REGULATION OF FLUIDS

AND ELECTROLYTES

Fluid Compartments of the Body

Intracellular Fluid (ICF) 67%
Extracellular Fluid (ECF) 33%

Plasma (6.6%)
Interstitial fluid (26.4%)
Lymph
Cerebrospinal fluid
Synovial fluid
Serous fluids
Aqueous humour

Plasma And Interstitial Fluid

Separated by blood capillaries
Water and solutes move by passive
diffusion
Components similar except for plasma
proteins and RBCs

ECF & ICF

Separated by cell membrane
Components different
Cell proteins in ICF
Unequal distribution of Na, K and their anions
due to the Na/K pump (pumps Na out and K into
cell)

Fluid Balance
Maintained by regulating the osmolarity of
the ECF

Fluid Input and Output

Input (2500 ml)
Eating 1000ml
Liquids 1200ml
Metabolic water 300ml

Output (2500ml)
Urination 1200ml
Defecation 150ml
Sensible perspiration 750ml
Insensible perspiration 400ml

Regulation of Water
Dehydration more water is lost than is
gained
Under conditions of excess water loss
without comparable electrolyte loss the ECF
becomes hypertonic
Water moves from the ICF to the ECF
Both ECF and ICF are now more relatively
concentrated and contain less water

Regulation of Water
Dehydration (contd)
Hypernatremia develops
Severe thirst, dryness and wrinkling of the skin
If plasma volume decreases and bp decreases shock
may develop

Hypotension (90 mmHg and less)

Pale, cool, moist skin
Confusion and disorientation
Heart rate increases, rapid , weak pulse
Cessation of urination
A drop in pH of blood; due to lactic acid produced by O2
deprived cells

Regulation of Water
Dehydration (contd)
Homeostatic Responses
ADH and Renin Secretion
Increased fluid Intake
ECF volume increases fluid shifts to ICF

Regulation of Water
Excess Water Gains
When ECF volume increases due to
increased water intake without
corresponding increases in electrolytes
ECF becomes hypotonic
Water shifts to ICF
Both ECF and ICF volumes larger than normal
and lower osmotic concentrations

Regulation of Water
Excess Water gains (contd)
Homeostatic Responses
ADH secretion decreases urine volume
increases

Regulation of Water
Excess Water Gains
If not corrected
Overhydration
Cells become distorted
Solute concentration around enzymes change
Cell function is disrupted

Regulation of Water
Overhydration is caused by
Ingestion of large volumes of freshwater
Inability to eliminate excess water due to chronic renal
failure or heart failure
Endocrine disorders excess ADH production
Signs of Overhydration
Hyponatremia
Drunken behavior, confusion, hallucinations,
convulsions, coma and then death

Regulation of Water
Treatment of Overhydration
Administration of Diuretics and
Infusion of a concentrated salt solution causing
a fluid shift from ICf to ECF

Electrolyte Balance
When the rates of gain and loss of each
electrolyte are equal in the body

Electrolyte Balance
Sodium (Na)
Gain and lose 1.1 3.3g each day
When there is a change in the gain or loss of Na
from the ECF there is no change in the
concentration of Na because there is always a
corresponding shift in water (ie osmosis occurs)

Electrolyte Balance
Sodium
If we eat a salty meal without adequate fluid
intake
Concentration of Na in the plasma increases
Fluid leaves the ICF and enters the ECF lowering Na
concentrations
Secretion of ADH due to osmoreceptors in pharynx
and hypothalamus

Electrolyte Balance
Sodium
In cases of dehydration where sodium is also
lost
Renin and Aldosterone are secreted

Overhydration
Plasma volume increases

Atrial and ventricular walls stretch

Natriuretic peptides secreted (ANP and BNP)
Thirst is reduced; ADH and Aldosterone secretion blocked
Salt and water losses increase at the kidneys

Electrolyte Balance
Potassium (K)
1.9 5.8g each day
Higher in the cell
Concentration in the ECF is controlled by the
rate of secretion along the DCT and collecting
system

Electrolyte Balance
Potassium
Rate of secretion at the DCT depends on:
Changes in K concentration in the ECF
Changes in pH (if ECF pH decreases H is secreted in
exchange for Na instead of K)
Aldosterone levels
Aldosterone acts on Na/K pumps causing reabsorption of
Na in exchange for K
When K is high in the ECF aldosterone is also secreted

Electrolyte Balance
Calcium (Ca)
0.8 -1.2g
Maintained by Parathyroid hormone,
calcitriol and calcitonin
PTH and Calcitriol increase calcium levels
Calcitonin decreases calcium levels

Electrolyte Balance
Calcium
Hypercalcemia caused by:
Hyperparathyroidism
Cancers of the breast, lungs, kidneys and bone
marrow
Excessive calcium or vitamin D supplements

Electrolyte Balance
Calcium
Hypocalcemia due to
Hypoparathyroidism
Vitamin D deficiency
Chronic renal failure

Electrolyte Balance
Magnesium (Mg) Balance
Magnesium is higher in the ICF than the ECF
0.3-0.4 g of Mg need to be consumed daily to
maintain balance
Mg is reabsorbed along the PCT

Electrolyte Balance
Phosphate
0.8 1.2 g needed each day
Reabsorbed along the PCT stimulated by
calcitriol

Electrolyte Balance
Chloride
Most abundant anion in the ECF
1.7 5.1 g needed each day
Absorbed along the digestive tract with sodium
and reabsorbed with sodium along the renal
tubule

Acid-Base Balance
pH of the ECF is 7.35 7.45
We are unable to survive if the pH goes
below 6.8 or above 7.7
Acidosis the physiological state that
results from plasma pH falling below 7.35
Alkalosis the physiological state that
results from plasma pH rising above 7.45

Acid-Base Balance
Acidosis and Alkalosis both affect most
greatly the cardiovascular and nervous
systems
Homeostatic control of pH is, therefore, of
great importance
Acidosis is more prevalent as the body
produces several acids through its cellular
activities

Mechanisms of pH Control
Acid-base balance is achieved by balancing
hydrogen ion gains and losses
i.e. that gained at the digestive tract and
through metabolic activities must equal that
produced in the urine and produced at the lungs

Mechanisms of pH Control
H+ are transported from their site of
production to their site of elimination by a
buffer
This prevents damage to tissues

Mechanisms of pH Control
There are three types of acids
Organic Acids participants in or by-products
of aerobic metabolism eg lactic acid
Volatile Acids can leave solution and enter
the atmosphere eg. Carbonic acid
Fixed Acids do not leave solution; remain in
body fluids until eliminated at the kidneys eg.
Sulphuric and phosphoric acids (produced by
catabolism of amino acids, phospholipids and
nucleic acids

Buffer Systems
Types of Buffer Systems
Protein
Carbonic Acid Bicarbonate
Phosphate

Protein Buffer Systems

Depend on the ability of amino-acids to
respond to pH changes by accepting or
releasing H+
Contribute to regulating ECF and ICF pH

Protein Buffer Systems

If pH increases the COOH (carboxyl) group
on the amino acid loses its H+ to become a
COO- (carboxylate ion)
Some amino acids have an R group that can
also donate an H+ if the pH increases above
normal
If the pH decreases the COO- and NH2 can
accept H+

Protein Buffer Systems

Proteins that can act as buffers include:
Plasma proteins
Extracellular protein fibres in interstitial fluid
Structural proteins in the ICF

Protein Buffer Systems

If pH of the ECF declines the H+ move into
the ICF where they are buffered
If pH increases in the ECF H+ move from
the ICF to the ECF in exchange for
potassium ions
This system is slow and cannot make rapid
and large-scale adjustments in the pH of the
ECF

Protein Buffer Systems

Haemoglobin Buffer System
The only intracellular buffer system that has an
immediate effect on the pH of the ECF and
helps prevent drastic changes in the pH when
the partial pressure of CO2 in the plasma
increases or decreases

Carbonic Acid-Bicarbonate Buffer

System
CO2 + H2O H2CO3 H+ + HCO3
Prevents changes in pH caused by organic acids
and fixed acids in the ECF
If pH decreases the H+ will be removed by HCO3 H2CO3 CO2 + H2O
The CO2 and H2O are released at the lungs
The reaction moves in the opposite direction if pH
increases ie H+ is released

Phosphate Buffer System

H2PO4- H+ + HPO42 i.e. Dihydrogen phosphate hydrogen +
monohydrogen phosphate
Supports the carbonic acid-bicarbonate
buffer system in the ECF but is of utmost
importance in the ICF
Also important in buffering urine

Respiratory Compensation
A change in the respiratory rate that helps to
stabilize the pH of the ECF
When respiration rate increases or decreases the
pH is altered by increasing or decreasing CO2
levels
Recall that when CO2 increases the pH decreases
and visa versa
Recall also that when CO2 increases the
respiratory centre is stimulated and respiratory
rate increases

Renal Compensation
A change in the rates of H+ and HCO3- secretion
and reabsorption by the kidneys in response to
changes in plasma pH

The process of elimination of H+ is dependent on

the availability of buffers in the renal tubule
i.e. the secretion of H+ cannot continue if the tubular
fluid declines to 4.0-4.5. At this point the H+ will leak
out of the tubular fluid (back into the blood) as fast as it
is secreted

Renal Compensation
The buffers involved in renal compensation
are:
Carbonic acid-bicarbonate
Phosphate

placed in the
tubule by filtration

Ammonia produced by tubular cells

Renal Compensation

Renal Responses to Acidosis

1.
2.
3.
4.

Secretion of H+
Buffer activity in tubules
Removal of CO2
Reabsorption of NaHCO3

Renal Compensation

Renal Responses to Alkalosis

1. H+ secretion decreases
2. Tubular cells do not reclaim the
bicarbonates in the tubular fluid
3. HCO3- secreted and a strong acid such as
HCl is reabsorbed along the collecting duct

Disturbances of Acid-Base Balance

Can occur under the following circumstances:

1. Cardiovascular Conditions eg heart failure and
hypotension

Affect pH of internal fluids by causing fluid shifts and by

changing glomerular filtration rates and respiratory efficiency

2. Disorders that affect circulating buffers, respiratory

performance or renal function eg emphysema or renal
failure
3. Conditions affecting the CNS

Will affect respiratory and cardiovascular reflexes

Respiratory Acidosis
Develops when the respiratory system
cannot eliminate all the CO2 generated by
tissues
Primary sign is low plasma pH due to
hypercapnia (elevated plasma CO2)
BUT the usual cause is
HYPOVENTILATION (abnormally low
respiratory rate) CO2 increases and pH
declines

Respiratory Acidosis
The body normally responds by increasing
respiratory rate
If respiratory rate does not increase
because the chemoreceptors fail to respond
to the decline in pH, breathing rate does not
increase or circulatory supply to the lungs is
inadequate pH will continue to decline
causing Acute Respiratory Acidosis

Respiratory Acidosis
Chronic Respiratory Acidosis
Develops when normal respiratory function is
compromised but the compensatory
mechanisms have not failed completely
Eg. Persons who have CNS injury and persons
whose respiratory centres have become desensitised
by alcohol or barbiturates

Respiratory Alkalosis
Occurs when respiratory activity lowers
plasma CO2 to below normal levels
(Hypocapnia)
Hypocapnia is caused by Hyperventilation

Respiratory Alkalosis
When pH increases (low CO2) due to
hyperventilation the condition corrects itself
by the chemoreceptors not being stimulated
so we do not get the urge to breathe
Respiratory Alkalosis rarely persists to
cause a clinical emergency

Respiratory Alkalosis

Common causes of Hyperventilation

1. Physical stresses eg pain
2. Psychological stresses eg extreme anxiety

Respiratory Alkalosis
Initial Symptoms:
Tingling of hands, lips and feet
Light-headedness

If pH continues to increase one may become unconscious

which removes any psychological stimuli, therefore,
breathing rate decreases
Breathing into a paper bag is a simple treatment for
respiratory alkalosis

Metabolic Acidosis

CAUSES
1. Production of a large number of fixed or
organic acids eg. Lactic Acidosis and
Ketoacidosis
2. Impaired ability to excrete H+ at the kidneys
due to glomerulonephritis or diuretics which
inhibit the Na/H transport system
3. Severe bicarbonate loss due to diarrhea

Metabolic Acidosis

Compensatory Mechanisms:
1. Respiratory Mechanism H+ interacting with
HCO3- CO2 and H2O
2. Renal Mechanism H+ secreted and HCO3reabsorbed

Combined Respiratory & Metabolic

Acidosis
Due to drowning
Lactic acid produced due to struggling muscles
CO2 increases if breathing stops
Treatment Artificial and Mechanical Respiratory
Assistance along with intravenous infusion of
isotonic solutions such as sodium lactate,
sodium gluconate or sodium bicarbonate
(release anions that can bind with the H+)

Metabolic Alkalosis
Results when HCO3- increases
HCO3- binds with H+ H2CO3
The resulting decline in H+ produces
symptoms of alkalosis

Metabolic Alkalosis
Can develop when HCl
is secreted by the
stomach causing
HCO3- to increase in
the ECF (Alkaline
Tide)

Metabolic Alkalosis
The temporary increase in pH due to the
release of HCO3- is not serious
BUT serious metabolic alkalosis can occur
due to bouts of repeated vomiting
Vomiting removes stomach acids, therefore,
the parietal cells are stimulated to produce
more HCl and therefore more HCO3-

Metabolic Alkalosis

Compensation Mechanisms and

Treatments
1. Breathing rate declines CO2 increases pH
declines
2. Increased loss of HCO3- from urine
3. Treatment of vomiting by using sodium
chloride or potassium chloride solutions
4. Acute cases treated with Ammonium Chloride
Metabolism of ammonium chloride releases HCl
H+ lowers pH