lecture presentation - fluid, electrolyte and acid base balance.ppt
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Fluid, electrolyte and acid base balanceTRANSCRIPT
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Fluids, electrolytes and acid-base balance
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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%)
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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
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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
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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
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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
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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
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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
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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)
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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
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Chemical buffer systems - bicarbonate
Bicarbonate – major ECF buffer
– H+ + HCO3- H2CO3
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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
-
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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
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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
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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
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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