Disorders of

Fluid and Electrolyte Balance

 Learning Outcomes

 Outline the fluid compartments, their composition and

factors that govern exchange of material between them.
 Outline the mechanisms that regulate body fluid volume
and electrolytes.
 Explain the basis of bedside assessment of intravascular
volume.
 Outline the causes and consequences of abnormalities of
plasma sodium, potassium, bicarbonate and albumin
concentrations.
 State the principles of management common fluid and
electrolyte disorders.
Body Fluid Compartments
Body Fluid Volumes
Body Fluid Compartments - interconnections
Body Fluid Compartments - interconnections

plasma Interstitial Intracellular

fluid fluid

Cell membrane

Capillary membrane
Composition of Body Fluids – electrolytes & pH
ECF ICF
Na+ (mmol/L) 135-147 10-15
K+ (mmol/L) 3.5-5.0 120-150
Cl- (mmol/L 95-105 20-30
HCO3- (mmol/L) 22-28 12-16
Ca++ (mmol/L) 2.1-2.8 ≈10-4
Phosphate (mmol/L) 1.0-1.4 42
 pH 7.4 7.1-7.2

ICF contains more proteins than ECF.

Proteins are negatively charged
 Regulation of Fluid Volume

A function of the kidney

Fluid volume is maintained by regulating Na + excretion –
influences mainly the ECF
Based on the intravascular volume

Major mechanisms
 Renin-andiotensin-aldosterone
 Glomerular and tubular mechanisms
 ADH, ANP
 Regulation of ECF Osmolality

A function of the kidney

Body fluid osmolality is maintained by regulating water
excretion - affects ECF directly and then ICF
Na+ being the main ECF ion, regulting osmolality is, in
practical terms, same as regulating Na + concentration

Major mechanism
 ADH
 Regulation of ECF K+

No direct mechanisms to regulate serum K +

Regulation is secondary to regulation of Na + and H +
 Regulation of ECF H+

Renal and respiratory regulation

Has an indirect effect on HCO3- levels

Renal:
Direct effect of plasma H+ and PCO2 on tubular cells

Respiratory:
Effect of plasma H+ and PCO2 through chemoreceptors
 Disorders of Intravascular Volume

Hypovolaemia - assessment
Symptoms –
Fatigue
Thirst
Dizziness and syncope – exertional or postural
Breathlessness
Confusion and altered levels of consciouness
 Disorders of Intravascular Volume

Hypovolaemia – assessment

Loss of skin turgour, dry mouth, sunken eyes

Delayed capillary filling
Cold extremities,
Peripheral cyanosis
Excessive sweating
Rapid and low volume pulse, significant increase in pulse on standing
Low blood pressure with low pulse pressure, postural hypotension
Altered mental status
Loss of weight
Low urine volume, high urine osmolality
 Disorders of Na+

Hyponatraemia
Serum Na+ of less than 135 mmol/L

Hypernatraemia
Serum Na+ of more than 145 mmol/L

Causes of Na+ disorders only uncommonly give rise to these

disorders. Most often they do not cause hypo/hypernatraemia
 Hyponatraemia

May occur with normal, decreased or increased

extracellular volume
 Causes of Hyponatraemia

Increased ECV Decreased ECV Normal ECV

Edematous states Hypovolemic states Normovolaemic
Excess of total body Decreased total body Normal Na+ and
Na+ and water Na+ and water excess of water
(dilutional)
• Congestive cardiac • Diuretic • Syndrome of
failure administration inappropriate
• Cirrhosis • Gastrointestinal loss antidiuretic hormone
• Nephrotic syndrome Excessive sweating
 Hyponatraemia

Symptoms:
Hyponatraemia may be asymptomatic until Na+ levels fall to very
low levels depending on -
the rapidity with which Na+ falls

Symptoms are neurological

Due to ovement of water into cells causing cerebral oedema
Nausea, vomiting, headache
Seizures
Symptoms of cerebral herniation
Respiratory failure, coma
 Treatment of Hyponatraemia

• Symptomatic hyponatraemia is a medical emergency.

Usually in acute hyponatraemia
In emergency situations treatment may be with
o Isotonic saline – more commonly
o Hypertonic saline – rarely
Even in an emergency the rate of correction should be slow
and full correction is avoided

• If asymptomatic and chronic it may not need immediate

correction, but correction of the underlying disorder
 Treatment of Hyponatraemia
Correction of hyponatraemia according to type
In all types, treatment of the primary cause is the mainstay of
treatment in chronic and asymptomatic hyponatraemia

Increased ECV Decreased ECV Normal ECV

Edematous states Hypovolemic states SIADH

Treatment: Treatment: Treatment:
Diuretics Water and Na Fluid restriction
RAS antagonists replacement Furosemide
Water & Na restriction Demeclocycline
CHF- cardiac glycosides
 Hypernatraemia

Less common than hyponatraemia

Causes
1. Na+ and water loss with proportionately more water loss
Renal disease – tubular disorders
Diabetes mellitus - hyperglycaemia
Gastrointestinal loss
Fever, sweat loss, burns
Diabetes insipidus

2. Excessive retention of Na+ and water with proportionately

more Na+
Primary hyperaldosteronism
 Hypernatraemia

Symptoms:
Occur due to cellular dehydration, mostly neurological
• Lethargy
• Confusion
• Coma
• Muscle damage, intracranial haemorrhage

• Severity of symptoms depend on how acutely

hypernatraemia develops
 Hypernatraemia

Treatment:
Slow replacement of water
• Dextrose based intravenous fluids
• Oral water intake
• Isotonic saline if hypernatraemia is very severe
 Disorders of K+

Hypokalaemia
Plasma K+ less than 3.5 mmol/L

Hyperkalemia
Plasma K+ more than 5.5 mmol/L
 Hypokalaemia

Causes
1. Increased loss
Gatrointestinal
Renal
Hyperaldosteronism – primary or secondary, Cushing
syndrome
2. Redistribution into cells
alkalosis
3. Magnesium deficiency
4. Drugs
Diuretics
5. Decreased intake
 Hypokalaemia

Clinical features and effects

1. Effects on excitable cells
Muscle weakness and paralysis
Paralytic ileus
Cardiac arrhythmias
2. Secondary effects through kidney
3. Increased Na+ loss, polyuria
4. Metabolic alkalosis
5. ECG changes – flattening of T waves, ST depression and QT
prolongation
 Hypokalaemia

Treatment
1. Correction of hypokalaemia
Oral K+ supplements
Slow intravenous administration if serious symptoms are
present
2. Treat underlying disease
3. Correct magnesium deficiency
 Hyperkalaemia

Causes
1. Renal retention
Renal disease
Addison disease
2. Movement out from ICF
Acidosis
3. Drugs
Spironolactone, ACE inhibitors, angiotensin II blockers
4. Cellular necrosis
 Hyperkalaemia

Clinical features
Hyperkalaemia can be asymptomatic until a late stage when
serious cardiac effects can occur

1. Cardiac arrhythmias including sinus arrest

2. ECG changes – tall T waves, widening of QRS, prolonged PR
interval, loss of P wave
3. Muscle weakness, paralysis
 Hyperkalaemia

Treatment
High level of hyperkalaemia should be considered a medical
emergency even in the absence of symptoms

1. Reduction of plasma K+ level

Decreasing oral intake and reduction of intestinal
absorption with K+ binding resins if K+ level is only
marginally high.
Dextrose+insulin infusion to increase movement of K+
into cells – has quick effect
Beta 2 agonists (albuterol)
Intravenous bicarbonate – has slow effect
 Hyperkalaemia

Treatment
2. Antagonise the effects of hyperkalaemia
Slow intravenous infusion of calcium gluconate

3. Removal of K+
Dialysis
Restore circulatory volume if depleted