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13 Fluid and Electrolyte Balance محاضرة
13 Fluid and Electrolyte Balance محاضرة
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
Digestive secretions are reabsorbed similarly to ingested fluids
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
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
© 2011 Pearson Education, Inc.
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
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.
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
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
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.
PCO2 pH
pH 2
PCO
Figure 24.5 3
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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
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
available supply of HCO3 is known as
CARBONIC ACID–BICARBONATE
the bicarbonate reserve.
BUFFER SYSTEM
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 CO2
H2O diffusing into the cell from
Carbonic the urine and from the ECF.
Naanhydrase
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
carbonic acid. Secretion secreting HCO3.
of HCO3
Figure 24.7 3
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CO2 generated by the tubule
The events in the cell is added to the CO2
Tubular Renal tubule cells ECF diffusing into the cell from the
secretion of bicarbonate fluid tubular fluid and from the ECF.
ions into the tubular
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
alveolar and plasma PCO2 increases. carbonic acid, the excess bicarbonate H must either be tied up by
This upsets the equilibrium and drives ions become part of the bicarbonate other buffer systems or excreted
the reaction to the right, generating reserve. at the kidneys. The underlying
additional H2CO3, which releases H problem, however, cannot be
and lowers plasma pH. eliminated without an increase in
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
If respiratory activity exceeds the rate of CO2 As bicarbonate ions and hydrogen
generation, alveolar and plasma PCO2 decline, ions are removed in the formation of
and this disturbs the equilibrium and drives carbonic acid, the bicarbonate ions—
the reactions to the left, removing H and but not the hydrogen ions—are
elevating plasma pH. replaced by the 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
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