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Biology 233
Human Anatomy and Physiology
Chapter 27 Lecture Outline
FLUID, ELECTROLYTE, & ACID-BASE HOMEOSTASIS
FLUID HOMEOSTASIS
water is 50-6-% of body mass (varies depending on body fat)
dissolves all molecules so reactions can take place
FLUID COMPARTMENTS
intracellular fluid (ICF) – cytosol
extracellular fluid (ECF) – fluid outside cells
interstitial fluid – 80% of ECF
plasma
Fluid Shifts Between Compartments
plasma(ECF)/interstitial fluid(ECF) exchange
filtration – shift from plasma to interstitial fluid
reabsorption – shift from interstitial fluid to plasma
net shift depends on:
blood hydrostatic pressure (BP)
blood colloid osmotic pressure (plasma osmolarity)
interstitial fluid(ECF)/intracellular fluid (ICF) exchange
shift is due to osmosis
normally osmolarity is the same in both compartments = no net shift
altering osmolarity of interstitial fluid causes fluid shifts
direction depends on concentration gradient produced
Note: Water is not actively transported between compartments. Shifts are normally
caused by altering osmolarity (solute concentration) in ECF.
FLUID BALANCE
Water Loss (2500ml/day)
urine – 1200
perspiration – 750ml
exhaled water vapor – 400ml
feces – 150ml
Water Gain (2500ml/day)
ingestion (drinking and eating) – 2200ml
metabolic water – 300ml
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Dehydration – water loss exceeds water gain
(excess perspiration, inadequate drinking, vomiting, diarrhea)
causes low blood volume and pressure, and hyperosmolarity of plasma
< filtration, > reabsorption = increases interstitial osmolarity
osmosis from ICF to interstitial fluid (cells shrink)
Body’s Response to Dehydration
>ADH secretion – more water reabsorption from urine
thirst center stimulated – more drinking
RAA pathway activated – thirst, > ADH secretion,
Na+ & water reabsorption
treatment – give hypotonic fluids
Overhydration – water gain exceeds water loss
(excessive drinking, inability to eliminate water in urine, excess ADH)
causes high blood volume and pressure, and hypoosmolarity of plasma
>filtration, < reabsorption = decreases interstitial osmolarity
osmosis from interstitial fluid to ICF (cells swell)
Body’s Response to Overhydration
< ADH secretion – more water excreted in urine
natriuretic peptides – reduce thirst, block ADH and aldosterone
treatment – diuretics, IV hypertonic fluids
IONS (ELECTROLYTES) IN BODY FLUIDS
electrolyte – ions from inorganic compound dissolved in water
(eg. Na+, Cl-, K+, Ca+2)
Main Ions in ECF (plasma and interstitial fluid)
Na+, Cl-, plasma protein anions, bicarbonate
Main Ions in ICF (cytosol)
K+, protein and organic phosphate anions
Other Important Ions
Ca+2, Mg+2, inorganic phosphate anions
(stored in bones)
FUNCTIONS OF IONS IN BODY FLUIDS
control osmosis between fluid compartments
ions are transported across membranes – water follows
participate in cell functions
action potentials in neurons
muscle contraction
regulate acid-base balance – eg. bicarbonate ions
cofactors for enzymes – eg. Ca+2 in blood clotting
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SODIUM
most abundant cation in ECF (90%)
136-148 mEq/liter in plasma (10mEq in cells)
Na/K pumps are responsible for high concentration in ECF
accounts for nearly half of ECF osmolarity
Sodium gain – diet (usually high)
Sodium loss – urine, perspiration
blood concentration is usually stable – balanced by osmosis
(fluid level regulated mainly by ADH)
Sodium Imbalances:
hyponatremia – low blood Na+ (due to overhydration)
> aldosterone – increases Na+ reabsorption in kidneys
< ADH – increases urine production (dilute)
causes depressed CNS function – mental impairment, coma death
treatment – diuretics, hypertonic NaCl solution
hypernatremia – high blood Na+ (due to dehydration)
> ADH – decreases urine production, increases thirst
causes thirst, tenting of skin, < BP leading to shock
treatment – rehydrate with hypotonic fluids
POTASSIUM
most abundant cation in ICF
140 mEq/liter in cells (3-5 mEq/liter in plasma)
Na/K pumps establish this gradient
Potassiuim gain – diet
Potassium loss – urine
blood concentration regulated by kidney secretion
Potassium Imbalances:
hyperkalemia – high blood K+ (eg. renal failure, acidosis)
causes cardiac arrhythmia
treatment – hypotonic fluid
hypokalemia – low blood K+ (eg. inadequate dietary intake, diuretics)
> aldosterone – increases secretion by renal tubules
causes weakness, paralysis
treatment – administer K+
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CALCIUM
most abundant mineral in body
99% stored in bones as mineral salts
4.5-5.5 mEq/liter in plasma
Calcium gain – diet (depends on calcitriol)
Calcium loss – urine, bile (small amounts)
Regulation of Blood Calcium
parathyroid hormone (PTH) – increases blood calcium
increases bone resorption
increases reabsorption of Ca+2 in kidneys
increases production of calcitriol
increases absorption of dietary Ca+2 in GI tract
calcitonin (not significant) – decreases blood calcium
decreases bone resorption
Calcium Imbalances:
hypercalcemia – high blood Ca+2 (hyperparathyroidism)
causes mental impairment, cardiac arrythmia, kidney stones
abnormal tissue calcification
treatment – hypotonic fluids, calcitonin
hypocalcemia – low blood Ca+2 (reduced intake, hypoparathyroidism)
causes muscle spasms, weak heartbeats, osteoporosis
treatment – administer Ca+2 and vitamin D
CHLORIDE
most abundant anion in ECF
100-108 mEq/liter in plasma (3mEq/L in cells)
Cl- follows Na+ to balance electrical charges
cells exchange Cl- for HCO3- in respiration (chloride shift)
chloride pumps form hydrochloric acid in gastric juice
ACID-BASE BALANCE
acid – dissociates in solution to form H+ (proton)
base – dissociates in solution to form OH- or another proton acceptor
decreases acidity by binding H+
pH scale measures H+ concentration of a solution
7 = neutral (acid=base)
<7 = acidic (more hydrogen ions)
>7 = basic or alkaline (fewer hydrogen ions)
strong acid – relatively complete dissociation = forms many H+
weak acid – incomplete dissociation = forms few H+
strong base – relatively complete binding of H+ = significantly reduces H+
weak base – incomplete binding of H+ = minor reduction in H+
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normal blood pH is 7.35-7.45
vital for normal metabolic functions
proteins (structural, enzymes) denature at high or low pH
pH changes disrupt cell membranes
pH changes alter balance of reversible reactions
acidosis – physiological state when pH < 7.35
CNS – disorientation, coma
heart – decreases contractility, causes arrhythmias
alkalosis – physiological state when pH > 7.45
CNS – convulsions, seizures
muscles – spasms, tetanus
Sources of Acids in Body
metabolism
CO2 production – carbonic acid
catabolizing proteins – sulfuric acid, phosphoric acid
hypoxia – lactic acid
starvation – ketone bodies
REGULATION OF BODY pH
3 Mechanisms:
1) BUFFER SYSTEMS – molecules that can temporarily bind excess H+
or donate H+ when they are low
Protein Buffer System (eg. hemoglobin, plasma proteins, others)
amino acids in ECF and ICF
amino group (NH2) – weak base
binds H+ when acidity increases
carboxyl group (COOH) – weak acid
donates H+ when acidity decreases
Phosphate Buffer System (in ICF)
dihydrogen phosphate (H2PO4-) – weak acid
donates H+ when acidity is low
monohydrogen phosphate (HPO4-2) – weak base
binds excess H+ when acidity is high
Carbonic Acid – Bicarbonate System (in ECF)
carbonic acid (H2CO3) – weak acid
donates H+ when acidity decreases
bicarbonate (HCO3-) – weak base
binds excess H+ when acidity increases
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2) RESPIRATORY COMPENSATION – altering ventilation to adjust pH
indirectly eliminates H+ by binding it in water
H+ + HCO3- <----> H2CO3 <----> CO2 + H2O
(CO2 diffuses out of blood in lungs and is exhaled)
increasing respirations = more CO2 exhaled = blood is less acidic
decreasing respirations = less CO2 exhaled = blood is more acidic
3) RENAL COMPENSATION – altering kidney activity to adjust pH
proton pumps normally actively secrete excess H+ and reabsorb HCO3secreted H+ is buffered in tubules (prevents H+ gradient forming)
ammonia (NH3) ---> ammonium ion (NH4+)
monohydrogen phosphate (HPO4-2) ---> H2PO4-
ACID – BASE DISTURBANCES
Respiratory Acidosis – low pH due to inadequate respiration
hypercapnia – high blood PCO2 (>45mmHg)
due to respiratory disorders - emphysema, pulmonary edema,
asthma, damage to respiratory center
cardiac disorders – reduced pulmonary perfusion
body’s response to respiratory acidosis
buffer systems bind H+ = > pH
respiratory compensation (if possible)
increased ventilation = <PCO2 = > pH
renal compensation – increased H+ secretion = > pH
increased HCO3- reabsorption = buffers H+ = >pH
Respiratory Alkalosis – high pH due to excessive respiration
hypocapnia – low blood PCO2 (<35mmHg)
due to hyperventilation – physical or emotional stress, high altitude
body’s response to respiratory alkalosis
buffers release H+
respiratory compensation (if possible)
decreased ventilation = > PCO2 = < pH
renal compensation – decreased H+ secretion = < pH
increased HCO3- secretion = less buffering of H+ = < pH
Metabolic Acidosis – low pH due to altered metabolic processes
accumulation of metabolic acids – ketoacidosis, lactic acidosis
failure to excrete H+ - renal disorders
loss of HCO3- - severe diarrhea
body’s response to metabolic acidosis – see respiratory acidosis
respiratory compensation is very effective
PCO2 is low when respiratory compensation is occurring
renal compensation not possible if problem has renal origin
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Metabolic Alkalosis – high pH due to altered metabolic processes
loss of acid – severe vomiting (HCl lost)
excess alkaline drugs – antacids
body’s response to metabolic alkalosis – see respiratory alkalosis
respiratory compensation is very effective
PCO2 is high when respiratory compensation is occurring
renal compensation not possible if problem has renal origin
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