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Chapter 16
Respiratory Physiology
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Objectives



Explain how the intrapulmonary and
intrapleural pressures vary during ventilation
and relate these pressure changes to Boyle’s
law.
Define the terms compliance and elasticity,
and explain now these lung properties affect
ventilation.
Discuss the significance of surface tension in
lung mechanics, explain how the law of
Laplace applies to lung function and describe
the role of pulmonary surfactant.
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Objectives



(continued)
Explain how inspiration and expiration are
accomplished in unforced breathing and
describe the accessory respiratory muscles
used in forced breathing.
Describe the roles of the medulla, pons, and
cerebral cortex in the regulation of breathing.
Explain how chemoreceptors in the medulla
and the peripheral chemoreceptors in the
aortic and carotid bodies respond to changes
in PC02, pH, and P02.
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Objectives



(continued)
Describe the loading and unloading reactions
and explain how the extent of these reactions
is influenced by the P02 and affinity of HB for
02.
Explain how oxygen transport is influenced by
changes in blood pH, temperature, and
explain the effect and physiological
significance of 2,3-DPG on oxygen transport.
Describe the hyperpnea of exercise and
explain how the anaerobic threshold is
affected by endurance training.
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Respiration

Includes 3 separate functions:

Ventilation:


Gas exchange:



Breathing.
Between air and capillaries in the lungs.
Between systemic capillaries and tissues of the
body.
02 utilization:

Cellular respiration.
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Ventilation




Mechanical process that moves air in and out of the
lungs.
[O2] of air is higher in the lungs than in the blood, O2
diffuses from air to the blood.
C02 moves from the blood to the air by diffusing
down its concentration gradient.
Gas exchange occurs entirely by diffusion.
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Alveoli

~ 300 million air sacs
(alveoli).



Large surface area (60–
80 m2).
Each alveolus is 1 cell
layer thick.
2 types of cells:

Alveolar type I:


Structural cells.
Alveolar type II:

Secrete surfactant.
Figure 16.1
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Respiratory Zone



Region of gas
exchange between
air and blood.
Includes respiratory
bronchioles and
alveolar sacs.
Must contain
alveoli.
Figure 16.4
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Conducting Zone



All the structures air
passes through before
reaching the
respiratory zone.
Warms and humidifies
inspired air.
Filters and cleans:


Insert fig. 16.5
Mucus secreted to trap
particles in the inspired
air.
Mucus moved by cilia to
be expectorated.
Figure 16.5
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Physical Properties of the Lungs

Compliance:

Distensibility (stretchability):


100 x more distensible than a balloon.


Ease with which the lungs can expand.
Compliance is reduced by factors that produce resistance
to distension.
Elasticity:


Tendency to return to initial size after distension.
High content of elastin proteins.

Very elastic and resist distension.

Recoil ability.
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Surface Tension

Force exerted by fluid in alveoli to resist
distension.



Lungs secrete and absorb fluid, leaving a very thin film of
fluid.
This film of fluid causes surface tension.
H20 molecules at the surface are attracted to
other H20 molecules by attractive forces.

Force is directed inward, raising pressure in alveoli.
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Law of Laplace

Pressure in alveoli is
directly proportional to
surface tension; and
inversely proportional to
radius of alveoli.

Insert fig. 16.11
Pressure in smaller
alveolus greater.
Figure 16.11
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Surfactant


Phospholipid produced
by alveolar type II cells.
Lowers surface tension.


Insert fig. 16.12
Reduces attractive forces of
hydrogen bonding by
becoming interspersed
between H20 molecules.
As alveoli radius
decreases, surfactant’s
ability to lower surface
tension increases.
Figure 16.12
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Boyle’s Law

Changes in intrapulmonary pressure occur as
a result of changes in lung volume.


Increase in lung volume decreases
intrapulmonary pressure.


Pressure of gas is inversely proportional to its
volume.
Air goes in.
Decrease in lung volume, raises
intrapulmonary pressure above atmosphere.

Air goes out.
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Lung Pressures

Intrapulmonary pressure:


Intrapleural pressure:



Intra-alveolar pressure (pressure in the alveoli).
Pressure in the intrapleural space.
Pressure is negative, due to lack of air in the
intrapleural space.
Transpulmonary pressure:


Pressure difference across the wall of the lung.
Intrapulmonary pressure – intrapleural pressure.

Keeps the lungs against the chest wall.
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Quiet Inspiration

Active process:




Contraction of diaphragm, increases thoracic
volume vertically.
Contraction of parasternal and internal
intercostals, increases thoracic volume laterally.
Increase in lung volume decreases pressure in
alveoli, and air rushes in.
Pressure changes:



Alveolar changes from 0 to –3 mm Hg.
Intrapleural changes from –4 to –6 mm Hg.
Transpulmonary pressure = +3 mm Hg.
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Expiration

Quiet expiration is a passive process.



After being stretched, lungs recoil.
Decrease in lung volume raises the pressure within alveoli
above atmosphere, and pushes air out.
Pressure changes:



Intrapulmonary pressure changes from –3 to +3 mm Hg.
Intrapleural pressure changes from –6 to –3 mm Hg.
Transpulmonary pressure = +6 mm Hg.
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Pulmonary Ventilation
Insert fig. 16.15
Figure 16.15
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Pulmonary Function Tests



Assessed by spirometry.
Subject breathes into a closed system in which air is
trapped within a bell floating in H20.
The bell moves up when the subject exhales and
down when the subject inhales.
Insert fig. 16.16
Figure 16.16
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Terms Used to Describe Lung Volumes
and Capacities
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Anatomical Dead Space


Not all of the inspired air reached the
alveoli.
As fresh air is inhaled it is mixed with air in
anatomical dead space.


Conducting zone and alveoli where [02] is lower
than normal and [C02] is higher than normal.
Alveolar ventilation = F x (TV- DS).



F = frequency (breaths/min.).
TV = tidal volume.
DS = dead space.
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Restrictive and Obstructive Disorders

Restrictive
disorder:



Vital capacity is
reduced.
FVC is normal.
Obstructive
disorder:


VC is normal.
FEV1 is < 80%.
Figure 16.17
Insert fig. 16.17
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Pulmonary Disorders

Dyspnea:


Shortness of breath.
COPD (chronic obstructive pulmonary
disease):

Asthma:

Obstructive air flow through bronchioles.

Caused by inflammation and mucus secretion.
 Inflammation contributes to increased airway
responsiveness to agents that promote bronchial
constriction.
 IgE, exercise.
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Pulmonary Disorders

Emphysema:


Alveolar tissue is destroyed.
Chronic progressive condition that reduces surface area for
gas exchange.


(continued)
Decreases ability of bronchioles to remain open during
expiration.
 Cigarette smoking stimulates macrophages and
leukocytes to secrete protein digesting enzymes that
destroy tissue.
Pulmonary fibrosis:

Normal structure of lungs disrupted by accumulation
of fibrous connective tissue proteins.

Anthracosis.
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Gas Exchange in the Lungs

Partial pressure:

The pressure that an
particular gas exerts
independently.
PATM = PN2 + P02 + PC02 + PH20=
760 mm Hg.
 02 is humidified = 105
mm Hg.


H20 contributes to
partial pressure (47 mm
Hg).


P02 (sea level) = 150
mm Hg.
PC02 = 40 mm Hg.
Figure 16.20
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Significance of Blood P0 and PC0
Measurements
2



At normal P02
arterial blood
= 100 mm Hg.
P02 level in
the systemic
veins is = 40
mm Hg; PC02
= 46 mm Hg.
Provides a
good index of
lung function.
2
Figure 16.23
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Pulmonary Circulation

Rate of blood flow through the pulmonary
circulation is = flow rate through the systemic
circulation.


Pulmonary vascular resistance is low.


Driving pressure is about 10 mm Hg.
Low pressure pathway produces less net filtration
than produced in the systemic capillaries.
Autoregulation:


Pulmonary arterioles constrict when alveolar P0
decreases.
Matches ventilation/perfusion ratio.
2
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Lung Ventilation/Perfusion Ratios

Functionally:


Alveoli at
apex are
underperfused
(overventilated).
Alveoli at the base
are underventilated
(overperfused).
Insert fig. 16.24
Figure 16.24
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Brain Stem Respiratory Centers

Rhythmicity center:


Controls automatic
breathing.
Iinteracting neurons
that fire either during
inspiration (I neurons)
or expiration
(E neurons).
Insert fig. 16.25
Figure 16.25
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Rhythmicity Center

I neurons located primarily in dorsal respiratory
group (DRG):


E neurons located in ventral respiratory group
(VRG):


Regulate activity of phrenic nerve.
Passive process.
Activity of E neurons inhibit I neurons.

Rhythmicity of I and E neurons may be due to
pacemaker neurons.
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Pons Respiratory Centers


Medullary rhythmicity center influenced
by pons.
Apneustic center:


Promotes inspiration by stimulating the I
neurons in the medulla.
Pneumotaxic center:


Antagonizes the apneustic center.
Inhibits inspiration.
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Chemoreceptors

Monitor changes in
blood PC0 , P0 , and pH.
Central:
2



2
Medulla.
Insert fig. 16.27
Peripheral:

Carotid and aortic
bodies.

Control breathing
indirectly.
Figure 16.27
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Central Chemoreceptors




More sensitive to changes in arterial PC0 .
H20 + C02
H2C03
H+
H+ cannot cross the blood brain barrier.
C02 can cross the blood brain barrier and
will form H2C03.
2

Lowers pH of CSF.

Directly stimulates central chemoreceptors.
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Peripheral Chemoreceptors

Are not stimulated directly by changes
in arterial PC0 .
H20 + C02
H2C03
H+
Stimulated by rise in [H+] of arterial
blood.
2



Increased [H+] stimulates peripheral
chemoreceptors.
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Chemoreceptor Control of
Breathing
Insert fig. 16.29
Figure 16.20
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Effects of Pulmonary Receptors
on Ventilation

Lungs contain receptors that influence the brain
stem respiratory control centers via sensory fibers
in vagus.

Unmyelinated C fibers can be stimulated by:

Capsaicin:


Histamine and bradykinin:



Produces apnea followed by rapid, shallow breathing.
Released in response to noxious agents.
Irritant receptors are rapidly adaptive receptors.
Hering-Breuer reflex:

Pulmonary stretch receptors activated during inspiration.

Inhibits respiratory centers to prevent undue tension on lungs.
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Hemoglobin



280 million
hemoglobin/RBC.
Each hemoglobin
has 4 polypeptide
chains and 4
hemes.
In the center of
each heme group
is 1 atom of iron
that can combine
with 1 molecule
02.
Insert fig. 16.32
Figure 16.32
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Hemoglobin

Methemoglobin:

Lacks electrons and cannot bind with 02.


(continued)
Blood normally contains a small amount.
Carboxyhemoglobin:

The bond with carbon monoxide is 210
times stronger than the bond with oxygen.

Transport of 02 to tissues is impaired.
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Hemoglobin

Oxygen-carrying capacity of blood determined by
its [hemoglobin].

Anemia:
[Hemoglobin] below normal.


Polycythemia:
[Hemoglobin] above normal.


Hemoglobin production controlled by erythropoietin.
Production stimulated by PC0 delivery to kidneys.


(continued)
2
Loading/unloading depends:
 P0 of environment.
 Affinity between hemoglobin and 02.
2
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Oxyhemoglobin Dissociation
Curve

Graphic illustration of the %
oxyhemoglobin saturation at
different values of P02.


Loading and unloading of 02.
 Steep portion of the
sigmoidal curve, small
changes in P02 produce
large differences in %
saturation (unload more
02).
Decreased pH, increased
temperature, and increased 2,3
DPG:

Affinity of hemoglobin for 02
decreases.
 Greater unloading of 02:
 Shift to the curve to
the right.
Figure 16.34
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Effects of pH and Temperature


Affinity is
decreased when
pH is decreased.
Increased
temperature and
2,3-DPG:
 Shift the curve
to the right.
Insert fig. 16.35
Figure 16.35
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C02 Transport

C02 transported in the blood:
HC03- (70%).
 Dissolved C02 (10%).
 Carbaminohemoglobin (20%).

H20 + C02 ca H2C03
High PC0
2
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Chloride Shift at Systemic
Capillaries


H20 + C02
H2C03
H+ + HC03At the tissues, C02 diffuses into the RBC; shifts
the reaction to the right.

Increased [HC03-] produced in RBC:


RBC becomes more +.



HC03- diffuses into the blood.
Cl- attracted in (Cl- shift).
H+ released buffered by combining with
deoxyhemoglobin.
HbC02 formed.

Unloading of 02.
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Carbon Dioxide Transport and
Chloride Shift
Insert fig. 16.38
Figure 16.38
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At Pulmonary Capillaries



H20 + C02
H2C03
H+ + HC03At the alveoli, C02 diffuses into the alveoli;
reaction shifts to the left.
Decreased [HC03-] in RBC, HC03- diffuses into
the RBC.

RBC becomes more -.


Deoxyhemoglobin converted to
oxyhemoglobin.


Cl- diffuses out (reverse Cl- shift).
Has weak affinity for H+.
Gives off HbC02.
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Reverse Chloride Shift in Lungs
Insert fig. 16.39
Figure 16.39
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Ventilation During Exercise




During exercise, breathing
becomes deeper and more
rapid.
Produce > total minute volume.
Neurogenic mechanism:

Sensory nerve activity from
exercising muscles
stimulates the respiratory
muscles.

Cerebral cortex input may
stimulate brain stem
centers.
Humoral mechanism:

PC0 and pH may be different
at chemoreceptors.

Cyclic variations in the
values that cannot be
detected by blood samples.
Insert fig. 16.41
2
Figure 16.41
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Lactate Threshold and
Endurance Training

Maximum rate of oxygen consumption that
can be obtained before blood lactic acid
levels rise as a result of anaerobic respiration.


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.
Have increased content of mitochondria in skeletal
muscles.
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Acclimatization to High Altitude


Adjustments in respiratory function when
moving to an area with higher altitude:
Changes in ventilation:

Hypoxic ventilatory response produces
hyperventilation.



Affinity of hemoglobin for 02:


Increases total minute volume.
Increased tidal volume.
Action of 2,3-DPG decreases affinity of
hemoglobin for 02.
Increased hemoglobin production:

Kidneys secrete erythropoietin.