Download Chapter 16 Respiration Respiration Organization of the respiratory

Chapter 16
Respiration
Respiration
• Functions of the respiratory system
–
–
–
–
–
–
–
– Breathing.
• Gas exchange:
– Occurs between air and blood in the lungs.
– Occurs between blood and tissues.
• 02 utilization:
– Cellular respiration.
Fig. 16.1
Fig not
in book
Type I cell
Steps in
Respiration
Type II cell
Fig. 16.4
Organization of the
respiratory system.
• The term respiration includes 3 separate
functions:
• Ventilation:
• Low -resistance
pathway for
airflow
• Defends against
yucky stuff
• Warms and
moistens air
• When you have
kids it enables
you to yell at
them.
ϖ No gas exchange
The conducting zone
Fig. 16.5
1
Respiratory Zone
• Region of gas
exchange between
air and blood.
• Includes respiratory
bronchioles.
• Must contain
alveoli.
• Gas exchange
occurs by diffusion.
Figure not in book
Fig. 16.4
Figure not in book
Fig. 16.8
Ventilation and Lung Mechanics
Step 1: Getting air into and out of lungs
Ventilation and Lung Mechanics
Step 1: Getting air into and out of lungs
• Remember: F = ΔP/R
– F = flow
– ΔP = pressure difference (mmHg)
– R = resistance to flow.
Fig not in book
2
Really, Really Important Point!
Fig not
in book
• During inspiration and expiration volume of
lungs is made to change.
¬ By Boyle’s law, these changes cause
changes in alveolar pressure which drives
air into or out of lungs.
Fig. 16.11
Volume of lungs depends on:
• Transpulmonary pressure - difference in
pressure between outside and inside of
lungs.
• Elasticity (stretchability) of lungs.
Surface Tension
• Law of Laplace:
• Pressure in alveoli is
directly proportional
to surface tension
and inversely
proportional to
radius of alveoli.
Creating the Intrapleural Pressure
• Pull of lungs inward and chestwall outward
on intrapleural fluid causes a negative
pressure within this space.
Fig. 16.15
3
Fig not in book
Fig not in book
Lung Compliance
Fig not in book
• CL = magnitude of change in lung volume
(ΔVL) produced by a given change in
transpulmonary pressure.
• CL = ΔVL/Δ (Palv - Pip)
• Greater the lung compliance the _______ it
is to expand the lungs at any given
transpulmonary pressure.
Determinants of Lung
Compliance
• Stretchability
• Surface tension at air-water interfaces
within alveoli.
– Assets of surfactant.
• Phospholipid
produced by
alveolar type II
cells.
• 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.
Surfactant
Fig. 16.12
4
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.
Fig. 16.14 See also table 16.2
• Tidal volume:
Amount of air expired with each breath.
• Vital capacity:
The maximum amount of air that can be forcefully exhaled
after maximum inhalation.
Schematic of a
spirometer (left)
and the spirometer
you will be using in
lab (above).
Spirogram
Fig. 16.16
Table 16.3 Terms Used to Describe Lung Volumes and
Capacities
Term
Definition
Lung Volumes
The four nonoverlapping components of the total lung
capacity
The volume of gas inspired or expired in an unforced
respiratory cycle
The maximum volume of gas that can be inspired during
forced breathing in addition to tidal volume
The maximum volume of gas that can be expired during
forced breathing in addition to tidal volume
The volume of gas remaining in the lungs after a maximum
expiration
Measurements that are the sum of two or more lung
volumes
The total amount of gas in the lungs after a maximum
inspiration
The maximum amount of gas that can be expired after a
maximum inspiration
The maximum amount of gas that can be inspired after a
normal tidal expiration
The amount of gas remaining in the lungs after a normal
tidal expiration
Tidal volume
Inspiratory reserve volume
Expiratory reserve volume
Residual volume
Lung Capacities
Total lung capacity
Vital capacity
Inspiratory capacity
Functional residual capacity
Figure not in book
5
Anatomical Dead Space
• Not all of the inspired air reaches the alveoli.
• As fresh air is inhaled it is mixed with anatomical
dead space.
• Conducting zone and alveoli where 02
concentration is lower than normal and C02
concentration is higher than normal.
• Alveolar ventilation: F x (TV- DS)
– F = frequency (breaths/min.).
– TV = tidal volume.
– DS = dead space.
Airway Radii and Resistance
• Airway radii affected by
– Physical factors
• “going down the wrong pipe”
• Asthma caused by chemical factors (see below).
– Neural factors
• Epinephrine
– Chemical factors
• CIGARETTE SMOKE, pollutants, viruses allergens,
bronchoconstrictor chemicals
Airway resistance and
restrictive vs. obstructive disorders
• Recall:
• F = (Patm - Palv) / R
• Resistance depends on:
–
–
–
Restrictive and Obstructive
Disorders
• Restrictive
disorder:
– Vital capacity is
reduced.
– FVC is normal.
• Obstructive
disorder:
– VC is normal.
– FEV1 is reduced.
Fig. 16.17
Gas Exchange
• Dalton’s Law:
• Total pressure of a gas mixture is = to the
sum of the pressures that each gas in the
mixture would exert independently.
• PATM = PN2 + P02 + PCo2 = 760 mm Hg
– 02 humidified.
• H20 contributes to partial pressure
(~ 47 mm Hg)
– P02 (sea level) = 150 mm Hg.
Fig. 16.20
6
Significance of Blood P02 and PC02
Measurements
• At normal P02
arterial blood is
about 100 mm
Hg.
• P02 systemic
veins =
~ 40 mm Hg.
• PC02 systemic
veins =
~ 46 mm Hg
Figure not in book - Applying numbers to previous figure.
Fig. 16.23
Gas Exchange
• Dalton’s Law:
• Total pressure of a gas mixture is = to
the sum of the pressures that each gas
in the mixture would exert
independently.
• PATM = PN2 + P0 + PCo2 = 760 mm Hg
Fig. 16.32
Measuring efficacy of lung function.
Defining Ventilation
• Minute ventilation - total ventilation per
minute
NOTE
these
numbers
• Alveolar Ventilation - total volume of fresh air
enter the alveoli per minute = efficacy of
breath
• Physiologic dead space - sum of anatomic and
alveolar dead space.
Fig. 16.23
7
Restrictive and Obstructive
Disorders
• Restrictive
disorder:
– Vital capacity is
reduced.
– FVC is normal.
• Obstructive
disorder:
– VC is normal.
– FEV1 is reduced.
Fig. 16.17
FEV1
Forced Expiratory Volume/sec.
• Fraction of total “forced” vital capacity
expired in 1 sec.
• The FEV1 of a person with obstructive lung
disease would be ________ 80% of vital
capacity.
• The FEV1 of a person with restrictive lung
disease would ________ 80% of vital
capacity.
Relevance of Partial Pressures
• High altitude => _______ in PO2 of inspired
air and _________ in alveolar PO2.
• Decreased alveolar ventilation => ______ in
PO2 of inspired air and ________ in
alveolar PO2.
• Increased cellular metabolism => ________
in alveolar PO2.
Alveolar Gas Pressure
• Alveolar PO2 and PCO2 determine the systemic
arterial PO2 and PCO2.
• Alveolar PO2 values determined by
– PO2 of atmospheric air
– Rate of alveolar ventilation
– Rate of total body oxygen consumption
• Alveolar PCO2 values determined by
– Rate of alveolar ventilation
– Rate of total body carbon dioxide production
Getting O2 into and CO2 out of
body: the bottom line(s)
• In alveoli
– PO2 and PCO2 on two sides of alveolar-capillary
membrane result in net diffusion, CO2 out and
O2 in.
– More capillaries involved, more total O2/CO2
exchange.
– Need for fewer or greater numbers of alveoli in
gas exchange (impairment of gas exchange:O2).
8
Getting O2 into and CO2 out of
body: the bottom line(s)
• In alveoli
– Ventilation-perfusion inequality = mismatching
of air supply and blood supply on an individual
alveoli.
– Lowers PO2 of systemic arterial blood.
– Caused by
Getting O2 into and CO2 out of
body: the bottom line(s)
• In tissues
– Low PO2 and high PCO2 in tissues results in net
movement of O2 into tissues and net CO2
movement out of tissues.
• We will revisit this momentarily.
• Ventilated blood in alveoli with no blood supply
• No blood flowing to some alveoli.
– Compensation by vasoconstriction
Breathing Lesson
(control of breathing)
• Medulla oblongata (medullary inspiratory
neurons).
• Pons
• Pulmonary stretch receptors
• Peripheral chemoreceptors • Central chemoreceptors
Regulation of Breathing
• Neurons in the
medulla oblongata
forms the rhythmicity
center:
– Controls automatic
breathing.
• Brain stem
respiratory centers:
– Medulla.
– Pons.
Fig. 16.25
Rhythmicity Center
• Dorsal respiratory group (DRG).
– Regulate activity of phrenic nerve.
– Project to and stimulate spinal interneurons that
innervate respiratory muscles.
– Considered the “I” neurons.
• Ventral respiratory group (VRG).
– Passive process.
– Controls motor neurons to the internal intercostal
muscles.
– Considered the “E” neurons.
Pons Respiratory Centers:
Influence medullary rhythmicity
• Apneustic center:
– Promote inspiration by stimulating the
inspiratory neurons in the medulla.
– Provide constant stimulus for inspiration.
• Pneumotaxic center:
– Antagonize the apneustic center.
– Inhibits inspiration.
• Activity of expiratory neurons inhibit inspiratory
neurons.
9
Adequacy of ventilation
• Hypoventilation
– increase in ratio of carbon dioxide production
to alveolar ventilation.
– hypercapnia
• Hyperventilation
– decrease in ratio of carbon dioxide production
to alveolar ventilation.
– hypocapnia
Fig. 16.28
Chemoreceptor Control
• Chemoreceptor input modifies the rate and depth
of breathing.
– Oxygen content of blood decreases more slowly
because of the large “reservoir” of oxygen attached to
hemoglobin.
– Chemoreceptors are more sensitive to changes in P C02.
H2C03
• H20 + C02
H+ + HC03• Rate and depth of ventilation adjusted to maintain
arterial PC02 of 40 mm Hg.
Chemoreceptors
• 2 groups of chemoreceptors
that monitor changes in
blood P C02, P 02, and pH.
• Central:
– Medulla.
• Peripheral:
– Carotid and aortic
bodies.
– Control breathing
indirectly via sensory
nerve fibers to the
medulla.
Fig. 16.27
Can say that chemoreceptor sensitivity to
PCO2 is augmented by low PO2.
Fig. 16.29
Fig. 16.31
10
Moving Oxygen in Blood
• Amount of oxygen dissolved in blood
directly proportional to PO2 of blood.
• But oxygen NOT very soluble in water
(blood).
• Hemoglobin to the rescue!!!!
Hemoglobin
Structure
Fig. 16.33
Hemoglobin
• Hemoglobin production controlled by
erythropoietin.
• Production stimulated by P02 delivery to kidneys.
• Loading/unloading depends:
– P02 of environment.
– Affinity between hemoglobin and 02.
• Oxyhemoglobin vs. Deoxyhemoglobin.
Fig. 16.34
• So what does
pH do to O2
affinity of
hemoglobin?
• Temperature?
• 2,3 DPG =
Fig. 16.35
More on 2,3DPG
I want my
OXYGEN!
• Anemia and
– Increased production of 2,3-DPG with low
hemoglobin concentration.
– Causes increased unloading of oxygen in
tissues.
• Fetal hemoglobin and
– Gamma chains in lieu of beta chains.
– Do not bind 2,3-DPG
– Becomes oxygen “pig”
11
Muscle Myoglobin
Inherited defects in hemoglobin
• Sickle-cell anemia
– Valine substitued for glutamic acid at position #6.
– Low PO2 causes cross-linking and formation of
paracrystalline gel - “sickling” of cells.
• Thalassemia
– Decreased synthesis of alpha or beta chain of
hemoglobin.
– Get increases in gamma chain synthesis.
• Slow-twitch skeletal fibers
and cardiac muscle cells are
rich in myoglobin.
– Higher affinity for 0 2 than
hemoglobin.
• Acts as a “go-between” in
the transfer of 0 2 from
blood to the mitochondria
within muscle cells.
• May also have an 02 storage
function in cardiac muscles.
Fig. 16.37
Carbon dioxide in blood
• Dissolved CO2: 1/10
• Carbaminohemoglobin: 1/5
• Bicarbonate: 7/10
Fig.
16.38
Figure not in book
Figure not in book
12
Fig not
in book
Fig. 16.39
Adequacy of ventilation
• Hypoventilation
– increase in ratio of carbon dioxide production
to alveolar ventilation.
– hypercapnia
• Hyperventilation
– decrease in ratio of carbon dioxide production
to alveolar ventilation.
– hypocapnia
Compensating acidosis or alkalosis.
• Metabolic acidosis or alkalosis -
• Respiratory acidosis or alkalosis -
Respiratory acidosis vs.
respiratory alkalosis
• Respiratory acidosis - increased arterial H + concentration
due to CO 2 retention.
• Metabolic acidosis - increased production of “nonvolatile”
acids or loss of blood bicarbonate, resulting in a fall of
blood pH.
• Respiratory alkalosis - lowering of arterial PCO2 and H+
concentration.
• Metabolic alkalosis - rise in blood pH produced by loss of
nonvolatile acids or by excessive accumulation of
bicarbonate base.
Chemoreceptors
• 2 groups of chemoreceptors
that monitor changes in
blood P C02, P 02, and pH.
• Central:
– Medulla.
• Peripheral:
– Carotid and aortic
bodies.
– Control breathing
indirectly via sensory
nerve fibers to the
medulla.
Fig. 16.27
13
Fig. not in book
Fig. not in book
Response to exercise
• Neurogenic
– Sensory nerve activity from exercising limbs
stimulate respiratory muscles.
– Input from cerebral cortex stimulates brain stem
respiratory centers.
• Humoral
– Changes in blood concentrations of gases and
signaling molecules.
Fig. not in book
• Hypoxic ventilatory
response to high
altitude (low PO2)
– produces
hyperventilation
– Increase in tidal
volume.
– Lowers arterial PCO2
– Produces respiratory
alkalosis which
eventually “blunts”
hyperventilatory
response.
Other respiratory changes due to
high altitudes
• Increased production
of 2,3-DPG.
• Increased production
of RBCs and
hemoglobin.
• “Barrel-chest”
Figure not in book
14
Figure not in book
Figure not in book
15