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13 Fluid and Electrolyte Balance
13 Fluid and Electrolyte Balance
Fluid,
Electrolyte,
and Acid-Base
Balance
PowerPoint® Lecture Presentations prepared by
Alexander G. Cheroske
Mesa Community College at Red Mountain
• 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.
ICF
ECF
Intracellular Interstitial
fluid 33% fluid 21.5%
Plasma 4.5%
Adult males
ICF ECF
Intracellular Interstitial
fluid 27% fluid 18%
Plasma 4.5%
Other
body
Solids 50% fluids
(organic and inorganic materials) (≤1%)
Adult females
Figure 24 Section 1 1
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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
Figure 24 Section 1 2
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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
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
150 mL lost
in feces
Figure 24.1 2
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Module 24.1: Fluid balance
Figure 24.1 3
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Changes to the ICF and ECF when water losses outpace water gains
Figure 24.1 4
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Module 24.1 Review
• 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
Kidneys
(primary site
of ion loss)
ICF ECF
Figure 24.2 1
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Figure 24.2 2
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Figure 24.2 3
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Figure 24.2 3
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Module 24.2 Review
Osmoreceptors
in hypothalamus
stimulated
HOMEOSTASIS
HOMEOSTASIS RESTORED
If you consume large DISTURBED
amounts of salt without Decreased Na
adequate fluid, as when Increased Na
levels in ECF
you eat salty potato levels in ECF
chips without taking a
drink, the plasma Na
concentration rises HOMEOSTASIS
temporarily.
Start
Normal Na
concentration
in ECF
Figure 24.3 1
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The mechanisms that regulate sodium balance
when sodium concentration in the ECF changes
HOMEOSTASIS
Start
Normal Na
concentration
in ECF
HOMEOSTASIS HOMEOSTASIS
DISTURBED RESTORED
Decreased Na
Increased Na
levels in ECF
levels in ECF
Figure 24.3 1
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Module 24.3: Water and sodium balance
HOMEOSTASIS
HOMEOSTASIS
RESTORED
DISTURBED
Figure 24.3 2
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The mechanisms that regulate water balance
when ECF volume changes
HOMEOSTASIS
Start
Normal ECF
HOMEOSTASIS volume HOMEOSTASIS
DISTURBED RESTORED
Falling ECF volume by fluid Rising ECF
loss or fluid and Na loss volume
Decreased blood
volume and Endocrine Responses Combined Effects
blood pressure
Increased renin secretion Increased urinary Na retention
and angiotensin II
activation Decreased urinary water loss
Increased aldosterone
Falling blood Increased thirst
release
pressure and
volume Increased ADH release Increased water intake
Figure 24.3 2
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Module 24.3 Review
KEY
Absorption The potassium ion
Renal K losses
Secretion concentration of the
are approximately
ICF is approximately
Diffusion through 100 mEq per day
leak channels 135 mEq/L.
Figure 24.4 1
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The role of aldosterone-sensitive exchange pumps
in the kidneys in determining the potassium The primary mechanism of
concentration in the ECF potassium secretion involves
an exchange pump that
ejects potassium ions while
reabsorbing sodium ions.
Tubular ECF
fluid
Sodium-potassium
exchange pump
Figure 24.4 2
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Events in the kidneys that affect potassium balance
Figure 24.4 3
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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
• 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
Figure 24 Section 2 1
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Section 2: Acid-Base Balance
• Classes of acids
• Fixed acids
• Do not leave solution
• Remain in body fluids until kidney excretion
• Examples: sulfuric and phosphoric acid
• 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
• 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 1
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The narrow range of normal pH of the ECF, and the conditions that result from pH shifts outside the normal range
Extremely Extremely
acidic basic
pH
Severe acidosis (pH below 7.0) can be deadly Severe alkalosis is also
because (1) central nervous system function dangerous, but serious cases
deteriorates, and the individual may become are relatively rare.
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.
Figure 24.5 2
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Module 24.5: Buffer systems
When carbon dioxide levels rise, more carbonic acid When the PCO2 falls, the reaction runs in reverse, and
forms, additional hydrogen ions and bicarbonate ions carbonic acid dissociates into carbon dioxide and
are released, and the pH goes down. water. This removes H ions from solution and
increases the pH.
PCO pH
2
pH P CO 2
Figure 24.5 3
© 2011 Pearson Education, Inc.
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
A buffer system in body fluids generally Adding H to the Removing H from the
consists of a combination of a weak acid (HY) solution upsets the solution also upsets the
and the anion (Y) released by its dissociation. equilibrium and results equilibrium and results
The anion functions as a weak base. In solution, in the formation of in the dissociation of
molecules of the weak acid exist in equilibrium additional molecules of additional molecules of
with its dissociation products. the weak acid. HY. This releases H.
H H HY H Y
HY H Y H Y
H HY
H
Figure 24.5 4
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Module 24.5 Review
Buffer Systems
occur in
Figure 24.6 1
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The reactions of the carbonic acid–bicarbonate buffer system 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
CARBONIC ACID–BICARBONATE available supply of HCO3 is known as
BUFFER SYSTEM the bicarbonate reserve.
CO2 CO2 H2O H2CO3 H HCO3 HCO3 Na NaHCO3
(carbonic acid) (bicarbonate ion) (sodium bicarbonate)
Lungs
Figure 24.6 4
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The events involved in the functioning of the hemoglobin buffer system
Tissue Plasma Plasma Lungs
cells
Red blood cells Red blood cells Released
with
exhalation
H2O H2O
Figure 24.6 2
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The mechanism by free amino acids function in
Start protein buffer systems
Increasing acidity (decreasing pH)
Normal pH
(7.35–7.45)
Figure 24.6 3
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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
Figure 24.7 1
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The activity of renal Tubular ECF Steps in CO2 removal and
Renal tubule cells
tubule cells in CO2 fluid HCO3 production
removal and HCO3
CO2 CO2 CO2 generated by the tubule
production CO2
cell is added to the CO 2
H2O diffusing into the cell from
Carbonic the urine and from the ECF.
Na anhydrase
H Carbonic anhydrase
H2CO3 converts CO2 and water to
carbonic acid, which then
H H HCO3 HCO3
dissociates.
Cl
The chloride ions exchanged
H for bicarbonate ions are
Cl HCO3 excreted in the tubular fluid.
Na
Bicarbonate ions and
sodium ions are transported
into the ECF, adding to the
bicarbonate reserve.
Figure 24.7 2
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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
Other Generation
Respiratory Response KIDNEYS
to Alkalosis buffer of H
systems
Decreased respiratory release H
Renal Response to Alkalosis
rate elevates PCO2,
effectively converting Kidney tubules respond by
CO2 molecules to conserving H ions and
Secretion secreting HCO3.
carbonic acid.
of HCO3
Figure 24.7 3
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CO2 generated by the tubule
The events in the cell is added to the CO 2
Tubular Renal tubule cells ECF
secretion of bicarbonate fluid diffusing into the cell from the
ions into the tubular tubular fluid and from the ECF.
fluid along the PCT, DCT, CO2 CO2 CO2
and collecting system
H2O Carbonic anyhydrase converts
Carbonic CO2 and water to carbonic
anhydrase acid, which then dissociates.
H2CO3
Figure 24.7 4
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Module 24.7 Review
CARBONIC ACID–BICARBONATE
BUFFER SYSTEM BICARBONATE RESERVE
When respiratory activity does not keep As bicarbonate ions and hydrogen ions To limit the pH effects of
pace with the rate of CO2 generation, are released through the dissociation of respiratory acidosis, the excess
carbonic acid, the excess bicarbonate H must either be tied up by
alveolar and plasma PCO2 increases.
ions become part of the bicarbonate other buffer systems or excreted
This upsets the equilibrium and drives at the kidneys. The underlying
the reaction to the right, generating reserve.
problem, however, cannot be
additional H2CO3, which releases H eliminated without an increase in
and lowers plasma pH. the respiratory rate.
Figure 24.8 1
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Responses to Acidosis
The integrated homeostatic responses
Respiratory compensation
to respiratory acidosis
Stimulation of arterial and CSF
chemoreceptors results in
Increased increased respiratory rate.
PCO2
Renal compensation
H ions are secreted and
HCO3 ions are generated. Combined Effects
Respiratory Acidosis Decreased PCO2
Buffer systems other than the
Elevated PCO2 results carbonic acid–bicarbonate Decreased H and
in a fall in plasma pH system accept H ions. increased HCO3
HOMEOSTASIS HOMEOSTASIS
DISTURBED RESTORED
Hypoventilation
HOMEOSTASIS Plasma pH
causing increased PCO2 Start returns to normal
Normal acid-
base balance
Figure 24.8 2
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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+)
CARBONIC ACID–BICARBONATE
BUFFER SYSTEM BICARBONATE RESERVE
Figure 24.8 3
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The integrated homeostatic responses to
respiratory alkalosis
HOMEOSTASIS
HOMEOSTASIS Start HOMEOSTASIS
DISTURBED Normal acid- RESTORED
base balance
Hyperventilation Plasma pH
causing decreased PCO2 returns to normal
Combined Effects
Respiratory Alkalosis Responses to Alkalosis
Increased PCO2
Lower PCO2 results Respiratory compensation
in a rise in plasma pH Inhibition of arterial and CSF Increased H and
chemoreceptors results in a decreased HCO3
decreased respiratory rate.
Renal compensation
Decreased H ions are generated and
PCO2 HCO3 ions are secreted.
Figure 24.8 4
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CLINICAL MODULE 24.8 Review