13 Fluid and Electrolyte Balance

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Transcript 13 Fluid and Electrolyte Balance

24
Fluid,
Electrolyte,
and Acid-Base
Balance
PowerPoint® Lecture Presentations prepared by
Alexander G. Cheroske
Mesa Community College at Red Mountain
© 2011 Pearson Education, Inc.
Section 1: Fluid and Electrolyte Balance
• Learning Outcomes
• 24.1 Explain what is meant by fluid balance, and
discuss its importance for homeostasis.
• 24.2 Explain what is meant by mineral balance, and
discuss its importance for homeostasis.
• 24.3 Summarize the relationship between sodium
and water in maintaining fluid and electrolyte
balance.
• 24.4 CLINICAL MODULE Explain factors that
control potassium balance, and discuss
hypokalemia and hyperkalemia.
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Section 1: Fluid and Electrolyte Balance
• Fluids constitute ~50%–60% of total body
composition
• Minerals (inorganic substances) are dissolved
within and form ions called electrolytes
• Fluid compartments
• Intracellular fluid (ICF)
• Water content varies most here due to variation in:
• Tissue types (muscle vs. fat)
• Distinct from ECF due to plasma membrane transport
• Extracellular fluid (ECF)
• Interstitial fluid volume varies
• Volume of blood (women < men)
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Total body composition of adult males
Total body composition of adult males and females
ICF
ECF
Intracellular
fluid 33%
Interstitial
fluid 21.5%
Plasma 4.5%
Solids 40%
(organic and inorganic materials)
Other
body
fluids
(≤1%)
Adult males
Total body composition of adult females
ECF
ICF
Intracellular
fluid 27%
Interstitial
fluid 18%
Plasma 4.5%
Solids 50%
(organic and inorganic materials)
Adult females
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Other
body
fluids
(≤1%)
Figure 24 Section 1
1
The solid components of a 70-kg (154-pound)
individual with a minimum of body fat
SOLID COMPONENTS
(31.5 kg; 69.3 lbs)
Kg
Proteins
Lipids
Minerals Carbohydrates Miscellaneous
Figure 24 Section 1
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2
Module 24.1: Fluid balance
• Fluid balance
• Water content stable over time
• Gains
• Primarily absorption along digestive tract
• As nutrients and ions are absorbed, osmotic gradient created
causing passive absorption of water
• Losses
• Mainly through urination (over 50%) but other routes as well
• Digestive secretions are reabsorbed similarly to ingested
fluids
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Figure 24.1
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1
Dietary Input
Digestive Secretions
Food and drink 2200 mL
Saliva 1500 mL
The digestive tract sites of water gain
through ingestion or secretion, or water
reabsorption, and of water loss
Gastric secretions 1500 mL
5200 mL
Liver (bile) 1000 mL
Pancreas (pancreatic
juice) 1000 mL
Water Reabsorption
Intestinal secretions 2000 mL
9200 mL
Small intestine
reabsorbs 8000 mL
1200 mL
Colon reabsorbs 1250 mL
1400
mL
Colonic mucous secretions
200 mL
150 mL lost
in feces
Figure 24.1
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Module 24.1: Fluid balance
• ICF and ECF compartments balance
• Very different composition
• Are at osmotic equilibrium
• Loss of water from ECF is replaced by water in ICF
• = Fluid shift
• Occurs in minutes to hours and restores osmotic equilibrium
• Dehydration
• Results in long-term transfer that cannot replace ECF water
loss
• Homeostatic mechanisms to increase ECF fluid volume will
be employed
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The major factors that affect ECF volume
ICF
Metabolic
water
(300 mL)
Water absorbed across
digestive epithelium
(2000 mL)
ECF
Water vapor lost
in respiration and
evaporation from
moist surfaces
(1150 mL)
Water lost in
feces (150 mL)
Water secreted
by sweat glands
(variable)
Plasma membranes
Water lost in urine
(1000 mL)
Figure 24.1
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Changes to the ICF and ECF when water losses outpace water gains
Intracellular
fluid (ICF)
Decreased ICF volume
Extracellular
fluid (ECF)
The ECF and ICF are in
balance, with the two
solutions isotonic.
ECF water loss
Water loss from ECF
reduces volume and
makes this solution
hypertonic with respect
to the ICF.
Increased
ECF volume
An osmotic water shift
from the ICF into the
ECF restores osmotic
equilibrium but
reduces the ICF
volume.
Figure 24.1
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Module 24.1 Review
a. Identify routes of fluid loss from the body.
b. Describe a fluid shift.
c. Explain dehydration and its effect on the
osmotic concentration of plasma.
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Module 24.2: Mineral balance
•
Mineral balance
•
Equilibrium between ion absorption and excretion
•
Major ion absorption through intestine and colon
•
Major ion excretion by kidneys
• Sweat glands excrete ions and water variably
•
Ion reserves mainly in skeleton
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Mineral balance, the balance between ion absorption (in the digestive tract) and ion excretion (primarily at the kidneys)
Ion Absorption
Ion absorption occurs across the
epithelial lining of the small intestine
and colon.
Ion reserves (primarily
in the skeleton)
Ion Excretion
Sweat gland
secretions
(secondary
site of ion loss)
Ion pool in body fluids
Kidneys
(primary site
of ion loss)
ICF
ECF
Figure 24.2
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Figure 24.2
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Figure 24.2
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3
Figure 24.2
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Module 24.2 Review
a. Define mineral balance.
b. Identify the significance of two important body
minerals: sodium and calcium.
c. Identify the ions absorbed by active transport.
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Module 24.3: Water and sodium balance
• Sodium balance (when sodium gains equal
losses)
• Relatively small changes in Na+ are accommodated
by changes in ECF volume
• Homeostatic responses involve two parts
1. ADH control of water loss/retention by kidneys and thirst
2. Fluid exchange between ECF and ICF
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The mechanisms that regulate sodium balance
when sodium concentration in the ECF changes
ADH Secretion Increases
The secretion of ADH
restricts water loss and
stimulates thirst, promoting
additional water
consumption.
Rising plasma
sodium levels
Recall of Fluids
Because the ECF
osmolarity increases,
water shifts out of the
ICF, increasing ECF
volume and lowering
ECF Na concentrations.
Osmoreceptors
in hypothalamus
stimulated
If you consume large
amounts of salt without
adequate fluid, as when
you eat salty potato
chips without taking a
drink, the plasma Na
concentration rises
temporarily.
HOMEOSTASIS
RESTORED
HOMEOSTASIS
DISTURBED
Decreased Na
levels in ECF
Na
Increased
levels in ECF
HOMEOSTASIS
Normal Na
concentration
in ECF
Start
Figure 24.3
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1
The mechanisms that regulate sodium balance
when sodium concentration in the ECF changes
HOMEOSTASIS
Normal Na
concentration
in ECF
HOMEOSTASIS
DISTURBED
HOMEOSTASIS
RESTORED
Decreased Na
levels in ECF
Osmoreceptors
in hypothalamus
inhibited
Falling plasma
sodium levels
Start
Increased Na
levels in ECF
ADH Secretion
Decreases
Water loss reduces
ECF volume,
concentrates ions
As soon as the osmotic
concentration of the ECF
drops by 2 percent or
more, ADH secretion
decreases, so thirst is
suppressed and water
losses at the kidneys
increase.
Figure 24.3
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1
Module 24.3: Water and sodium balance
• Sodium balance (continued)
• Exchange changes in Na+ are accommodated by
changes in blood pressure and volume
• Hyponatremia (natrium, sodium)
• Low ECF Na+ concentration (<136 mEq/L)
• Can occur from overhydration or inadequate salt intake
• Hypernatremia
• High ECF Na+ concentration (>145 mEq/L)
• Commonly from dehydration
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Module 24.3: Water and sodium balance
• Sodium balance (continued)
• Exchange changes in Na+ are accommodated by
changes in blood pressure and volume (continued)
• Increased blood volume and pressure
• Natriuretic peptides released
• Increased Na+ and water loss in urine
• Reduced thirst
• Inhibition of ADH, aldosterone, epinephrine, and
norepinephrine release
• Decreased blood volume and pressure
• Endocrine response
• Increased ADH, aldosterone, RAAS mechanism
• Opposite bodily responses to above
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The mechanisms that regulate water balance
when ECF volume changes
Responses to Natriuretic Peptides
Rising blood
pressure and
volume
Increased water loss in urine
Natriuretic peptides
released by cardiac
muscle cells
Increased Na loss in urine
Combined
Effects
Reduced
blood
volume
Reduced thirst
Inhibition of ADH, aldosterone,
epinephrine, and norepinephrine
release
Reduced
blood
pressure
Increased blood
volume and
atrial distension
HOMEOSTASIS
RESTORED
HOMEOSTASIS
DISTURBED
Falling ECF
volume
Rising ECF volume by fluid
gain or fluid and Na gain
HOMEOSTASIS
Start
Normal ECF
volume
Figure 24.3
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The mechanisms that regulate water balance
when ECF volume changes
HOMEOSTASIS
Start
Normal ECF
volume
HOMEOSTASIS
DISTURBED
Falling ECF volume by fluid
loss or fluid and Na loss
Decreased blood
volume and
blood pressure
Falling blood
pressure and
volume
HOMEOSTASIS
RESTORED
Rising ECF
volume
Endocrine Responses
Combined Effects
Increased renin secretion
and angiotensin II
activation
Increased aldosterone
release
Increased ADH release
Increased urinary Na retention
Decreased urinary water loss
Increased thirst
Increased water intake
Figure 24.3
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Module 24.3 Review
a. What effect does inhibition of osmoreceptors have
on ADH secretion and thirst?
b. What effect does aldosterone have on sodium ion
concentration in the ECF?
c. Briefly summarize the relationship between sodium
ion concentration and the ECF.
© 2011 Pearson Education, Inc.
CLINICAL MODULE 24.4: Potassium
imbalance
• Potassium balance (K+ gain = loss)
• Major gain is through digestive tract absorption
• ~100 mEq (1.9–5.8 g)/day
• Major loss is excretion by kidneys
• Primary ECF potassium regulation by kidneys since intake fairly
constant
• Controlled by aldosterone regulating Na+/K+ exchange pumps in
DCT and collecting duct of nephron
• Low ECF pH can cause H+ to be substituted for K+
• Potassium is highest in ICF due to Na+/K+ exchange pump
• ~135 mEq/L in ICF vs. ~5 mEq/L in ECF
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The major factors involved in potassium balance
Factors Controlling Potassium Balance
Approximately 100
mEq (1.9–5.8 g) of
potassium ions are
absorbed by the
digestive tract each
day.
Roughly
98 percent of the
potassium
content of the
human body is in
the ICF, rather
than the ECF.
The K concentration in the
ECF is relatively low. The rate
of K entry from the ICF
through leak channels is
balanced by the rate of K
recovery by the Na/K
exchange pump.
When potassium
balance exists,
the rate of urinary
K excretion
matches the rate
of digestive tract
absorption.
The potassium ion
concentration in the
ECF is approximately
5 mEq/L.
KEY

Absorption

Secretion

Diffusion through
leak channels
The potassium ion
concentration of the
ICF is approximately
135 mEq/L.
Renal K losses
are approximately
100 mEq per day
Figure 24.4
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The role of aldosterone-sensitive exchange pumps
in the kidneys in determining the potassium
concentration in the ECF
The primary mechanism of
potassium secretion involves
an exchange pump that
ejects potassium ions while
reabsorbing sodium ions.
Tubular
fluid
KEY
 Aldosteronesensitive
exchange
pump

ECF
The sodium ions are then pumped out
of the cell in exchange for potassium
ions in the ECF. This is the same pump
that ejects sodium ions entering the
cytosol through leak channels.
Sodium-potassium
exchange pump
Figure 24.4
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Events in the kidneys that affect potassium balance
Distal
convoluted
tubule
Collecting
duct
Under normal conditions, the
aldosterone-sensitive pumps
exchange K in the ECF for
Na in the tubular fluid. The
net result is a rise in plasma
sodium levels and increased
K loss in the urine.
When the pH falls in the ECF
and the concentration of H is
relatively high, the exchange
pumps bind H instead of K.
This helps to stabilize the pH
of the ECF, but at the cost of
rising K levels in the ECF.
Figure 24.4
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CLINICAL MODULE 24.4: Potassium
imbalance
• Disturbances of potassium balance
• Hypokalemia (kalium, potassium)
• Below 2 mEq/L in plasma
• Can be caused by:
• Diuretics
• Aldosteronism (excessive aldosterone secretion)
• Symptoms
• Muscular weakness, followed by paralysis
• Potentially lethal when affecting heart
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CLINICAL MODULE 24.4: Potassium
imbalance
• Disturbances of potassium balance (continued)
• Hyperkalemia
• Above 8 mEq/L in plasma
• Can be caused by:
• Chronically low pH
• Kidney failure
• Drugs promoting diuresis by blocking Na+/K+ pumps
• Symptoms
• Muscular spasm including heart arrhythmias
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CLINICAL MODULE 24.4 Review
a. Define hypokalemia and hyperkalemia.
b. What organs are primarily responsible for
regulating the potassium ion concentration of the
ECF?
c. Identify factors that cause potassium excretion.
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Section 2: Acid-Base Balance
•
Learning Outcomes
• 24.5 Explain the role of buffer systems in maintaining
acid-base balance and pH.
• 24.6 Explain the role of buffer systems in regulating
the pH of the intracellular fluid and the
extracellular fluid.
• 24.7 Describe the compensatory mechanisms
involved in the maintenance of acid-base
balance.
• 24.8 CLINICAL MODULE Describe respiratory
acidosis and respiratory alkalosis.
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Section 2: Acid-Base Balance
•
Acid-base balance (H+ production = loss)
•
Normal plasma pH: 7.35–7.45
•
H+ gains: many metabolic activities produce
acids
•
CO2 (to carbonic acid) from aerobic respiration
•
Lactic acid from glycolysis
•
H+ losses and storage
•
Respiratory system eliminates CO2
•
H+ excretion from kidneys
•
Buffers temporarily store H+
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The major factors involved in the maintenance
of acid-base balance
The respiratory system
plays a key role by
eliminating
carbon dioxide.
Active tissues
continuously generate
carbon dioxide, which in
solution forms carbonic
acid. Additional acids,
such as lactic acid, are
produced in the course of
normal metabolic
operations.
Normal
plasma pH
(7.35–7.45)
Tissue cells
Buffer Systems
The kidneys play a major
role by secreting
hydrogen ions into the
urine and generating
buffers that enter the
bloodstream. The rate of
excretion rises and falls
as needed to maintain
normal plasma pH. As a
result, the normal pH of
urine varies widely but
averages 6.0—slightly
acidic.
Buffer systems can
temporarily store H
and thereby provide
short-term pH
stability.
Figure 24 Section 2
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1
Section 2: Acid-Base Balance
•
Classes of acids
•
Fixed acids
•
Do not leave solution
•
•
Examples: sulfuric and phosphoric acid
•
•
Remain in body fluids until kidney excretion
Generated during catabolism of amino acids, phospholipids,
and nucleic acids
Organic acids
•
Part of cellular metabolism
•
•
Examples: lactic acid and ketones
Most metabolized rapidly so no accumulation
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Section 2: Acid-Base Balance
•
Classes of acids (continued)
•
Volatile acids
•
Can leave body by external respiration
•
Example: carbonic acid (H2CO3)
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Module 24.5: Buffer systems
• pH imbalance
• ECH pH normally between 7.35 and 7.45
• Acidemia (plasma pH <7.35): acidosis (physiological
state)
• More common due to acid-producing metabolic activities
• Effects
• CNS function deteriorates, may cause coma
• Cardiac contractions grow weak and irregular
• Peripheral vasodilation causes BP drop
• Alkalemia (plasma pH >7.45): alkalosis (physiological
state)
• Can be dangerous but relatively rare
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Figure 24.5
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1
The narrow range of normal pH of the ECF, and the conditions that result from pH shifts outside the normal range
The pH of the ECF
(extracellular fluid)
normally ranges from
7.35 to 7.45.
When the pH of plasma falls below
7.5, acidemia exists. The
physiological state that results is
called acidosis.
When the pH of plasma rises
above 7.45, alkalemia exists.
The physiological state that
results is called alkalosis.
Extremely
acidic
Extremely
basic
pH
Severe acidosis (pH below 7.0) can be deadly
because (1) central nervous system function
deteriorates, and the individual may become
comatose; (2) cardiac contractions grow weak and
irregular, and signs and symptoms of heart failure
may develop; and (3) peripheral vasodilation
produces a dramatic drop in blood pressure,
potentially producing circulatory collapse.
Severe alkalosis is also
dangerous, but serious cases
are relatively rare.
Figure 24.5
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2
Module 24.5: Buffer systems
• CO2 partial pressure effects on pH
• Most important factor affecting body pH
• H2O + CO2  H2CO3  H+ + HCO3–
• Reversible reaction that can buffer body pH
• Adjustments in respiratory rate can affect body pH
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The inverse relationship between the PCO2 and pH
PCO2
40–45
mm Hg
pH
7.35–7.45
HOMEOSTASIS
If PCO2 rises
H2O  CO2
H2CO3
H  HCO3
When carbon dioxide levels rise, more carbonic acid
forms, additional hydrogen ions and bicarbonate ions
are released, and the pH goes down.
If PCO2 falls
H  HCO3
H2CO3
H2O  CO2
When the PCO2 falls, the reaction runs in reverse, and
carbonic acid dissociates into carbon dioxide and
water. This removes H ions from solution and
increases the pH.
Figure 24.5
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Module 24.5: Buffer systems
• Buffer
• Substance that opposes changes to pH by removing
or adding H+
• Generally consists of:
• Weak acid (HY)
• Anion released by its dissociation (Y–)
• HY  H+ + Y– and H+ + Y–  HY
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The reactions that occur when pH buffer systems function
A buffer system in body fluids generally
consists of a combination of a weak acid (HY)
and the anion (Y) released by its dissociation.
The anion functions as a weak base. In solution,
molecules of the weak acid exist in equilibrium
with its dissociation products.
HY
H

Y
Adding H to the
solution upsets the
equilibrium and results
in the formation of
additional molecules of
the weak acid.
H  Y
H
H  HY
Removing H from the
solution also upsets the
equilibrium and results
in the dissociation of
additional molecules of
HY. This releases H.
H  HY
H  Y
H
Figure 24.5
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Module 24.5 Review
a. Define acidemia and alkalemia.
b. What is the most important factor affecting the pH
of the ECF?
c. Summarize the relationship between CO2 levels
and pH.
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Module 24.6: Major body buffer systems
•
Three major body buffer systems
•
All can only temporarily affect pH (H+ not eliminated)
1.
Phosphate buffer system
•
2.
Buffers pH of ICF and urine
Carbonic acid–bicarbonate buffer system
•
Most important in ECF
•
Fully reversible
•
Bicarbonate reserves (from NaHCO3 in ECF) contribute
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Module 24.6: Major body buffer systems
•
Three major body buffer systems (continued)
3. Protein buffer systems (in ICF and ECF)
•
Usually operate under acid conditions (bind H+)
•
•
Binding to carboxyl group (COOH–) and amino group
(—NH2)
Examples:
•
Hemoglobin buffer system
•
CO2 + H2O  H2CO3  HCO3– + Hb-H+
•
Only intracellular system with immediate effects
•
Amino acid buffers (all proteins)
•
Plasma proteins
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The body’s three major buffer systems
Buffer Systems
occur in
Intracellular fluid (ICF)
Phosphate Buffer
System
Has an important
role in buffering the
pH of the ICF and
of urine
Extracellular fluid (ECF)
Protein Buffer Systems
Contribute to the regulation of pH in the ECF and ICF;
interact extensively with the other two buffer systems
Carbonic Acid–
Bicarbonate Buffer
System
Is most important in the
ECF
Hemoglobin
buffer system
(RBCs only)
Amino acid
buffers
(All proteins)
Plasma
protein
buffers
Figure 24.6
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1
The reactions of the carbonic acid–bicarbonate buffer system
CARBONIC ACID–BICARBONATE
BUFFER SYSTEM
CO2
CO2  H2O
Lungs
H2CO3
(carbonic acid)
Start
H

HCO3
(bicarbonate ion)
Addition of H
from metabolic
activity
BICARBONATE RESERVE
Body fluids contain a large reserve of
HCO3, primarily in the form of dissolved
molecules of the weak base sodium
bicarbonate (NaHCO3). This readily
available supply of HCO3 is known as
the bicarbonate reserve.
HCO3  Na
NaHCO3
(sodium bicarbonate)
The primary function of the carbonic
acid–bicarbonate buffer system is to
protect against the effects of the organic
and fixed acids generated through
metabolic activity. In effect, it takes the H
released by these acids and generates
carbonic acid that dissociates into water
and carbon dioxide, which can easily be
eliminated at the lungs.
Figure 24.6
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4
The events involved in the functioning of the hemoglobin buffer system
Tissue
cells
Plasma
Lungs
Plasma
Red blood cells
Red blood cells
H2O
H2O
CO2
H2CO3
HCO3  Hb
H
Hb H  HCO3
Released
with
exhalation
H2CO3
CO2
Figure 24.6
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2
Start
Normal pH
The mechanism by free amino acids function in
protein buffer systems
Increasing acidity (decreasing pH)
(7.35–7.45)
At the normal pH of
body fluids (7.35–
7.45), the carboxyl
groups of most amino
acids have released
their hydrogen ions.
If pH drops, the carboxylate ion (COO)
and the amino group (—NH2) of a free
amino acid can act as weak bases and
accept additional hydrogen ions, forming a
carboxyl group (—COOH) and an amino
ion (—NH3), respectively. Many of the
R-groups can also accept hydrogen ions,
forming RH.
Figure 24.6
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3
Module 24.6: Major body buffer systems
•
Disorders
•
Metabolic acid-base disorders
•
Production or loss of excessive amounts of fixed or
organic acids
•
Carbonic acid–bicarbonate system works to counter
•
Respiratory acid-base disorders
•
Imbalance of CO2 generation and elimination
•
Must be corrected by depth and rate of respiration
changes
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Module 24.6 Review
a. Identify the body’s three major buffer systems.
b. Describe the carbonic acid–bicarbonate buffer
system.
c. Describe the roles of the phosphate buffer system.
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Module 24.7: Metabolic acid-base disorders
•
Metabolic acid-base disorders
•
Metabolic acidosis
•
•
Develops when large numbers of H+ are released by organic
or fixed acids
Accommodated by respiratory and renal responses
•
•
Respiratory response
•
Increased respiratory rate lowers PCO2
•
H+ + HCO3–  H2CO3  H2O + CO2
Renal response
•
Occurs in PCT, DCT, and collecting system
•
H2O + CO2  H2CO3  H+ + HCO3–

H+ secreted into urine

HCO3– reabsorbed into ECF
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The responses to metabolic acidosis
Start
Addition
of H
CARBONIC ACID–BICARBONATE BUFFER SYSTEM
CO2
CO2  H2O
Lungs
Respiratory Response
to Acidosis
Increased respiratory
rate lowers PCO2,
effectively converting
carbonic acid molecules
to water.
H2CO3
(carbonic acid)
Other
buffer
systems
absorb H
H
 HCO3
(bicarbonate ion)
KIDNEYS
BICARBONATE RESERVE
HCO3  Na
NaHCO3
(sodium bicarbonate)
Generation
of HCO3
Renal Response to Acidosis
Secretion
of H
Kidney tubules respond by (1) secreting H
ions, (2) removing CO2, and (3) reabsorbing
HCO3 to help replenish the bicarbonate
reserve.
Figure 24.7
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1
The activity of renal
tubule cells in CO2
removal and HCO3
production
Tubular
fluid
CO2
CO2

H2O
Carbonic
Na anhydrase
H
H
ECF
Renal tubule cells
CO2
H2CO3
H
HCO3
HCO3
Cl
H
Cl
HCO3
Na
Steps in CO2 removal and
HCO3 production
CO2 generated by the tubule
cell is added to the CO2
diffusing into the cell from
the urine and from the ECF.
Carbonic anhydrase
converts CO2 and water to
carbonic acid, which then
dissociates.
The chloride ions exchanged
for bicarbonate ions are
excreted in the tubular fluid.
Bicarbonate ions and
sodium ions are transported
into the ECF, adding to the
bicarbonate reserve.
Figure 24.7
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2
Module 24.7: Metabolic acid-base disorders
•
Metabolic alkalosis
•
Develops when large numbers of H+ are removed
from body fluids
•
Rate of kidney H+ secretion declines
•
Tubular cells do not reclaim bicarbonate
•
Collecting system transports bicarbonate into urine and
retains acid (HCl) in ECF
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Module 24.7: Metabolic acid-base disorders
•
Metabolic alkalosis (continued)
•
Accommodated by respiratory and renal
responses
•
•
Respiratory response
•
Decreased respiratory rate raises PCO2
•
H2O + CO2  H2CO3  H+ + HCO3–
Renal response
•
Occurs in PCT, DCT, and collecting system
•
H2O + CO2  H2CO3  H+ + HCO3–
•
HCO3– secreted into urine (in exchange for Cl–)
•
H+ actively reabsorbed into ECF
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The responses to metabolic alkalosis
Start
Removal
of H
CARBONIC ACID–BICARBONATE BUFFER SYSTEM
Lungs
CO2  H2O
Respiratory Response
to Alkalosis
Decreased respiratory
rate elevates PCO2,
effectively converting
CO2 molecules to
carbonic acid.
H2CO3
(carbonic acid)
Other
buffer
systems
release H
H
 HCO3
(bicarbonate ion)
Generation
of H
BICARBONATE RESERVE
HCO3  Na
NaHCO3
(sodium bicarbonate)
KIDNEYS
Renal Response to Alkalosis
Secretion
of HCO3
Kidney tubules respond by
conserving H ions and
secreting HCO3.
Figure 24.7
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3
The events in the
secretion of bicarbonate
ions into the tubular
fluid along the PCT, DCT,
and collecting system
Tubular
fluid
Renal tubule cells
CO2

H2O
CO2
ECF
CO2 generated by the tubule
cell is added to the CO2
diffusing into the cell from the
tubular fluid and from the ECF.
CO2
Carbonic anyhydrase converts
CO2 and water to carbonic
acid, which then dissociates.
Carbonic
anhydrase
H2CO3
HCO3
HCO3
Cl
H
H
Cl
The hydrogen ions are actively
transported into the ECF,
accompanied by the diffusion
of chloride ions.
HCO3 is pumped into the
tubular fluid in exchange for
chloride ions that will diffuse
into the ECF.
Figure 24.7
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4
Module 24.7 Review
a. Describe metabolic acidosis.
b. Describe metabolic alkalosis.
c. lf the kidneys are conserving HCO3– and
eliminating H+ in acidic urine, which is
occurring: metabolic alkalosis or metabolic
acidosis?
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CLINICAL MODULE 24.8: Respiratory
acid-base disorders
•
Respiratory acid-base disorders
•
Respiratory acidosis
•
CO2 generation outpaces rate of CO2 elimination at lungs
•
Shifts bicarbonate buffer system toward generating more
carbonic acid
•
H2O + CO2  H2CO3  H+ + HCO3–
•
HCO3– goes into bicarbonate reserve
•
H+ must be neutralized by any of the buffer systems
• Respiratory (increased respiratory rate)
• Renal (H+ secreted and HCO3– reabsorbed)
• Proteins (bind free H+)
© 2011 Pearson Education, Inc.
The events in respiratory acidosis
CARBONIC ACID–BICARBONATE
BUFFER SYSTEM
CO2
CO2  H2O
Lungs
H2CO2
(carbonic acid)
When respiratory activity does not keep
pace with the rate of CO2 generation,
alveolar and plasma PCO2 increases.
This upsets the equilibrium and drives
the reaction to the right, generating
additional H2CO3, which releases H
and lowers plasma pH.
H

HCO3
(bicarbonate ion)
BICARBONATE RESERVE
HCO3  Na
As bicarbonate ions and hydrogen ions
are released through the dissociation of
carbonic acid, the excess bicarbonate
ions become part of the bicarbonate
reserve.
NaHCO3
(sodium bicarbonate)
To limit the pH effects of
respiratory acidosis, the excess
H must either be tied up by
other buffer systems or excreted
at the kidneys. The underlying
problem, however, cannot be
eliminated without an increase in
the respiratory rate.
Figure 24.8
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1
Responses to Acidosis
The integrated homeostatic responses
to respiratory acidosis
Increased
PCO2
Respiratory compensation
Stimulation of arterial and CSF
chemoreceptors results in
increased respiratory rate.
Renal compensation
H ions are secreted and
HCO3 ions are generated.
Respiratory Acidosis
Elevated PCO2 results
in a fall in plasma pH
Buffer systems other than the
carbonic acid–bicarbonate
system accept H ions.
Decreased PCO2
Decreased H and
increased HCO3
HOMEOSTASIS
RESTORED
HOMEOSTASIS
DISTURBED
Hypoventilation
causing increased PCO2
Combined Effects
HOMEOSTASIS
Start
Normal acidbase balance
Plasma pH
returns to normal
Figure 24.8
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2
CLINICAL MODULE 24.8: Respiratory
acid-base disorders
•
Respiratory alkalosis
•
CO2 elimination at lungs outpaces CO2 generation rate
•
Shifts bicarbonate buffer system toward generating more
carbonic acid
•
H+ + HCO3–  H2CO3  H2O + CO2
•
•
H+ removed as CO2 exhaled and water formed
Buffer system responses
•
Respiratory (decreased respiratory rate)
•
Renal (HCO3– secreted and H+ reabsorbed)
•
Proteins (release free H+)
© 2011 Pearson Education, Inc.
The events in respiratory alkalosis
CARBONIC ACID–BICARBONATE
BUFFER SYSTEM
CO2
CO2  H2O
Lungs
H2CO2
(carbonic acid)
If respiratory activity exceeds the rate of CO2
generation, alveolar and plasma PCO2 decline,
and this disturbs the equilibrium and drives
the reactions to the left, removing H and
elevating plasma pH.
H

HCO3
(bicarbonate ion)
BICARBONATE RESERVE
HCO3  Na
NaHCO3
(sodium bicarbonate)
As bicarbonate ions and hydrogen
ions are removed in the formation of
carbonic acid, the bicarbonate ions—
but not the hydrogen ions—are
replaced by the bicarbonate reserve.
Figure 24.8
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3
The integrated homeostatic responses to
respiratory alkalosis
HOMEOSTASIS
HOMEOSTASIS
DISTURBED
Start
Normal acidbase balance
HOMEOSTASIS
RESTORED
Plasma pH
returns to normal
Hyperventilation
causing decreased PCO2
Respiratory Alkalosis
Responses to Alkalosis
Lower PCO2 results
in a rise in plasma pH
Respiratory compensation
Inhibition of arterial and CSF
chemoreceptors results in a
decreased respiratory rate.
Combined Effects
Increased PCO2
Increased H and
decreased HCO3
Renal compensation
Decreased
PCO2
H ions are generated and
HCO3 ions are secreted.
Buffer systems other than the
carbonic acid–bicarbonate system
release H ions.
Figure 24.8
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4
CLINICAL MODULE 24.8 Review
a. Define respiratory acidosis and respiratory
alkalosis.
b. What would happen to the plasma PCO2 of a
patient who has an airway obstruction?
c. How would a decrease in the pH of body fluids
affect the respiratory rate?
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