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Fluids, electrolytes and acid-base balance

Body Fluids - distribution

Body fluids constitute 55-60% of body mass

Higher in males due to greater muscle mass and lower fat

Total body water declines throughout life with changes in muscle mass and fat Water occupies 2 main fluid compartments:

Intracellular (~2/3 of total water)


Extracellular (~1/3 total water)

plasma (20%) interstitial fluid (80%)

Water balance

Normally body fluid volume remains constant

water loss = water gain ~60% ingested liquids ~30% ingested in foods ~10% metabolic water (from oxidation) ~4% faeces ~28% insensible water loss (skin & lungs) ~8% perspiration ~60% urine

Water gain:

Water loss:

Additional fluid loss in menstrual flow in females of reproductive age

Regulation of body water gain and loss

Regulation of body water gain depends mainly on regulating volume of water intake

Thirst centre in hypothalamus governs urge to drink Nerve impulses from osmoreceptors in hypothalamus

Thirst centre stimulated by :

in PV or in plasma osmolality

Hypothalamic osmoreceptors lose water to plasma Increased transmission of nerve impulses to thirst centre

dry mouth and pharynx - less saliva from blood plasma in PV = BP

increased angiotensin II (via JGA)

stimulates thirst centre

Regulation of body water (and solute) loss depends mainly on urinary excretion

Fluid movements

Ions formed when electrolytes dissolve and dissociate

Certain ions largely confined to

particular fluid compartments

control osmosis of water between fluid compartments

water moves between body compartments according to osmotic gradient

Moves from areas of low osmolality to high osmolality

Electrolyte balance - Sodium

Sodium

Most abundant ion in extracellular fluid


has

primary role in controlling ECF volume and


relatively impermeable to Na+ so stays in

water distribution
cells

ECF

Regulation of sodium balance

Na+ balance regulated by kidneys


angiotensin II increases Na+ absorption in PCT aldosterone increases Na+ absorption in collecting ducts

Na+ content of body may change, but concentration constant due to corresponding changes in water volume

Regulation of potassium balance

Potassium

Most abundant cation in intracellular fluid

Relative ICF:ECF K+ concentration important for regulating resting membrane potential

K+ balance regulated by changing amount secreted by kidney tubules

When plasma K+ high aldosterone secreted and


stimulates principal cells of collecting ducts to secrete K+ into filtrate

Acid-base balance

Biochemical reactions influenced by pH of surrounding fluids (pH = -log[H+]) pH of tissues regulated by:

chemical buffers (very rapid)


Bicarbonate Phosphate Protein

respiratory compensation

Elimination of volatile acid (carbonic acid) by exhalation of CO2 Excretion of non-volatile acids (cannot be eliminated by exhaling CO2)

renal compensation

Chemical buffer systems - proteins

Most abundant buffers in ICF and blood plasma

Carboxyl groups can act as an acid

R-COOH R-COO- + H+

Amino group can act as a base:

R-NH2 + H+ R-NH3+

Side chains on some amino acids can also buffer

Chemical buffer systems - bicarbonate

Bicarbonate major ECF buffer

H+ + HCO3- H2CO3

Chemical buffer systems - phosphate


Important in urine and ICF Phosphate buffer system consists of:

dihydrogen phosphate (H2PO4-) weak acid


OH-

+ H2PO4- H2O + HPO42-

monohydrogen phosphate (HPO42-) weak base


H+

+ HPO42- H2PO4-

Acid-base imbalances

Arterial blood pH normally 7.4


Acidosis pH below 7.35 Alkalosis pH above 7.45

ie 0.05 pH units above or below normal

Acidosis

Depression of CNS activity through depression of synaptic transmission

Alkalosis

Overexcitability of CNS and peripheral nerves

Neurons conduct impulses continuously in the absence of appropriate stimuli

Can lead to spasms, convulsions and death

Acid base imbalances

Respiratory acidosis and alkalosis

Disorders resulting from changes in partial pressure of

CO2 in arterial blood

Metabolic acidosis and alkalosis

Disorders resulting from changes in HCO3- concentration in arterial blood

Respiratory compensation

Can compensate for metabolic acidosis/alkalosis

H+ buffered by bicarbonate to form CO2 (or vice versa)

H+ + HCO3- H2CO3 CO2 + H2O

Rising or falling H+ from changes in metabolic acid production stimulate peripheral chemoreceptors increases or decreases ventilation to eliminate more or less CO2

Can achieve compensation in minutes to hours

Renal compensation

Can compensate for respiratory acidosis/alkalosis Also only means of eliminating nonvolatile acids (ie acids that cannot be converted to CO2)

PCT

Na+/H+ antiporters secrete H+

Collecting duct (most important):

One type of intercalated cell reduces blood acid load

secretes H+ into tubular fluid against concentration gradient using proton pumps (H+ATPases)

H+ in urine can be 1000 times higher than blood

Second type of intercalated cell increases blood acid load

secretes HCO3- into tubular fluid and reabsorbs H+

Can achieve compensation in days to weeks