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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
Water gain:– ~60% ingested liquids– ~30% ingested in foods– ~10% metabolic water (from oxidation)
Water loss:– ~4% faeces– ~28% insensible water loss (skin &
lungs)– ~8% perspiration– ~60% urine
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
Thirst centre stimulated by :– Nerve impulses from osmoreceptors in
hypothalamus 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
water distribution
cells relatively impermeable to Na+ so stays in
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
– renal compensation
Excretion of non-volatile acids (cannot be eliminated by exhaling CO2)
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 + HPO4
2-
– 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