RESPIRATORY

PHYSIOLOGY

Presentation Adapted from the publication by The McGraw-Hill

Companies. DO NOT REPRODUCE.
 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.
 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.
 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 hyperapnea of exercise and
explain how the anaerobic threshold is
affected by endurance training.
 RESPIRATION

• Includes 3 separate functions:

• Ventilation:
• Breathing.
• Gas exchange:
• Between air and capillaries in the lungs.
• Between systemic capillaries and tissues of the body.
• 02 utilization:
• Cellular respiration.
 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.
 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
 RESPIRATORY ZONE
• Region of gas
exchange
between air and
blood.
• Includes
respiratory
bronchioles and
alveolar sacs.
• Must contain
alveoli.
Figure 16.4
 CONDUCTING ZONE

• All the structures air

passes through
before reaching the Insert fig. 16.5
respiratory zone.
• Warms and humidifies
inspired air.
• Filters and cleans:
• Mucus secreted to
trap particles in the
inspired air.
• Mucus moved by cilia
to be expectorated.

Figure 16.5
 PHYSICAL PROPERTIES OF
• Compliance: THE LUNGS
• Distensibility (stretchability):
• Ease with which the lungs can expand.
• 100 x more distensible than a balloon.
• 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.
 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.
 LAW OF LAPLACE

• Pressure in alveoli is
directly proportional to
surface tension; and Insert fig. 16.11
inversely proportional
to radius of alveoli.
• Pressure in smaller
alveolus greater.

Figure 16.11
 SURFACTANT

• Phospholipid produced
by alveolar type II cells.
Insert fig. 16.12
• Lowers surface tension.
• 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
 BOYLE’S LAW

• Changes in intrapulmonary pressure occur

as a result of changes in lung volume.
• Pressure of gas is inversely proportional to its
volume.
• Increase in lung volume decreases
intrapulmonary pressure.
• Air goes in.
• Decrease in lung volume, raises
intrapulmonary pressure above
atmosphere.
• Air goes out.
 LUNG
• Intrapulmonary pressure:
PRESSURES
• Intra-alveolar pressure (pressure in the alveoli).
• Intrapleural pressure:
• 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.
 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.
 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.
 PULMONARY VENTILATION

Insert fig. 16.15

Figure 16.15
 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
Terms Used to Describe Lung Volumes
and Capacities
 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.
 RESTRICTIVE AND OBSTRUCTIVE DISORDERS

• Restrictive
disorder:
• Vital capacity
is reduced. Insert fig. 16.17
• FVC is normal.
• Obstructive
disorder:
• VC is normal.
• FEV1 is < 80%.

Figure 16.17
 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.
 PULMONARY DISORDERS (CONTINUED)

• Emphysema:
• Alveolar tissue is destroyed.
• Chronic progressive condition that reduces surface
area for gas exchange.
• 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.
 GAS EXCHANGE IN THE LUNGS

• Partial pressure:
• The pressure that an
particular gas exerts
independently.
• PATM = PN + P0 + PC0 + PH 0=
2 2 2 2

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
 SIGNIFICANCE OF BLOOD P0 AND 2

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.
Figure 16.23
 PULMONARY CIRCULATION
• Rate of blood flow through the pulmonary
circulation is = flow rate through the
systemic circulation.
• Driving pressure is about 10 mm Hg.
• Pulmonary vascular resistance is low.
• Low pressure pathway produces less net
filtration than produced in the systemic
capillaries.
• Autoregulation:
• Pulmonary arterioles constrict when alveolar
P0 decreases.
2

• Matches ventilation/perfusion ratio.

 LUNG VENTILATION/PERFUSION RATIOS

• Functionally:
• Alveoli at Insert fig. 16.24
apex are
underperfused
(overventilated).
• Alveoli at the base
are
underventilated
(overperfused).

Figure 16.24
 BRAIN STEM RESPIRATORY CENTERS

• Rhythmicity center:
• Controls automatic
breathing.
Insert fig. 16.25
• Iinteracting neurons
that fire either during
inspiration (I
neurons) or
expiration (E
neurons). Figure 16.25
 RHYTHMICITY CENTER
• I neurons located primarily in dorsal respiratory
group (DRG):
• Regulate activity of phrenic nerve.
• E neurons located in ventral respiratory group
(VRG):
• Passive process.
• Activity of E neurons inhibit I neurons.
• Rhythmicity of I and E neurons may be due to
pacemaker neurons.
 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.
 CHEMORECEPTORS

• Monitor changes in
blood PC0 , P0 , and
2 2

pH.
Insert fig. 16.27
• Central:
• Medulla.
• Peripheral:
• Carotid and aortic
bodies.
• Control breathing
indirectly.

Figure 16.27
 CENTRAL
CHEMORECEPTORS
• More sensitive to changes in arterial PC0 . 2

• H20 + C02
H2brain
• H+ cannot cross the blood C03barrier. H+
• C02 can cross the blood brain barrier and will form
H2C03.
• Lowers pH of CSF.
• Directly stimulates central chemoreceptors.
 PERIPHERAL
CHEMORECEPTORS
• Are not stimulated directly by changes in arterial PC02.
• H20 + C02 H2C03 H+
• Stimulated by rise in [H+] of arterial blood.
• Increased [H+] stimulates peripheral chemoreceptors.
 CHEMORECEPTOR
CONTROL OF BREATHING

Insert fig. 16.29

Figure 16.20
 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:
• Produces apnea followed by rapid, shallow breathing.
• Histamine and bradykinin:
• 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.
 HEMOGLOBIN

• 280 million
hemoglobin/RBC.
Insert fig. 16.32
• 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.

Figure 16.32
 HEMOGLOBIN (CONTINUED)

• Methemoglobin:
• Lacks electrons and cannot bind with 02.
• 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.
 HEMOGLOBIN (CONTINUED)

• 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.
2

• Loading/unloading depends:
• P0 of environment.
2

• Affinity between hemoglobin and 02.

 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
 EFFECTS OF PH AND TEMPERATURE

• Affinity is
decreased when
pH is decreased.
• Increased Insert fig. 16.35
temperature and
2,3-DPG:
• Shift the curve
to the right.

Figure 16.35
 C02 TRANSPORT

• C02 transported in the blood:

• HC03- (70%).
• Dissolved C02 (10%).
• Carbaminohemoglobin (20%).

H20 + C02 ca H2C03

High PC0 2
 CHLORIDE SHIFT AT
SYSTEMIC+CAPILLARIES
• H20 + C02 H2C03 H + HC03
-

• At the tissues, C02 diffuses into the RBC;

shifts the reaction to the right.
• Increased [HC03-] produced in RBC:
• HC03- diffuses into the blood.
• RBC becomes more +.
• Cl- attracted in (Cl- shift).
• H+ released buffered by combining with
deoxyhemoglobin.
• HbC02 formed.
• Unloading of 02.
CARBON DIOXIDE TRANSPORT
AND CHLORIDE SHIFT

Insert fig. 16.38

Figure 16.38
 AT PULMONARY
CAPILLARIES
• H20 + C02 H2C03 H+ + HC03-
• At the alveoli, C02 diffuses into the alveoli;
reaction shifts to the left.
• Decreased [HC03-] in RBC, HC03- diffuses into
the RBC.
• RBC becomes more -.
• Cl- diffuses out (reverse Cl- shift).
• Deoxyhemoglobin converted to
oxyhemoglobin.
• Has weak affinity for H+.
• Gives off HbC02.
REVERSE CHLORIDE SHIFT IN
LUNGS
Insert fig. 16.39

Figure 16.39
 VENTILATION DURING EXERCISE
• During exercise, breathing
becomes deeper and more
rapid.
• Produce > total minute volume. Insert fig. 16.41
• 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
2

different at
chemoreceptors.
• Cyclic variations in the
values that cannot be
detected by blood
samples.
Figure 16.41
 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.
 ACCLIMATIZATION TO HIGH
ALTITUDE
• Adjustments in respiratory function when
moving to an area with higher altitude:
• Changes in ventilation:
• Hypoxic ventilatory response produces
hyperventilation.
• Increases total minute volume.
• Increased tidal volume.
• Affinity of hemoglobin for 02:
• Action of 2,3-DPG decreases affinity of
hemoglobin for 02.
• Increased hemoglobin production:
• Kidneys secrete erythropoietin.
Thank You.