UNIVERSITY OF NAIROBI

SCHOOL OF MEDICINE
DEPARTMENT OF CLINICAL CHEMISTRY
Wednesday 10th February, 2010
TYPES OF ELECTROLYTES
Examples;

Sodium
Potassium
Magnesium

The above are intracellular while the extracellular are;

Sodium
Chloride
Bicarbonate

In propagation of a nerve impulse, sodium interchanges with potassium to pass on a

signal
Sodium

It is the most important to the extracellular fluid osmolarity; others include urea

and glucose
The reference value is 135 145mmol/liter
Features that affect sodium levels are hyper and hyponatrimia

Hyponatrimia

Retention of water
Congestive heart failure
Liver failure
Renal failure
Loss of sodium from the body; via the GIT, skin, respiratory system, urinary
system etc and include vomiting, diarrhea, diuretics in the kidney,

hypoaldosterodism etc
Loss via the skin is through burns and excessive sweating

Pseudohyponatrimia

Clinical Features of Hyponatrimia

Water moves from intacellular to extracellular

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Generalized weakness
Altered state of consciousness and coma

Hypernatrimia

Associated with increase in the extracellular fluid osmolarity

Signs and Symptoms

Peripheral edema
Dysnia
Pulmonary edema
Venous congestion
Hypertension
Effusions
Weight gain
Cell shrinking in the CNS thus causes; tremors, irritability, confusion, coma,
hemiplegia

Causes of Hypernatrimia

Pure water loss; unreplaced insensible losses, diabetes insipidus

Hypotonic fluid losses; polyuric phase of acute renal failure, through the GIT in
cases of vomiting and diarrhea and abuse of laxatives (drugs given to get rid of

constipation), skin with burns and excessive sweating

Hypertonic sodium gain; when there is a net gain by the body via fluid whose
sodium concentration is great as compared to that in plasma e.g. patients with
Cushs syndrome and patients receiving hypertonic infusions

Potassium

I s predominantly intracellular
Aldosterone exchanges sodium with potassium or hydrogen ions
There are factors that affects transport of potassium in and out of the cell;
Insulin; Promotes entry of potassium into the cell
pH; Acidic pH prevents entry of potassium into the cells; alkalinic pH
promotes entry
Catecholamines; promote entry of potassium into the cells

Hyperkalemia

The reference rate is 3.5 5.0 mmol/liter hence hyperkalemia is when the
concentration is > 5.0mmol/liter
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Causes
Pre-analytical causes

Hemolysis; When hemolysis occurs, the extracellular concentration of potassium

goes up because it was intracellular then after hemolysis they are freed
Delayed separation of serum; as soon as the specimen is received, tests should be
done immediately or the fluid compartments should be separated to avoid infusion

of effusion of electrolytes in either direction

Transcellular potassium movement a.k.a sodium-potassium shift; includes
acidosis, insulin insufficiency, tissue hypoxia, crash injuries, violent muscular

ability after an epileptic fitz, the potassium levels go up

Increased intake of potassium; tablets taken orally may be excessive or
intravenous potassium injections in a hospital set up. Transfusion of old blood

increases blood potassium levels

Reduced excretion; seen in renal failure, in cases of hypoaldosterodism, in
Ardisons disease and use of potassium sparing diuretics

Clinical Features

Affecting contractile tissues especially myocardium

Levels above 7.5mmol/l are fatal
Cardiac arrest
Arrhythmia
Characteristic ECG changes like an absent P-wave and a widened QRS complex
Numbness
Generalized weaknesses

Management

Aims at protecting the heart from the effects of hyperkalemia by introducing

calcium
Promote entry of calcium into the cell
Administration of insulin with glucose to prevent hypoglycemia
Use of Beta 2 antagonist that promotes entry of potassium into the cells

Use of ion exchange resins n Dialysis

Restricting potassium intake

Hypokalemia
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Causes

Primary mineralcorticoids excess in Cushs syndrome and Korns Syndrome

Secondary mineralcorticoid excess; cardiac failure, nephritic symptom, renal

failure, liver failure

Transcellular potassium movement; alkalosis, insulin excess, beta agonists
Reduced potassium intake; poor diet, patients on IV line dependency

Routes of Potassium Loss

Via kidney through diuretics

Via GIT; diarrhea, laxatives and vomiting
Via the skin; sweating

Signs and Symptoms of Hypokalemia

Generalized weakness
Constipation
Hypothermia
Confusion
Cardiac arrhythmias
Potentiation of Digoxin syndrome/toxicity
Polyuria and polydipsia
Loss of concentrating ability by the kidney
Metabolic alkalosis; there is no enough potassium to exchange with sodium in the
body hence hydrogen ions are lost more developing metabolic acidosis