SCIT 1408 Applied Human Anatomy and Physiology II - Fluids Chapter 26

Body Water Content
Infants 73% or >, water
Females ~ 50%, water
Males ~ 60%, water
Old age ~ 45%, water
Total water content declines with age
Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings
Fluid Compartments
ICF intracellular fluid; (2/3 total fluid volume)
ECF extracellular fluid; (1/3 total fluid volume)
Plasma the fluid portion of the blood
Interstitial fluid (IF) fluid in spaces between cells
Other minor ECFs
Lymph, CSF, eye humors, synovial fluid, serous

fluid, and GI secretions
Fluid Compartments
PLAY
InterActive Physiology :
Introduction to Body Fluids, page 10
Figure 26.1
Composition of Body Fluids
Water = universal solvent
Solutes are:
Electrolytes
inorganic salts, all acids and bases, & some proteins
Dissociate in H20, > particles, > osmosis factor
Nonelectrolytes
glucose, lipids, creatinine, & urea
Do not dissociate, 1 particle, < osmosis factor
Water moves according to osmotic gradients
PLAY
Introduction to Body Fluids, page 11
Electrolyte Concentration
mEq/L - # electrical charges/ L soln
mEq/L = (concentration of ion in [mg/L]/the

atomic weight of ion) number of electrical
charges on one ion
For single charged ions, 1 mEq = 1 mOsm
For bivalent ions, 1 mEq = 1/2 mOsm
1 mOsm = # solute particles in 1 g or 1 ml H20
Electrolyte Composition of Body Fluids
Body Fluid Compartments
ECF
ICF
Figure 26.2
Fluid Movement Among Compartments
Compartmental exchange is regulated by osmotic

and hydrostatic pressures
IF in capillary beds returned to blood via lymph
Exchanges between IF & ICF via semi-permeable

cell membranes
Two-way water flow is substantial
Nutrients flow into ICF, wastes flow out (1-way

flow)
Extracellular and Intracellular Fluids
Osmolalities of all body fluids are equal
changes in solute concentrations are quickly

followed by osmotic changes
ICF volume due to ECF [solute]
Plasma
PLAY
only fluid that circulates throughout the body

links external and internal environments
Introduction to Body Fluids, pages 1922
Continuous Mixing of Body Fluids
Figure 26.3
Water Intake and Output for Proper Hydration
> plasma osmolality

triggers release of
ADH & stimulates
thirst
Figure 26.4
Regulation of Water Intake
The hypothalamic thirst center is stimulated:
By a decline in plasma volume of 10%15%
By increases in plasma osmolality of 12%
Via baroreceptor input, angiotensin II, other stimuli
Not always stimulated when fluid vol is < as in

exercise
Thirst turned off by mouth moisture, stomach

stretch receptors
PLAY
Water Homeostasis, page 18
Regulation of Water Intake: Thirst Mechanism
Figure 26.5
Regulation of Water Output
Obligatory H20 losses include:
Insensible water losses from lungs and skin
H20 in undigested food residues in feces
Kidneys excrete 900-1200 mOsm of solutes to

maintain blood homeostasis
Urine solutes must be flushed out of the body in

H20 ---- H20 follows Na+
PLAY
Water Homeostasis, pages 310
Influence and Regulation of ADH
Water reabsorption in collecting ducts directly

proportional to ADH release
< ADH = dilute urine, < volume of body fluids
> ADH = concentrated urine, > body fluids via > of

aquaporins in collecting duct membranes
Regulation of ADH release = hypothalmus
> ADH release: > fever; > sweating, vomiting,

diarrhea; severe blood loss, burns
PLAY
Mechanisms and Consequences of ADH

Release
Figure 26.6
Disorders of Water Balance: Dehydration
H20 loss > H20 intake;
negative fluid balance
From: hemorrhage, burns, vomiting, diarrhea,

sweating, water deprivation, > diuretics
Signs/symptoms: cottonmouth, thirst, dry flushed

skin, oliguria
Prolonged dehydration: < H20 in ECF
wt loss
Fever
mental confusion
hypovolemic shock, < electrolytes
Disorders of Water Balance: Dehydration
Figure 26.7a
Disorders of Water Balance:

Hypotonic Hydration
Figure 26.7b
Disorders of Water Balance:

Hypotonic Hydration
From: Renal insufficiency or >>> ingestion of H20
Hyponatremia
ECF diluted sodium level normal but > water
H20 moves into cells
Nausea, vomiting, cramping, cerebral edema
Immediate threat to neurons
Disorders of Water Balance: Edema
> fluid in the interstitial space, tissue swelling
Caused by: > flow of fluids out of the blood or

< return of fluids to blood
> flow of fluids out of the blood :
> BP, > capillary permeability (inflammation)
Damaged venous valves, blocked blood vessels
CHF, hypertension, high blood volume
Edema
< return of fluids to blood (imbalance in colloid

osmotic pressures)
Hypoproteinemia < plasma proteins
In capillary beds, fluid leaves at the arterial ends, < plasma

proteins fail to pull fluid back in at venous end
From: protein malnutrition, liver disease,

glomerulonephritis
Blocked lymphatic vessels
Leaked proteins collect in IF, > fluid from

blood; leads to < BP, < circulation
Electrolyte Homeostasis, pages 1216
Electrolyte Balance
Electrolyte balance refers mainly to salt balance
Salts ingested, lost in urine, feces, sweat
Na+, K+, Ca++ regulation very important:
Neuromuscular excitability
Secretory activity
Membrane permeability
Controlling fluid movements
Sodium in Fluid and Electrolyte Balance
Sodium > cation in the ECF; > osmotic pressure
Sodium salts: NaHCO3, NaCl
Account for 90-95% of all solutes in the ECF
Contribute 280 mOsm of the total 300 mOsm ECF

solute concentration
Plasma membranes fairly impermeable to Na+ but

some does leak into cells & is pumped out by Na+K+ pumps
When [Na+] changes, H20 volume changes- ECF

[Na+] remains pretty constant
Sodium in Fluid and Electrolyte Balance
Changes in plasma sodium levels affect:
Plasma volume & BP
ICF & IF volumes
Na+ levels chiefly controlled by kidneys &

coupled to acid-base balance
PLAY
Electrolyte Homeostasis, pages 46, 1822
Regulation of Sodium Balance: Aldosterone
Sodium reabsorption
65% of Na+in filtrate reabsorbed in PCT
25% reclaimed in the loops of Henle
IF, > aldosterone levels

1. all remaining Na+ is reabsorbed
2. > aquaporins inserted into DCT & collecting
ducts, increasing membrane permeability to H20
3. H20 follows Na+ & both are reabsorbed
JGA stimulates renin-angiotensin mechanism to

release aldosterone when:
1. Sympathetic nervous system stimulation
2. Decreased filtrate osmolality
3. Decreased stretch (due to decreased blood
pressure)
Adrenal cortex releases aldosterone if :

1. > K+ in plasma (ECF)
2. < Na+ in plasma (not nearly as sensitive)
> Aldosterone- effects mediated very slowly

1. < urine output
2. > BP
PLAY
Figure 26.8
Addisons Disease
Hypoaldosteronism
Hypovolemia a high risk
Maintenance of Blood Pressure Homeostasis

Correcting < BP
Baroreceptors in
aorta, carotids, heart
Figure 26.9
Mechanisms and Consequences of ANP

Release
Correcting > BP
Figure 26.10
Influence of Other Hormones on Na+ Balance
Estrogens:
> NaCl reabsorption by renal tubules
May cause water retention during menstrual cycles
> edema during pregnancy
Progesterone:
< Na+ reabsorption, > Na+ & H20 loss
Glucocorticoids
> Na+ reabsorption, > edema
Regulation of Potassium Balance
K+ > intracellular cation; Maintains RMP
> ECF K+ (hyperkalemia), < membrane potential
< ECF K+ (hypokalemia) = hyperpolarization &

nonresponsiveness
Imbalance effects excitable cells especially
Neurons
Muscles
Heart- sudden death
Regulation of Potassium Balance

ICF: ECF- H+ exchange with K+ for cation balance
Acidosis, ECF K+ rises
Alkalosis, ECF K+ falls
Regulatory Site: Cortical Collecting Ducts
10- 15% of filtrate K+ lost in urine regardless of need
Must ingest K+ foods over time to keep proper K+

levels
> ECF K+, principal cells in collecting ducts > K+

secreted into filtrate; from diet high in K+
< ECF K+, < secretion/excretion; from diet low in K+
Type A intercalated cells can reabsorb some K+ left in

the filtrate
Influence of Aldosterone on K+ secretion
> Aldosterone, > K+ secretion, > Na+ reabsorption

by principal cells
> ECF K+ around the adrenal cortex causes:
Release of aldosterone
Potassium secretion
Potassium controls its own ECF concentration via

feedback regulation of aldosterone release
Homeostatic Imbalance
Dietary Salt substitutes contain > K+
Must have adequate aldosterone levels to prevent

hyperkalemia
Too much aldosterone, (adrenocortical tumor),

hypokalemia, hyperpolarization of neurons &
paralysis
Regulation of Calcium
Ca++ in ECF is important for:
Hypocalcemia:
> excitability, causes muscle tetany
Hypercalcemia:
Blood clotting, membrane permeability, secretory

behavior, neuromuscular cells
< excitability, May cause heart arrhythmias
Calcium balance is controlled by parathyroid

hormone (PTH) and calcitonin (minor)
Regulation of Calcium and Phosphate
PTH > ECF Ca++ from:
Bones mostly from here
Small intestine > intestinal absorption
Kidneys > Ca++ reabsorption, which goes with

< phosphate reabsorption
Normal Ca++ inhibits PTH release
Acid-Base Balance
Normal pH of body fluids:
Arterial blood = 7.4
Venous blood & IF = 7.35
ICF = 7.0
Alkalosis or alkalemia = arterial blood pH > 7.45
Acidosis or acidemia = arterial pH < 7.35
(physiological acidosis b/c it is below normal even

though it is above neutral pH & not acidic)
Hydrogen Ions
Most from cellular metabolism
[H+] Regulation:
Chemical buffer systems act within seconds
Respiratory center acts within 1-3 minutes
Renal require hrs- days
Acids- H+ donors
Bases- H+ acceptors
Strong and Weak Acids

Strong:
Completely
dissociates
Weak:
Partially
dissociates
Figure 26.11
Chemical Buffer Systems
3 major chemical buffer systems
Bicarbonate buffer system- important ECF buffer
Phosphate buffer system
Protein buffer system
Any drifts in pH are resisted by the entire chemical

buffering system
Bicarbonate Buffer System
A mixture of carbonic acid (H2CO3) weak acid
& sodium bicarbonate (NaHCO3) weak base
If HCl added: Bicarbonate ties up H+, > H2CO3
HCl + NaHCO3
Acid/Base Homeostasis, pages 1617
H2CO3 + NaCl
Phosphate Buffer System
Nearly identical to the bicarbonate system
Sodium salts of dihydrogen phosphate (H2PO4), a

weak acid
Monohydrogen phosphate (HPO42), a weak base
This system is an effective buffer in urine and

intracellular fluid
PLAY
Acid/Base Homeostasis, page 18
Protein Buffer System
Plasma & intracellular proteins - most plentiful and

powerful buffers; eg. hgb
Some amino acids of proteins have:
Carboxyl groups- (weak acids)
Amino groups- (weak bases)
Amphoteric molecules are protein molecules that

can function as a weak acid or a weak base
PLAY
Physiological Buffer Systems
The respiratory system regulation:
CO2 + H2O H2CO3 H+ + HCO3

reversible rxn
PLAY
Physiological Buffer Systems
During carbon dioxide unloading, H+ incorporated

into H2O
When hypercapnia or rising plasma H+ occurs:
Deeper, more rapid breathing expels > CO2
< H+
Alkalosis causes slower, shallow breathing, > H+
Lung dysfunction causes acid-base imbalance

(respiratory acidosis or respiratory alkalosis)
PLAY
Renal Mechanisms of Acid-Base Balance
Chemical buffers can tie up excess acids or bases,

but they cannot eliminate them from the body
The lungs can eliminate carbonic acid by

eliminating carbon dioxide
Only the kidneys can rid the body of metabolic

acids (phosphoric, uric, & lactic acids, & ketones)
and prevent metabolic acidosis
The ultimate acid-base regulatory organs are

the kidneys

1. Conserving (reabsorbing) or generating new
HCO3
2. Excreting HCO3
Losing a HCO3 is the same as gaining a H+
Reabsorbing a HCO3 is the same as losing a H+
Hydrogen ion secretion occurs in the PCT and in

type A intercalated cells
Hydrogen ions from the dissociation of carbonic

acid
PLAY
H2CO3 H+ + HCO3
Tubules impermeable to HCO3; cannot
reabsorb but can conserve via an indirect way
Reabsorption of Bicarbonate
1. In tubule cells : CO2 + H2O H2CO3
2. H2CO3 H+ + HCO3
3. For each H+ secreted, a Na+ & HCO3 are reabsorbed by
the PCT cells
4. Secreted H+ form H2CO3 in filtrate - in tubule lumen
5. H2CO3 then dissociates to CO2 + H2O
6. CO2 diffuses into tubule cell, > H+ secretion
thus, HCO3 disappears from filtrate at the same rate that it
enters the peritubular capillary blood
Reabsorption of Bicarbonate
Carbonic acid formed

in filtrate dissociates
to release carbon
dioxide and water
Carbon dioxide then

diffuses into tubule
cells, where it acts to
trigger further
hydrogen ion
secretion
PLAY
Figure 26.12
Generating New Bicarbonate Ions
Type A intercalated cells of Collecting ducts

generate new HCO3 by 2 mechanisms:
1. Renal excretion of acid via secretion and

excretion of H+
2. Renal excretion of acid via secretion and
excretion of NH4+ ( ammonium ions)
PLAY
Hydrogen Ion Excretion
Dietary H+ must be counteracted by generating

new HCO3
The excreted H+ must bind to buffers in the urine

(phosphate buffer system)
Intercalated cells actively secrete H+ into urine,

which is buffered and excreted
HCO3 generated is:
Moved into the interstitial space via a cotransport

system
Passively moved into the peritubular capillary

blood
Hydrogen Ion Excretion
In response to
acidosis:
Kidneys generate
bicarbonate ions
and add them to the
blood
An equal amount of
hydrogen ions are
added to the urine
Figure 26.13
Ammonium Ion Excretion
This method uses NH4+ produced by the

metabolism of glutamine in PCT cells
Each glutamine metabolized produces two

ammonium ions and two bicarbonate ions
Bicarbonate moves to the blood and ammonium

ions are excreted in urine
Ammonium Ion Excretion
Figure 26.14
Bicarbonate Ion Secretion
When the body is in alkalosis, type B intercalated

cells:
Secrete HCO3
Reabsorb H+ , acidify the blood
The mechanism is the opposite of type A

intercalated cells and the HCO3 reabsorption
process
Even during alkalosis, the nephrons and collecting

ducts excrete fewer HCO3 than they conserve
PLAY
Respiratory Acidosis and Alkalosis
Respiratory system fails to balance pH
Abnormal PCO2 indicates < respiratory function
Normal PCO2 : 35 - 45 mm Hg
Respiratory acidosis: PCO2 > 45mm Hg
Respiratory alkalosis: PCO2 < 35 mm Hg
Respiratory Acidosis and Alkalosis
Respiratory acidosis:
> common cause of acid-base imbalance
> CO2, < pH
From shallow breathing or < gas exchange
pneumonia, cystic fibrosis, emphysema
Respiratory alkalosis:
< CO2, > pH
Hyperventilation
Stress, pain
Metabolic Acidosis
Second most common cause of acid-base

imbalance
< pH, < HCO3
From:
> alcohol, > loss HCO3
> lactic acid from exercise or shock, ketosis,

kidney failure
Metabolic Alkalosis
> pH, > HCO3
From:
Vomiting of the acid contents of the stomach
Intake of excess base (e.g., from antacids)
Constipation, in which excessive bicarbonate is

reabsorbed
Effects of Acidosis & Alkalosis
pH < 7.0
CNS depressed
Coma
Death
pH > 7.8
CNS overstimulated
Muscle tetany
> agitation, nervousness
convulsions
Respiratory and Renal Compensations
Respiratory System attempts to correct metabolic

acid-base imbalances
Renal System attempts to correct imbalances

caused by respiratory disease
Respiratory Compensation of Metabolic Acidosis
> rate & depth of breathing b/c > H+ & < HCO3
stimulate respiratory centers
As CO2 is blown off during respiratory

compensation to get rid of H+, PCO2 levels <
In respiratory acidosis, the respiratory rate is often

depressed and is the immediate cause of the
acidosis
Respiratory Compensation of Metabolic Alkalosis
Compensation exhibits slow, shallow breathing,

allowing CO2 to accumulate in the blood
Compensation is revealed by:
> pH (over 7.45)
> HCO3
Rising PCO2
PLAY
Renal Compensation of Respiratory Acidosis
To correct respiratory acid-base imbalance, renal

mechanisms are stepped up
Acidosis has > PCO2 and > HCO3
> PCO2 is the cause of acidosis
> HCO3 indicate the kidneys are retaining

HCO3 to offset the acidosis
Renal Compensation of Respiratory Alkalosis
< PCO2
> pH
The kidneys eliminate HCO3 by:
failing to reclaim it
actively secreting it
Developmental Aspects
Water content of the body is > at birth (70-80%);

declines with age; 58% at adulthood
> muscle mass, > water (adult males)
Homeostatic mechanisms slow down with age
Elders > risk of dehydration- < responsive to thirst
The very young and the very old are the most
frequent victims of fluid, acid-base, and electrolyte
imbalances
Problems with Fluid, Electrolyte, and AcidBase Balance
Occur in the young, reflecting:
Low residual lung volume
High rate of fluid intake and output
High metabolic rate yielding more metabolic

wastes
High rate of insensible water loss
Inefficiency of kidneys in infants

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Body Water Content

Infants 73% or >, water

Females ~ 50%, water

Males ~ 60%, water

Old age ~ 45%, water

Total water content declines with age

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

ICF intracellular fluid; (2/3 total fluid volume)

ECF extracellular fluid; (1/3 total fluid volume)

Plasma the fluid portion of the blood

Interstitial fluid (IF) fluid in spaces between cells

Other minor ECFs

Lymph, CSF, eye humors, synovial fluid, serous

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Composition of Body Fluids

Water = universal solvent

inorganic salts, all acids and bases, & some proteins

Dissociate in H20, > particles, > osmosis factor

glucose, lipids, creatinine, & urea

Do not dissociate, 1 particle, < osmosis factor

Water moves according to osmotic gradients

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

mEq/L - # electrical charges/ L soln

mEq/L = (concentration of ion in [mg/L]/the

For single charged ions, 1 mEq = 1 mOsm

For bivalent ions, 1 mEq = 1/2 mOsm

1 mOsm = # solute particles in 1 g or 1 ml H20

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Electrolyte Composition of Body Fluids

Body Fluid Compartments

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Fluid Movement Among Compartments

Compartmental exchange is regulated by osmotic

IF in capillary beds returned to blood via lymph

Exchanges between IF & ICF via semi-permeable

Two-way water flow is substantial

Nutrients flow into ICF, wastes flow out (1-way

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Extracellular and Intracellular Fluids

Osmolalities of all body fluids are equal

changes in solute concentrations are quickly

ICF volume due to ECF [solute]

only fluid that circulates throughout the body

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Continuous Mixing of Body Fluids

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Water Intake and Output for Proper Hydration

> plasma osmolality

Regulation of Water Intake

The hypothalamic thirst center is stimulated:

By a decline in plasma volume of 10%15%

By increases in plasma osmolality of 12%

Via baroreceptor input, angiotensin II, other stimuli

Not always stimulated when fluid vol is < as in

Thirst turned off by mouth moisture, stomach

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Water Intake: Thirst Mechanism

Copyright 2006 Pearson Education, Inc., publishing as Benjamin Cummings

Regulation of Water Output

Obligatory H20 losses include:

Insensible water losses from lungs and skin

H20 in undigested food residues in feces

Kidneys excrete 900-1200 mOsm of solutes to