HYPOKALAEMIA

FATHIMA SHIFANA
114
 Pathophysiology

Potassium
 Most abundant intracellular cation in the human
body
 Normal plasma level : 3.5-5.5 mmol/L
 Maintenance of k balance is essential for many
cellular functions and neuromuscular
transmission
 98% is located in the cell
 Intracellular k+ concentration-150
mmol/L
 Extracellular concentration- 4-5 mmol/L
 Difference is maintained by Na+-K+
ATPase
 Ratio of k+ concentration inside and
outside the cell- major determinant of
resting membrane potential
Acid base status

Alkalemia –promote K+ uptake by the cells

Acidemia –diminishes K+ uptake by the cells
 Acidosis Alkalosis

H+ K+
K+ H+
RENAL HANDLING OF K+
 Glomerulus – freely filtered
 PCT and thick ascending limb of henle-
reabsorbed
 DCT and cortical collecting duct- secreted
 Excretion is increased by
 Aldosterone
 High sodium delivery to collecting duct –
Diuretics
 High urine flow- osmotic diuresis
 High serum potassium level
 Hypokalaemia

 Defined as plasma concentration of K+ less than

3.5 mmol/L
 Clinical manifestations of hypokalemia vary
greatly between individual patients &their
severity depends on degree of hypokalemia
Mild Hypokalaemia : 3.0 – 3.5 mmol/L :
asymptomatic
Moderate Hypokalaemia: 2.5 - 3.0 mmol/L :
symptomatic
Severe Hypokalaemia <2.5 mmol/L
PSEUDOHYPOKALAEMIA

 “Pseudohypokalemia" occurs in acute

myelogenous leukemia
 large number of abnormal leucocytes in the
blood specimen (stored at room temperature) –
can take up extracellular potassium
 apparent hypokalaemia – artefact of storage
procedure
 Clinical features
 Anorexia , Nausea
 Skeletal muscle
 Weakness
 Cramps
 Tetany
 Paralysis
 Rhabdomyolysis
 Smooth muscle
 Constipation
 Ileus
 Urinary retention
 Endocrine
 Carbohydrate intolerance
 • Cvs
ECG changes
Atrial or ventricular arrhythmias
Decreased amplitude and broadening of T wave
Prominent ‘U’ wave
Premature ventricular contractions
Depressed ST segments
 Causes

Hypokalemia
Increased loss

Decreased Redistribution Extra

intake into cell renal
renal
Decreased K intake

 Dietary – starvation
 IV therapy(potassium free)
Redistribution into cell
 Alkalosis
 Insulin Excess
 Beta-2 agonist
 Alpha antagonist
 Hypokalemic periodic paralysis
 Hypothermia
 Barium toxicity
Increased urinary excretion
 Activation of mineralocorticoid receptor
 Conn syndrome
 Cushing’s syndrome
 Glucocorticoid excess
 Liquorice
 Genetic disorder
 Liddle syndrome
 Bartters syndrome
 Gitelmans syndrome
 Renal tubular acidosis (type 1 and 2)
 Diuretics:
Loop diuretics
Thiazides
Increased gastrointestinal loss
 Upper gastrointestinal tract
 Vomiting
 Nasogastric aspiration
 Lower gastrointestinal tract
 Diarrhoea
 Laxative abuse
 Bowel obstruction
 Ureterosigmoidostomy
Management
 Diagnosis and treatment of the cause
 oral potassium supplements for mild to
moderate deficiency – milk , fruit juice , tender
coconut water
 Syrup potassium chloride – 15 ml contains 20
mmol of potassium
 In setting of abnormal kidney function and
mild to moderate, 20 meq/dl of oral potassium
is generally sufficient to prevent
hypokalaemia, but 40-100 meq/dl over a
period of days to weeks is needed to treat
hypokalaemia and fully replete potassium
stores
 Intravenous potassium chloride is indicated for
patients with severe hypokalaemia and for those
who cannot take oral supplementation
 For severe deficiency potassium may be given
through a peripheral intravenous line in a
concentration up to 40 mmol/L and at rates
upto to 10 mmol/h
 Concentration of upto 20 mmol/h may be given
through a central venous catheter
 Continuous ECG monitoring is indicated and
the serum potassium level should be checked
every 3-6 hours
 Avoid glucose containing fluid to prevent
further shifts of potassium into the cells
 Magnesium deficiency should be corrected ,
particularly in refractory hypokalaemia
Thank you