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Chapter 16
Respiratory Physiology
16-1
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Chapter 16 Outline
Respiratory
Structures
Physical Aspects of Ventilation
Mechanics of Breathing
Pulmonary Disorders
Factors Affecting Ventilation
Control of Ventilation
Hemoglobin
CO2 Transport & Acid-Base Balance
Exercise & Altitude Effects
16-2
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Respiration
Encompasses
3 related functions: ventilation, gas
exchange, & 02 utilization (cellular respiration)
Ventilation moves air in & out of lungs for gas
exchange with blood (external respiration)
Gas exchange between blood & tissues, & O2
use by tissues is internal respiration
Gas exchange is passive via diffusion
16-3
Respiratory Structures
16-4
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Structure of Respiratory System

Air passes from mouth to trachea to right & left bronchi to
bronchioles to terminal bronchioles to respiratory bronchioles to
alveoli
Fig 16.4
16-5
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Structure of Respiratory System continued
Gas exchange occurs only in respiratory bronchioles & alveoli
(= respiratory zone)
 All other structures constitute the conducting zone
 Are polyhedral in shape & clustered at ends of respiratory
bronchioles, like units of honeycomb

Fig 16.4
16-6
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Structure of Respiratory System continued

Gas exchange occurs
across the 300 million
alveoli (60-80 m2 total
surface area)
 Only 2 thin cells are
between lung air &
blood: 1 alveolar & 1
endothelial cell
Insert 16.1
Fig 16.1
16-7
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Alveoli
 Are
polyhedral in shape & clustered at ends of
respiratory bronchioles, like units of honeycomb
Air in 1 cluster can pass to others through pores
16-8
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Conducting Zone
 Warms
&
humidifies inspired
air
 Mucus lining filters
& cleans inspired
air
Mucus moved by
cilia to be
expectorated
Insert fig. 16.5
Fig 16.5
16-9
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Thoracic Cavity
 Is
created by the diaphragm, a dome-shaped sheet of
skeletal muscle
 Contains heart, large blood vessels, trachea,
esophagus, thymus, & lungs
 Below diaphragm is abdominopelvic cavity
Contains liver, pancreas, GI tract, spleen, &
genitourinary tract
 Intrapleural space is thin fluid layer between visceral
pleura covering lungs & parietal pleura lining thoracic
cavity walls
16-10
Physical Aspects of Ventilation
16-11
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Physical Aspects of Ventilation
Ventilation
results from pressure differences induced
by changes in lung volumes
Air moves from higher to lower pressure
Compliance, elasticity, & surface tension of lungs
influence ease of ventilation
16-12
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Intrapulmonary & Intrapleural Pressures

Visceral & parietal pleurae normally adhere to each other so
that lungs remain in contact with chest walls
Fig 16.8
 & expand & contract with thoracic cavity
16-13
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Intrapulmonary & Intrapleural Pressures


During inspiration, intrapulmonary pressure is about -3 mm Hg
pressure; during expiration is about +3 mm Hg
Positive transmural pressure (intrapulmonary - intrapleural
pressure) keeps lungs inflated
16-14
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Boyle’s Law (P = 1/V)
 Implies
that changes in intrapulmonary pressure occur
as a result of changes in lung volume
Pressure of gas is inversely proportional to volume
 Increase in lung volume decreases intrapulmonary
pressure causing inspiration
 Decrease in lung volume raises intrapulmonary
pressure causing expiration
16-15
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Compliance
Is
how easily lung expands with pressure
Or change in lung volume per change in transmural
pressure (DV/DP)
Is reduced by factors that cause resistance to
distension
16-16
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Elasticity
 Is
tendency to return to initial size after distension
 Due to high content of elastin proteins
 Elastic tension increases during inspiration & is
reduced by recoil during expiration
16-17
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Surface Tension (ST)
 And
elasticity are forces that promote alveolar
collapse & resist distension
 Lungs secrete & absorb fluid, normally leaving a thin
film of fluid on alveolar surface
Fluid absorption occurs by osmosis driven by Na+
active transport
Fluid secretion is driven by active transport of Clout of alveolar epithelial cells
This film causes ST because H20 molecules are
attracted to other H20 molecules
Force of ST is directed inward, raising pressure
in alveoli
16-18
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Surface Tension continued
 Law
of Laplace states
that pressure in alveolus
is directly proportional to
ST; & inversely to radius
of alveoli
 Thus, pressure in
smaller alveoli would
be greater than in
larger alveoli, if ST
were same in both
Fig 16.11 Insert fig. 16.11
16-19
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Surfactant


Consists of
phospholipids secreted
by type II alveolar cells
Lowers ST by getting
between H20
molecules, reducing
their ability to attract
each other via
hydrogen bonding
Fig 16.12
16-20
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Surfactant continued
 Prevents
ST from collapsing alveoli
 Surfactant secretion begins in late fetal life
 Premies are often born with immature surfactant
system (= Respiratory Distress Syndrome or RDS)
Have trouble inflating lungs
 In adults, septic shock may cause acute respiratory
distress syndrome (ARDS) which decreases
compliance & surfactant secretion
16-21
Mechanics of Breathing
16-22
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Mechanics of Breathing
 Pulmonary
ventilation consists of inspiration (= inhalation) &
expiration (= exhalation)
 Accomplished by alternately increasing & decreasing
volumes of thorax & lungs
Fig 16.13
expiration
inspiration
16-23
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Quiet Breathing



Inspiration occurs mainly
because diaphragm
contracts, increasing
thoracic volume vertically
Parasternal & external
intercostal contraction
contributes a little by
raising ribs, increasing
thoracic volume laterally
Expiration is due to
passive recoil
Fig 16.14
16-24
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Deep Breathing
Inspiration involves
contraction of extra
muscles to elevate ribs:
scalenes, pectoralis
minor, &
sternocleidomastoid
muscles
 Expiration involves
contraction of internal
intercostals &
abdominal muscles

Fig 16.14
16-25
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Mechanics of Pulmonary Ventilation
Insert fig. 16.15
Fig 16.15
16-26
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Pulmonary Function Tests
 Assessed
clinically by spirometry, a method that
measures volumes of air moved during inspiration &
expiration
 Anatomical dead space is air in conducting zone
where no gas exchange occurs
16-27
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Pulmonary Function Tests continued


Tidal volume is amount of air expired/breath in quiet breathing
Vital capacity is amount of air that can be forcefully exhaled
after a maximum inhalation
 = sum of inspiratory reserve, tidal volume, & expiratory
reserve
Fig 16.16
16-28
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16-29
Pulmonary Disorders
16-30
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Restrictive Disorders
 Are
characterized by reduced vital capacity but with
normal forced vital capacity
E.g. pulmonary fibrosis
16-31
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Obstructive Disorders

Have normal vital
capacity but
expiration is retarded
 E.g. asthma
 Diagnosed by
tests, such as
forced expiratory
volume, that
measure rate of
expiration
Insert fig. 16.17
Fig 16.17
16-32
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Pulmonary Disorders
Are
frequently accompanied by dyspnea, a feeling of
shortness of breath
Asthma results from episodes of obstruction of air flow
thru bronchioles
Caused by inflammation, mucus secretion, &
broncho constriction
Inflammation contributes to increased airway
responsiveness to agents that promote bronchial
constriction
Provoked by allergic reactions that release IgE, by
exercise, by breathing cold, dry air, or by aspirin
16-33
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Pulmonary Disorders continued
Emphysema
is a chronic, progressive condition that
destroys alveolar tissue, resulting in fewer, larger
alveoli
Reduces surface area for gas exchange & ability of
bronchioles to remain open during expiration
Collapse of bronchiole during expiration causes air
trapping, decreasing gas exchange
Commonly occurs in long-term smokers
Cigarette smoking stimulates macrophages &
leukocytes to secrete protein-digesting enzymes
that destroy tissue
16-34
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emphysema
normal lung
Fig 16.18
16-35
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Pulmonary Disorders continued
Sometimes
lung damage leads to pulmonary fibrosis
instead of emphysema
Characterized by accumulation of fibrous connective
tissue
Occurs from inhalation of particles <6m in size,
such as in black lung disease (anthracosis) from
coal dust
16-36
Factors Affecting Gas Exchange
16-37
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Partial Pressure of Gases
 Partial
pressure is pressure that a particular gas in a
mixture exerts independently
 Dalton’s Law states that total pressure of a gas
mixture is the sum of partial pressures of each gas in
mixture
 Atmospheric pressure at sea level is 760 mm Hg
PATM = PN2 + P02 + PC02 + PH20 = 760 mm Hg
16-38
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Gas Exchange in Lungs
 Is
driven by
differences in
partial
pressures of
gases
between
alveoli &
capillaries
Fig 16.20
16-39
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Gas Exchange in Lungs continued

Is facilitated by enormous surface area of alveoli, short diffusion
distance between alveolar air & capillaries, & tremendous
density of capillaries
Fig 16.21
16-40
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Partial Pressures of Gases in Blood
When blood & alveolar air are at equilibrium the amount of O2
in blood reaches a maximum value
 Henry’s Law says that this value depends on solubility of O2 in
blood (a constant), temperature of blood (a constant), & partial
pressure of O2
 So the amount of O2 dissolved in blood depends directly on its
partial pressure (PO2), which varies with altitude

16-41
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Blood PO2 & PCO2 Measurements




Provide good
index of lung
function
At normal PO2
arterial blood
has about 100
mmHg PO2
PO2 is about 40
mmHg in
systemic veins
PC02 is 46
mmHg in
systemic veins
Fig 16.23
16-42
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Pulmonary Circulation
 Rate
of blood flow through pulmonary circuit equals
flow through systemic circulation
 But is pumped at lower pressure (about 15 mm Hg)
Pulmonary vascular resistance is low
Low pressure produces less net filtration than in
systemic capillaries
Avoids pulmonary edema
 Pulmonary arterioles constrict where alveolar PO2 is
low & dilate where high
This matches ventilation to perfusion
16-43
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Lung Ventilation/Perfusion Ratios
 Normally,
alveoli at
apex of lungs are
underperfused &
overventilated
 Alveoli at base are
overperfused &
underventilated
Insert fig. 16.24
Fig 16.24
16-44
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Disorders Caused by High Partial Pressures
of Gases
 Total
atmospheric pressure increases by an
atmosphere for every 10m below sea level
 At depth, increased O2 & N2 can be dangerous to body
 Breathing 100% O2 at < 2 atmospheres can be
tolerated for few hrs
O2 toxicity can develop rapidly at > 2 atmospheres
Probably because of oxidation damage
16-45
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Disorders Caused by High Partial Pressures
of Gases




At sea level, nitrogen is physiologically inert
It dissolves slowly in blood
Under hyperbaric conditions takes more than hour for
dangerous amounts to accumulate
 Nitrogen narcosis resembles alcohol intoxication
Amount of nitrogen dissolved in blood as diver ascends
decreases due to decrease in PN2
 If ascent is too rapid, decompression sickness occurs as
bubbles of nitrogen gas form in tissues & enter blood,
blocking small blood vessels & producing “bends”
16-46
Control of Ventilation
16-47
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Brain Stem Respiratory Centers

Automatic breathing is
generated by a rhythmicity
center in medulla oblongata
Fig 16.25
 Consists of inspiratory
neurons that drive
Insert fig. 16.25
inspiration & expiratory
neurons that inhibit
inspiratory neurons
Their activity varies in
a reciprocal way &
may be due to
pacemaker neurons
16-48
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Brain Stem Respiratory Centers continued
Inspiratory
neurons stimulate spinal motor neurons
that innervate respiratory muscles
Expiration is passive & occurs when inspiratories are
inhibited
16-49
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Pons Respiratory Centers
Activities
of medullary rhythmicity center is influenced
by centers in pons
Apneustic center promotes inspiration by stimulating
inspiratories in medulla
Pneumotaxic center antagonizes apneustic center,
inhibiting inspiration
16-50
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Chemoreceptors


Automatic breathing is
influenced by activity of
chemoreceptors that
monitor blood PC02, P02,
& pH
 Central
chemoreceptors are in
medulla
Peripheral
chemoreceptors are in
large arteries near heart
(aortic bodies) & in
carotids (carotid bodies)
Fig 16.26
16-51
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CNS Control of
Breathing
Fig 16.27
16-52
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Effects of Blood PC02 & pH on Ventilation
 Chemoreceptors
modify ventilation to maintain normal
CO2, O2, & pH levels
PCO2 is most crucial because of its effects on blood
pH
H20 + C02  H2C03  H+ + HC03-
 Hyperventilation
causes low C02 (hypocapnia)
 Hypoventilation causes high C02 (hypercapnia)
16-53
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Effects of Blood PC02 & pH on Ventilation
continued
 Brain
chemoreceptors are responsible for greatest
effects on ventilation
H+ can't cross BBB but C02 can, which is why it is
monitored & has greatest effects
Rate and depth of ventilation adjusted to maintain
arterial PC02 of 40 mm Hg
 Peripheral chemoreceptors do not respond to PC02,
only to H+ levels
16-54
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Fig 16.30
16-55
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Chemoreceptor Control of Breathing
Fig 16.29
16-56
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Effects of Blood P02 on Ventilation
 Low
blood P02 (hypoxemia) has little affect on
ventilation
Does influence chemoreceptor sensitivity to PC02
P02 has to fall to about half normal before
ventilation is significantly affected
Emphysema blunts chemoreceptor response to
PC02
Oftentimes ventilation is stimulated by hypoxic
drive rather than PC02
16-57
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Effects of Pulmonary Receptors on
Ventilation


Lungs have receptors that influence brain respiratory control
centers via sensory fibers in vagus
 Unmyelinated C fibers are stimulated by noxious substances
such as capsaicin
Causes apnea followed by rapid, shallow breathing
 Irritant receptors are rapidly adapting; respond to smoke,
smog, & particulates
Causes cough
Hering-Breuer reflex is mediated by stretch receptors activated
during inspiration
 Inhibits respiratory centers to prevent overinflation of lungs
16-58
Hemoglobin
16-59
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Hemoglobin (Hb) & 02 Transport
 Loading
of Hb with O2 occurs in lungs; unloading in
tissues
 Affinity of Hb for O2 changes with a number of
physiological variables
16-60
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Hemoglobin (Hb) & 02 Transport


Each Hb has 4
globin polypeptide
chains & 4 heme
groups that bind
02
Each heme has a
ferrous ion that
can bind 1 02
 So each Hb
can carry 4 02s
Fig 16.33
16-61
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Hemoglobin (Hb) & 02 Transport continued
Most 02 in blood is
bound to Hb inside
RBCs as
oxyhemoglobin
 Each RBC has about
280 million molecules
of Hb
 Hb greatly increases
02 carrying capacity
of blood

Insert fig. 16.32
Fig 16.32
16-62
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Hemoglobin (Hb) & 02 Transport continued
 Methemoglobin
contains ferric iron (Fe3+) -- the
oxidized form
Lacks electron to bind with 02
Blood normally contains a small amount
 Carboxyhemoglobin is heme combined with carbon
monoxide
Bond with carbon monoxide is 210 times stronger
than bond with oxygen
So heme can't bind 02
16-63
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Hemoglobin (Hb) & 02 Transport continued
 02-carrying
capacity of blood depends on its Hb levels
In anemia, Hb levels are below normal
In polycythemia, Hb levels are above normal
 Hb production controlled by erythropoietin (EPO)
Production stimulated by low P02 in kidneys
 Hb levels in men are higher because androgens
promote RBC production
16-64
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Hemoglobin (Hb) & 02 Transport continued
 High
P02 of lungs favors loading; low P02 in tissues
favors unloading
 Ideally, Hb-02 affinity should allow maximum loading in
lungs & unloading in tissues
16-65
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Oxyhemoglobin Dissociation Curve



Gives % of Hb sites
that have bound 02 at
different P02s
 Reflects loading &
unloading of 02
Differences in %
saturation in lungs &
tissues are shown at
right
In steep part of
curve, small changes
in P02 cause big
changes in %
saturation
Fig 16.34
16-66
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Oxyhemoglobin Dissociation Curve
Fig 16.35


Is affected by changes
in Hb-02 affinity caused
by pH & temperature
Affinity decreases
when pH decreases
(Bohr Effect) or temp
increases
 Occurs in tissues
where temp, C02 &
acidity are high
 Causes Hb-02 curve
to shift right & more
unloading of 02
16-67
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Effect of 2,3 DPG on 02 Transport
RBCs have no mitochondria; can’t perform aerobic respiration
 2,3-DPG is a byproduct of glycolysis in RBCs
 Its production is increased by low 02 levels
 Causes Hb to have lower 02 affinity, shifting curve to right
 In anemia, total blood Hb levels fall, causing each RBC to
produce more DPG
 Fetal hemoglobin (HbF) has 2 g-chains in place of b-chains of
HbA
 HbF can’t bind DPG, causing it to have higher 02 affinity
Facilitates 02 transfer from mom to baby

16-68
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Sickle-cell Anemia

Sickle-cell anemia affects 8-11% of African Americans
 HbS has valine substituted for glutamic acid at 1 site on b
chains
 At low P02, HbS crosslinks to form a “paracrystalline gel”
inside RBCs
Makes RBCs less flexible & more fragile
Fig 16.36
16-69
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Thalassemia
 Thalassemia
affects primarily people of Mediterranean
descent
Has decreased synthesis of a or b chains;
increased synthesis of g chains
16-70
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Myoglobin
 Is
a red pigment found exclusively in striated muscle
Slow-twitch skeletal & cardiac muscle fibers are rich
in myoglobin
16-71
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Myoglobin
Has only 1 globin;
binds only 1 02
 Has higher affinity for
02 than Hb; is shifted to
extreme left
 Releases 02 only at low
P02
 Serves in 02 storage,
particularly in heart
during systole

Insert fig. 13.37
Fig 16.37
16-72
CO2 Transport & Acid-Base Balance
16-73
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C02 Transport
C02
transported in blood as dissolved C02 (10%),
carbaminohemoglobin (20%), & bicarbonate ion,
HC03-, (70%)
In RBCs carbonic anhydrase catalyzes formation of
H2CO3 from C02 + H2O
16-74
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Chloride Shift
 High
C02 levels in tissues causes the reaction
C02 + H2O  H2C03  H+ + HC03- to shift right in
RBCs
Results in high H+ & HC03- levels in RBCs
H+ is buffered by proteins
HC03- diffuses down concentration & charge
gradient into blood causing RBC to become more
+
So Cl- moves into RBC (chloride shift)
16-75
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Chloride Shift
Fig 16.38
16-76
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Reverse Chloride Shift
lungs, C02 + H2O 
H2C03  H+ + HC03-, moves
to left as C02 is breathed out
 Binding of 02 to Hb
decreases its affinity for H+
 H+ combines with HC03& more C02 is formed
 Cl- diffuses down
concentration & charge
gradient out of RBC
(reverse chloride shift)
 In
Fig 16.39
16-77
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Acid-Base Balance in Blood
Blood
pH is maintained within narrow pH range by
lungs & kidneys (normal = 7.4)
Most important buffer in blood is bicarbonate
H20 + C02  H2C03  H+ + HC03Excess H+ is buffered by HC03Kidney's role is to excrete H+ into urine
16-78
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Effect of Bicarbonate on Blood pH
Fig 16.40
Insert fig. 16.40
16-79
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Acid-Base Balance in Blood continued
2
major classes of acids in body:
A volatile acid can be converted to a gas
E.g. C02 in bicarbonate buffer system can be
breathed out
 H20 + C02  H2C03  H+ + HC03All other acids are nonvolatile & cannot leave blood
E.g. lactic acid, fatty acids, ketone bodies
16-80
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Acid-Base Balance in Blood continued
Acidosis
is when pH < 7.35; alkalosis is pH > 7.45
Respiratory acidosis caused by hypoventilation
Causes rise in blood C02 & thus carbonic acid
Respiratory alkalosis caused by hyperventilation
Results in too little C02
16-81
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Acid-Base Balance in Blood continued
Metabolic
acidosis results from excess of nonvolatile
acids
E.g. excess ketone bodies in diabetes or loss of
HC03- (for buffering) in diarrhea
Metabolic alkalosis caused by too much HC03- or too
little nonvolatile acids (e.g. from vomiting out stomach
acid)
16-82
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Acid-Base Balance in Blood continued
Normal
pH is obtained when ratio of HCO3- to C02 is
20 : 1
Henderson-Hasselbalch equation uses C02 & HCO3levels to calculate pH:
pH = 6.1 + log = [HCO3-]
[0.03PC02]
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Respiratory Acid-Base Balance
Ventilation
usually adjusted to metabolic rate to
maintain normal CO2 levels
With hypoventilation not enough CO2 is breathed out in
lungs
Acidity builds, causing respiratory acidosis
With hyperventilation too much CO2 is breathed out in
lungs
Acidity drops, causing respiratory alkalosis
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Exercise & Altitude Effects
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Ventilation During Exercise
 During
exercise,
arterial PO2, PCO2,
& pH remain fairly
constant
Fig 16.41
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Ventilation During Exercise

During exercise, breathing becomes deeper & more rapid,
delivering much more air to lungs (hyperpnea)
 2 mechanisms have been proposed to underlie this
increase:
With neurogenic mechanism, sensory activity from
exercising muscles stimulates ventilation; and/or motor
activity from cerebral cortex stimulates CNS respiratory
centers
With humoral mechanism, either PC02 & pH may be
different at chemoreceptors than in arteries
Or there may be cyclic variations in their values that
cannot be detected by blood samples
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Lactate Threshold
 Is
maximum rate of oxygen consumption before blood
lactic acid levels rise as a result of anaerobic
respiration
Occurs when 50-70% maximum 02 uptake has been
reached
 Endurance-trained athletes have higher lactate
threshold, because of higher cardiac output
Have higher rate of oxygen delivery to muscles &
greater numbers of mitochondria & aerobic
enzymes
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Acclimatization to High Altitude
Involves increased ventilation, increased DPG, & increased Hb
levels
 Hypoxic ventilatory response initiates hyperventilation which
decreases PC02 which slows ventilation
 Chronic hypoxia increases NO production in lungs which
dilates capillaries there
NO binds to Hb & is unloaded in tissues where may also
increase dilation & blood flow
NO may also stimulate CNS respiratory centers
 Altitude increases DPG, causing Hb-02 curve to shift to right
 Hypoxia causes kidneys to secrete EPO which increases RBCs

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