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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.

© 2011 Pearson Education, Inc.


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 ‫ت نقسم ا لسوائل‬
Intracellular fluid (ICF)
Water content varies most here due to variation in:
‫تختلف معظم محتويات الماء هنا نتيجة الي اختالف في‬:-
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)

© 2011 Pearson Education, Inc.


Total body composition of adult males

Total body composition of adult males and females

ICF
ECF
Intracellular Interstitial
fluid 33% fluid 21.5%

Plasma 4.5%

Solids 40% Other


(organic and inorganic materials) body
fluids
(≤1%)

Adult males

Total body composition of adult females

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
© 2011 Pearson Education, Inc.
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 2
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


Figure 24.1 1
© 2011 Pearson Education, Inc.
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

Colonic mucous secretions


200 mL
Colon reabsorbs 1250 mL 1400
mL

150 mL lost
in feces
Figure 24.1 2
© 2011 Pearson Education, Inc.
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 ‫ازاحة ا لسوائل‬
Occurs in minutes to hours and restores osmotic equilibrium
‫اعادة معادلة الضغط االسموزي‬
Dehydration
Results in long-term transfer that cannot replace ECF water loss
Homeostatic mechanisms to increase ECF fluid volume will be employed

© 2011 Pearson Education, Inc.


Water absorbed across
digestive epithelium
The major factors that affect ECF volume (2000 mL)
Water vapor lost
in respiration and
evaporation from
moist surfaces
(1150 mL)

Metabolic Water lost in


ICF water ECF feces (150 mL)
(300 mL)
Water secreted
by sweat glands
(variable)

Plasma membranes Water lost in urine


(1000 mL)

Figure 24.1 3
© 2011 Pearson Education, Inc.
Changes to the ICF and ECF when water losses outpace water gains

Intracellular Extracellular The ECF and ICF are in


fluid (ICF) fluid (ECF) 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.

An osmotic water shift


Decreased ICF volume Increased from the ICF into the
ECF volume ECF restores osmotic
equilibrium but
reduces the ICF
volume.

Figure 24.1 4
© 2011 Pearson Education, Inc.
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.

© 2011 Pearson Education, Inc.


Module 24.2: Mineral balance

Mineral balance ‫ت وازنا لسوائم ا لمع دنيه‬


Equilibrium‫ ا??لتوازن‬between ion absorption and excretion
Major ion aabsorption through intestine and ccolon
‫االمتصاص االساسي لاليونات خالل االمعاء والقيولون‬
Major ion excretion by kidneys
Sweat glands excrete ions and water variably ?‫مختلفه‬
Ion reserves mainly in skeleton

© 2011 Pearson Education, Inc.


Mineral balance, the balance between ion absorption (in the digestive tract) and ion excretion (primarily at the kidneys)
Ion Absorption Ion reserves (primarily Ion Excretion
in the skeleton)
Ion absorption occurs across the Sweat gland
epithelial lining of the small intestine secretions
and colon. (secondary
site of ion loss)

Ion pool in body fluids

Kidneys
(primary site
of ion loss)

ICF ECF

Figure 24.2 1
© 2011 Pearson Education, Inc.
Figure 24.2 2
© 2011 Pearson Education, Inc.
Figure 24.2 3
© 2011 Pearson Education, Inc.
Figure 24.2 3
© 2011 Pearson Education, Inc.
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.

© 2011 Pearson Education, Inc.


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
• ADH control of water loss/retention by kidneys and thirst
• Fluid exchange between ECF and ICF

© 2011 Pearson Education, Inc.


The mechanisms that regulate sodium balance ADH Secretion Increases
when sodium concentration in the ECF changes Recall of Fluids
The secretion of ADH
Because the ECF
restricts water loss and
osmolarity increases,
stimulates thirst, promoting
water shifts out of the
additional water
ICF, increasing ECF
Rising plasma consumption.
volume and lowering
sodium levels
ECF Na concentrations.

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
© 2011 Pearson Education, Inc.
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

Osmoreceptors Water loss reduces


in hypothalamus ECF volume,
inhibited ADH Secretion concentrates ions
Decreases
As soon as the osmotic
concentration of the ECF
drops by 2 percent or
more, ADH secretion
Falling plasma decreases, so thirst is
sodium levels suppressed and water
losses at the kidneys
increase.

Figure 24.3 1
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


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

© 2011 Pearson Education, Inc.


The mechanisms that regulate water balance Responses to Natriuretic Peptides Combined
when ECF volume changes Effects
Increased Na loss in urine
Reduced
Rising blood Increased water loss in urine blood
pressure and Natriuretic peptides volume
volume released by cardiac Reduced thirst
muscle cells Reduced
Inhibition of ADH, aldosterone, blood
epinephrine, and norepinephrine pressure
release
Increased blood
volume and
atrial distension

HOMEOSTASIS
HOMEOSTASIS
RESTORED
DISTURBED

Rising ECF volume by fluid Falling ECF


gain or fluid and Na gain volume
HOMEOSTASIS
Start
Normal ECF
volume

Figure 24.3 2
© 2011 Pearson Education, Inc.
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

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

© 2011 Pearson Education, Inc.


The major factors involved in potassium balance
Factors Controlling Potassium Balance
Approximately 100 Roughly The K concentration in the When potassium
mEq (1.9–5.8 g) of 98 percent of the ECF is relatively low. The rate balance exists,
potassium ions are potassium of K entry from the ICF the rate of urinary
absorbed by the content of the through leak channels is K excretion
digestive tract each human body is in balanced by the rate of K matches the rate
day. the ICF, rather recovery by the Na/K of digestive tract
than the ECF. exchange pump. absorption.

The potassium ion


concentration in the
ECF is approximately
5 mEq/L.

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
© 2011 Pearson Education, Inc.
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

KEY The sodium ions are then pumped out


of the cell in exchange for potassium
 Aldosterone- ions in the ECF. This is the same pump
sensitive that ejects sodium ions entering the
exchange
pump cytosol through leak channels.

 Sodium-potassium
exchange pump

Figure 24.4 2
© 2011 Pearson Education, Inc.
Events in the kidneys that affect potassium balance

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
Distal sodium levels and increased
convoluted K loss in the urine.
tubule
When the pH falls in the ECF
and the concentration of H is
relatively high, the exchange
Collecting pumps bind H instead of K.
duct This helps to stabilize the pH
of the ECF, but at the cost of
rising K levels in the ECF.

Figure 24.4 3
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


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

© 2011 Pearson Education, Inc.


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.

© 2011 Pearson Education, Inc.


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.

© 2011 Pearson Education, Inc.


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+

© 2011 Pearson Education, Inc.


The major factors involved in the maintenance
of acid-base balance
The respiratory system
plays a key role by
eliminating
carbon dioxide.

The kidneys play a major


role by secreting
hydrogen ions into the
Active tissues urine and generating
continuously generate buffers that enter the
carbon dioxide, which in Normal bloodstream. The rate of
solution forms carbonic plasma pH excretion rises and falls
acid. Additional acids, (7.35–7.45) as needed to maintain
such as lactic acid, are normal plasma pH. As a
produced in the course of Tissue cells result, the normal pH of
normal metabolic urine varies widely but
averages 6.0—slightly
operations. acidic.
Buffer Systems

Buffer systems can


temporarily store H
and thereby provide
short-term pH
stability.

Figure 24 Section 2 1
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


Section 2: Acid-Base Balance

Classes of acids (continued)


Volatile acids
Can leave body by external respiration
Example: carbonic acid (H2CO3)

© 2011 Pearson Education, Inc.


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

© 2011 Pearson Education, Inc.


Figure 24.5 1
© 2011 Pearson Education, Inc.
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 When the pH of plasma rises


7.5, acidemia exists. The above 7.45, alkalemia exists.
physiological state that results is The physiological state that
called acidosis. results is called alkalosis.

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
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


The inverse relationship between the PCO2 and pH
PCO2 pH
40–45 7.35–7.45
mm Hg HOMEOSTASIS

If PCO2 rises If PCO2 falls

H2O  CO2 H2CO3 H  HCO3 H  HCO3 H2CO3 H2O  CO2

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
© 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

© 2011 Pearson Education, Inc.


The reactions that occur when pH buffer systems function

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
© 2011 Pearson Education, Inc.
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.

© 2011 Pearson Education, Inc.


Module 24.6: Major body buffer systems

Three major body buffer systems


All can only temporarily affect pH (H+ not eliminated)

• Phosphate buffer system


Buffers pH of ICF and urine
• Carbonic acid–bicarbonate buffer system
Most important in ECF
Fully reversible
Bicarbonate reserves (from NaHCO3 in ECF) contribute

© 2011 Pearson Education, Inc.


Module 24.6: Major body buffer systems

Three major body buffer systems


(continued)
• 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

© 2011 Pearson Education, Inc.


The body’s three major buffer systems

Buffer Systems
occur in

Intracellular fluid (ICF) Extracellular fluid (ECF)

Phosphate Buffer Protein Buffer Systems Carbonic Acid–


System Bicarbonate Buffer
Contribute to the regulation of pH in the ECF and ICF;
System
Has an important interact extensively with the other two buffer systems
role in buffering the Is most important in the
pH of the ICF and ECF
of urine

Hemoglobin Amino acid Plasma


buffer system buffers protein
(RBCs only) (All proteins) buffers

Figure 24.6 1
© 2011 Pearson Education, Inc.
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

The primary function of the carbonic


acid–bicarbonate buffer system is to
protect against the effects of the organic
Addition of H and fixed acids generated through
Start from metabolic metabolic activity. In effect, it takes the H
activity 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 4
© 2011 Pearson Education, Inc.
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

CO2 H2CO3 HCO3  Hb H Hb H  HCO3 H2CO3 CO2

Figure 24.6 2
© 2011 Pearson Education, Inc.
The mechanism by free amino acids function in
Start protein buffer systems
Increasing acidity (decreasing pH)
Normal pH
(7.35–7.45)

At the normal pH of If pH drops, the carboxylate ion (COO)


body fluids (7.35– and the amino group (—NH2) of a free
7.45), the carboxyl amino acid can act as weak bases and
groups of most amino accept additional hydrogen ions, forming a
acids have released carboxyl group (—COOH) and an amino
their hydrogen ions. ion (—NH3), respectively. Many of the
R-groups can also accept hydrogen ions,
forming RH.

Figure 24.6 3
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


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.

© 2011 Pearson Education, Inc.


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

© 2011 Pearson Education, Inc.


The responses to metabolic acidosis Addition
Start
of H

CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE

CO2 CO2  H2O H2CO3 H  HCO3 HCO3  Na NaHCO3


(carbonic acid) (bicarbonate ion) (sodium bicarbonate)
Lungs
Generation
Other of HCO3
Respiratory Response KIDNEYS
to Acidosis buffer
systems Renal Response to Acidosis
Increased respiratory absorb H
rate lowers PCO2, Kidney tubules respond by (1) secreting H
effectively converting ions, (2) removing CO2, and (3) reabsorbing
carbonic acid molecules HCO3 to help replenish the bicarbonate
Secretion reserve.
to water. of H

Figure 24.7 1
© 2011 Pearson Education, Inc.
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.
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
© 2011 Pearson Education, Inc.
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

© 2011 Pearson Education, Inc.


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

© 2011 Pearson Education, Inc.


The responses to metabolic alkalosis Removal
Start
of H

CARBONIC ACID–BICARBONATE BUFFER SYSTEM BICARBONATE RESERVE

Lungs CO2  H2O H2CO3 H  HCO3 HCO3  Na NaHCO3


(carbonic acid) (bicarbonate ion) (sodium bicarbonate)

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
© 2011 Pearson Education, Inc.
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

HCO3 HCO3 H H The hydrogen ions are actively


transported into the ECF,
Cl Cl 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 4
© 2011 Pearson Education, Inc.
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?

© 2011 Pearson Education, Inc.


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 BICARBONATE RESERVE

CO2 CO2  H2O H2CO2 H  HCO3 HCO3  Na NaHCO3


(carbonic acid) (bicarbonate ion) (sodium bicarbonate)
Lungs

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
© 2011 Pearson Education, Inc.
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
© 2011 Pearson Education, Inc.
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 BICARBONATE RESERVE

CO2 CO2  H2O H2CO2 H  HCO3 HCO3  Na NaHCO3


(carbonic acid) (bicarbonate ion) (sodium bicarbonate)
Lungs

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
© 2011 Pearson Education, Inc.
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

Respiratory Alkalosis Combined Effects


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.

Buffer systems other than the


carbonic acid–bicarbonate system
release H ions.

Figure 24.8 4
© 2011 Pearson Education, Inc.
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?

© 2011 Pearson Education, Inc.

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