FLUID AND ELECTROLYTE

DR ANIZA MOHAMMED JELANI

DEPARTMENT OF CHEMICAL
PATHOLOGY
 CONTENT
1. Water:
 Normal body water balance

2. Electrolyte:
 Sodium homeostasis

 Disorders of serum sodium

 Potassium homeostasis

 Disorders of serum potassium

 Chloride homeostasis

 Disorders of serum chloride

 WATER DISTRIBUTION

• Water comprises about 60% of body weight

(affected by age, sex)
-Less in female & elderly
• 66% in intracellular compartment

• 33% in extracellular compartment :- mostly

extravascular.
• Minimal day to day fluctuations in body water

due to fine balance between intake and output

 TOTAL WATER (42 L)

PLASMA (3.5L)
INTERSTITIAL FLUID
(10.5L)

INTRACELLULAR WATER EXTRACELLULA

(28L) R WATER
(14L)
INTRACELLULAR-EXTRACELLULAR WATER
DISTRIBUTION

 Water is not actively transported in the body

 The movement of fluid between ECF and ICF is
determined by the osmotic gradient.
 Normally the osmotic gradient between these
compartment is equal (isotonic).
 The osmotic activity is governed mainly by
sodium (ECF)
 Other contributor to the osmotic activity of
ECF include anions
(HCO3- , Cl-), glucose and urea.
 EXTRACELLULAR WATER DISTRIBUTION-
INTRAVASCULAR/EXTRAVASCULAR
COMPARTMENT

 The intravascular and extravascular components of the

ECF are separated by the capillary membrane.
 The hydrostatic pressure within the circulation tends to
drive fluid out, the oncotic pressure of the plasma
proteins, e.g. albumin, draws fluid in and maintains the
relative constancy of the plasma volume as a proportion
of the ECF
 WATER INTAKE AND OUTPUT

 Major factor determining water intake is thirst

which is under the control of thirst centre in the
hypothalamus.
 Control of thirst centre is by:

 Tonicity of ECF (high tonicity stimulates thirst

centre)
 Blood volume (low volume stimulates thirst
centre)
 Miscellaneous: pain, stress
 TONICITY & OSMOLALITY
TONICITY
 Effective osmotic pressure of a solution relative to
plasma
 Effective osmolality of a solution
 A measure of only particles that exert an osmotic effect
 Changes in the tonicity of the ECF stimulate the
mechanisms for water intake or loss.

OSMOLALITY
 A measure of total number of particles
(ion,molecules) present in solution
 WATER INTAKE AND OUTPUT
 Major water loss occurs via the kidney.
 Others through skin (sweating) and respiration.

 Control of fluid loss by the kidney is done by its

ability to excrete and reabsorb water that pass
through the glomerular filtration.
 Arginine vassopressin hormone (AVP) plays an
important role in controlling the renal fluid
handling.
 ARGININE VASSOPRESSIN (AVP)
 Also known as Antidiuretic Hormone (ADH)
 A hypothalamic polypeptide that is transported along
the axons of the synthesizing neurons into the posterior
pituitary gland.
 Released into the systemic circulation after appropriate
stimuli (osmotic and volume stimuli)
 Acts principally on renal collecting tubules to increase
water reabsorption
 
 ROLE OF AVP

 Arginine vasopressin (AVP) acts on the renal collecting

ducts to increase their permeability and subsequent water
reabsorption.
 Factors controlling AVP synthesis and release:

 Tonicity of the ECF: hypertonicity of ECF stimulates

AVP.
 Blood volume: Hypovolaemia stimulates baroreceptor at
the right atrium and carotid sinus - increase AVP release.
 AVP release can also be triggered by:

 Stress, nausea, drugs eg opiates,barbiturates.

 PHYSIOLOGICAL RESPONSES TO WATER LOSS
Water loss

Increased ECF osmolality

Stimulation of Stimulation of hypothalamic Redistribution of

AVP release thirst centre water from ICF

Renal water Increased water intake Increased ECF

retention water

Restoration of ECF osmolality

 SODIUM HOMEOSTASIS

 Total body Na+ in an adult man is 4000mmol.

 70% of body Na+ is freely exchangeable and 30% being
complexed in bone.
 Normal ecf [Na+] is 135 – 145 mmol/L

 Na+ input and output normally are balance.

 Na+ is the predominant cation in the ECF compartment, thus

become a major determinant of the osmotic activity of the ECF.
 Changes in ECF [Na+] will cause changes in water distribution
between the two compartments.
 ECF [Na+]

ECF osmolality

AVP
Thirst (water intake) Water shift from
(renal water reabsorption)
ICF to ECF
 ECF [Na+]

ECF osmolality

AVP
Thirst (decreased Water shift from
(renal water excretion)
water intake) ECF to ICF
 Na+ balance depends on the renal regulation of Na+ excretion. This
is determined by the intravascular volume.
 Low intravascular volume causes increase renal sodium retention
 High intravascular volume causes increase renal loss of sodium

• Factors controlling renal handling of sodium:

1) GFR (increased renal blood flow,higher GFR,more Na excreted)
2) Aldosterone ( low intravascular volume stimulates renin
angiotensin mechanism causes Na reabsorption)
3) Atrial natriuretic peptide (high intravascular volume stimulates
receptor in atrium, increased GFR,more Na excreted)
 HYPONATRAEMIA

•Serum Na of less than 130 mmol/L is clinically significant.

•Causes:

1.HYPERTONIC HYPONATRAEMIA
2.HYPOTONIC HYPONATRAEMIA
3. PSEUDOHYPONATRAEMIA
HYPERTONIC HYPONATRAEMIA
 (high serum osmolality)

-hyperglycaemia
 HYPOTONIC HYPONATRAEMIA
 (Low serum osmolality)
a)-Hypovolaemia:
 Extrarenal-GIT loss: diarrhoea, vomiting
-skin loss
 Renal-diuretic therapy
-salt losing nephritis
-Addison’s disease
Cont.
HYPOTONIC HYPONATRAEMIA

b) Euvolaemia:

 Increased intake + hypovolaemia: haemorrhage,

burns
 Drugs
 Stress
 Post surgery, psychogenic
 Endocrine:hypothyroid, cortisol deficiency
 Renal insufficiency
Cont.
 HYPOTONIC HYPONATRAEMIA

c)Hypervolaemia (oedematous state)

 CCF
 Nephrotic syndrome
 Liver cirrhosis
 PSEUDOHYPONATRAEMIA
 Hyperlipidaemia
 Hyperproteinaemia
 HYPERNATRAEMIA

Serum Na+ more than 145 mmol/L

Less common than hyponatraemia.
CAUSES OF HYPERNATRAEMIA
 PURE WATER DEPLETION
 Too old, too young or too sick to drink
 Access to water denied
 Oesophageal obstruction
 Thirst centre lesions
CAUSES OF HYPERNATRAEMIA
 SODIUM AND WATER DEPLETION (hypotonic fluid loss)
 Extrarenal:

a. GIT:vomiting,diarrhoea

b. Skin:Excessive sweating
 Renal

a. Osmotic diuresis:glucose,mannitol

b. Diabetes insipidus:neurogenic,nephrogenic
 The volume of urine produced is variable depending on the
origin of the loss
 Clinically patient is hypovolaemic.
CAUSES OF HYPERNATRAEMIA
 SALT GAIN (without proportional gain in water)
 Iatrogenic:IV hypertonic saline/NaHCO3
 Salt ingestion
 Primary mineralocorticoid excess

 Clinically patient is hypervolaemic

 Complications: pulmonary oedema,circulatory overload.
 POTASSIUM HOMEOSTASIS
 Human body contains 3000-5000 mmol of K+ in total.

 Most of them are intracellular (120 -150 mmol/L) - It is the

predominant intracellular cation

 Only 2% of total body K+ is located in the extracellular

compartment. However it is important for the maintenance of
cell membrane polarization.

 Depending on diet, K+ intake is 1-2 mmol/kg/day. Most of them

absorbed in the gut with only 10 mmol/day appear in faeces.

 Majority of K+ excretion is in the kidney. Others via faeces and

sweat.
 POTASSIUM HOMEOSTASIS
1.RENAL K+ HANDLING
>90% of K+ that pass through the glomerulus is reabsorbed in the proximal
tubules.
Majority of K+ excretion occur in distal tubules:-

i.Movement of K+ together with H+ from the tubular cells into the lumen
neutralize the membrane potential generated by the active reabsorption of Na +
into the tubular cells.
ii.Factors affecting K+ excretion:
 Aldosterone
 Hydrogen ions
 Na+ load
 The rate of tubular fluid flow –diuretic, osmotic diuresis,GFR
 POTASSIUM HOMEOSTASIS

2. POTTASIUM MOVEMENT ACROSS THE CELL

MEMBRANE

 K+moves across the cell membrane via Na+K+ ATPase pump.

Factors affecting K+ transfer:

Insulin
stimulates cellular uptake of K+
 Cathecolamines

Hydrogen ion-move across the cell membrane in exchange

with K+
Aldosterone-increase uptake of ECF K+
 HYPOKALAEMIA

 Serum K+ of less than 3.5 mmol/L.

 Significant hypokalaemia clinically manifest as disturbance of

neuromuscular function ie paralytic ileus, muscular weakness
 CAUSES OF HYPOKALAEMIA
 DECREASED INTAKE  RENAL LOSS
 Inappropriate IV therapy  Metabolic acidosis
 Anorexia nervosa  Diuretic therapy
 Chronic alcoholism  Mineralocorticoid excess
 TRANCELLULAR SHIFT syndromes
 Insulin
 RTA
 Β adrenergic agonists
 Bartter’s syndrome
 Rapid cellular proliferation
 Mg depletion
 Gentamycin therapy
 EXTRARENAL LOSS
 Leukaemia
 Vomiting
 Diarhoea
 Laxative abuse
 Villous adenoma of colon
 Urine diversion to gut
 HYPERKALAEMIA

 Serum K+ of more than 5 mmol/L

 Leads to severe clinical manifestation ie cardiac arrest in
asystole or ventricular fibrillation
 Spurious hyperkalaemia, a common finding due to leakage of
K+ from blood cells in vitro.
 CAUSES OF HYPERKALAEMIA
 PSEUDOHYPERKALAEMIA
 Hemolysis
 Leucocytosis
 Thrombocytosis
 INCREASE INTAKE TO ECF
 Exogenous-oral/IV therapy
 Endogenous-Tissue necrosis (crush injury,burns)
 DISTURBED INTRACELLULAR/EXTRACELLULAR
DISTRIBUTION
 Acidaemia
 Insulin deficiency
 Drugs:digoxin,succinylcholine
 Hypertonicity:glucose, sodium
 Hyperkalaemic periodic paralysis
 CAUSES OF HYPERKALAEMIA
 DECREASED RENAL EXCRETION
 Renal failure-acute/chronic
 Drugs-pottasium sparing diuretics, captopril,heparin etc
 Mineralocorticoid deficiency syndromes
 Mineralocorticoid resistant syndromes
 CHLORIDE
 Major anion in ECF

 Essential electrolyte of all body fluid

 Responsible for maintaining acid/base balance,

transmitting nerve impulses and regulating fluid in and
out of cells.
HYPERCHLORAEMIA
associated with..
 Hypernatraemia
 Normal anion gap metabolic acidosis

- Renal Tubular acidosis

 Diarrhoea
HYPOCHLORAEMIA
associated with..
 Hyponatraemia
 Metabolic alkalosis

 Vomiting
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