscular Manifestations

Cardiac Manifestations

Most dangerous complication.

Renal Manifestations

Gastrointestinal Manifestations

ECG Changes in Hypokalaemia

ECG changes correlate poorly with potassium level but remain clinically critical.

Classic Changes:

A. Urinary Potassium Measurement

Urine K⁺	Interpretation
<20 mEq/day	Extrarenal loss or redistribution
>20 mEq/day	Renal potassium loss

B. Spot Urine Potassium/Creatinine Ratio

C. Acid–Base Status

Condition	Likely Cause
Metabolic alkalosis	Vomiting, diuretics, hyperaldosteronism
Metabolic acidosis	Diarrhea, RTA

D. Magnesium Levels

Mandatory in all unexplained cases.

Potassium Replacement Therapy

Oral Replacement (Preferred if stable)

Formulation	Typical Dose	Advantages	Disadvantages / Precautions
Potassium Chloride (KCl) Tablets	20–100 mEq/day in divided doses	Most commonly used; corrects both potassium deficit and chloride depletion	Gastric irritation, ulcer risk if not taken with water/food
Sustained-release Potassium Chloride	20–80 mEq/day	Less gastric irritation, slower absorption	Risk of GI ulcer if tablet lodges in esophagus
Liquid Potassium Chloride Solution / Syrup	20–100 mEq/day divided	Better for NG tube / dysphagia patients; faster absorption	Unpleasant taste, GI irritation
Effervescent Potassium Chloride Tablets	Dissolved in water; 20–80 mEq/day	Better palatability and absorption	Requires preparation; may cause bloating
Potassium Citrate	20–60 mEq/day	Provides alkalinizing effect; prevents renal stones	Can worsen metabolic alkalosis
Potassium Bicarbonate	25–100 mEq/day	Corrects acidosis along with potassium	Not useful in alkalosis
Potassium Gluconate	Multiple tablets required	Better GI tolerance	Low potency; rarely used in ICU
Potassium Phosphate (Oral)	Dose individualized	Corrects both potassium and phosphate deficiency, use in Refeeding syndrome	Risk hyperphosphatemia

IV Potassium Replacement

Parameter	Peripheral Line	Central Line
Maximum concentration	40 mEq/L	Up to 80–120 mEq/L
Maximum infusion rate	10 mEq/hour	20 mEq/hour
Extreme life-threatening situations	Not recommended	Up to 40 mEq/hour (ICU with monitoring)
ECG monitoring	Recommended if >10 mEq/hr	Mandatory
Risk	Phlebitis, extravasation	Arrhythmias, rapid hyperkalaemia