Transcript respiratory system

RESPIRATORY SYSTEM
FUNCTIONAL ANATOMY
OF
THE RESPIRATORY SYSTEM
• Respiratory System:
– Pulmonary ventilation: movement of air into and out of the lungs
so that gases there are continuously changed and refreshed
(commonly called breathing)
– External respiration: movement of oxygen from the lungs to the
blood and of carbon dioxide from the blood to the lungs
• Circulatory System:
– Transport of respiratory gases:
• Transport of oxygen from the lungs to the tissue cells of the body
• Transport of carbon dioxide from the tissue cells to the lungs
• Accomplished by the cardiovascular system using blood as the
transporting fluid
– Internal respiration: movement of oxygen from blood to the
tissue cells and of carbon dioxide from tissue cells to blood
FUNCTIONAL ANATOMY
OF
THE RESPIRATORY SYSTEM
• Respiratory and circulatory systems are
closely coupled, and if either system fails,
the body’s cells begin to die from oxygen
starvation
• Because it moves air, the respiratory
system is also involved with the sense of
smell and with speech
RESPIRATORY ORGANS
• The respiratory system
includes:
–
–
–
–
–
–
–
–
–
Nose
Nasal cavity
Pharynx
Larynx
Trachea
Bronchi
Bronchioles
Lungs
Alveoli
RESPIRATORY SYSTEM
• Two Zones:
– Conducting:
• Includes all the passageways that provide rigid
conduits for air to reach the gas exchange locations
• Cleanses, humidifies, and warms incoming air
– Respiratory:
• Actual site of gas exchange, is composed of the
respiratory bronchioles, alveolar ducts, and alveoli
• All microscopic structures
RESPIRATORY ORGANS
EXTERNAL NOSE
NOSE
• The nose is divided
into the external
nose, which is formed
by hyaline cartilage
and bones of the
skull, and the nasal
cavity, which is
entirely within the
skull
INTERNAL NASAL CAVITY
•
•
•
•
Divided by a midline nasal septum
– Anteriorly cartilage
– Posteriorly vomer and ethmoid
bone
Continuous posteriorly with the nasal
portion of the pharynx through the
posterior nasal apertures (internal
nares)
Roof of the nasal cavity is formed by
the ethmoid and sphenoid bones of the
skull
Floor is formed by the palate, which
separates the nasal cavity from the
oral cavity
– Anterior: maxillary processes and
palatine bone
– Posterior: muscular and soft
INTERNAL NASAL CAVITY
VESTIBULE
• The part of the nasal
cavity just superior to the
nostrils
• Lined with skin
containing sebaceous
and sweat glands and
numerous hair follicles
• Hairs (vibrissae) filter
coarse particles (dust,
pollen) from inspired air
INTERNAL NASAL CAVITY
TWO TYPES OF MUCOSA
•
Olfactory:
– Lines the slitlike superior region
– Contains smell receptors
•
Respiratory:
– Mucous glands: secrete mucus
– Serous glands: secrete a watery
fluid containing enzymes
– Epithelial cells: secrete defensins
(natural antibiotics that help get rid
of invading microbes)
•
•
The sticky mucus traps inspired
dust, bacteria, and other debris,
while lysozyme attacks and
destroys bacteria chemically
High water content of the mucus
film acts to humidify the inhaled
air
INTERNAL NASAL CAVITY
RESPIRATORY MUCOSA
• Ciliated cells create a gentle
current that moves the sheet of
contaminated mucus posteriorly
toward the throat, where it is
swallowed and digested by
stomach juices
– Cold air causes them to
become sluggish
• Mucus accumulates and
dribbles out the nostrils
• Richly supplied with sensory
nerve endings:
– Contact with irritating particles
triggers a sneeze reflex—
forcing air outward in a violent
burst
INTERNAL NASAL CAVITY
RESPIRATORY MUCOSA
• Rich plexuses of
capillaries and thinwalled veins underlie
the nasal epithelium
and warm incoming
air as it flows across
the mucosal surface
INTERNAL NASAL CAVITY
• Protruding medially from each
lateral wall of the nasal cavity
are three curved scroll-like
mucosa-covered projections:
increase the mucosal surface
area exposed to the air and
enhance air turbulence in the
cavity
– Superior conchae
– Middle conchae
– Inferior conchae
• Groove inferior to each concha
is a meatus
THE NOSE
AND
PARANASAL SINUSES
•
•
The nose provides a resonance
chamber for speech
The nasal cavity is surrounded by
paranasal sinuses within the frontal,
maxillary, sphenoid, and ethmoid
bones that serve to lighten the
skull, warm and moisten air, and
produce mucus which drains into
the nasal cavity
– The suctioning effect created by
nose blowing helps drain the
sinuses
HOMEOSTATIC IMBALANCE
• Rhinitis: inflammation of the nasal mucosa accompanied
by excessive mucus production, nasal congestion, and
postnasal drip
– Caused by cold viruses, streptococcal bacteria, and various
allergens
• Sinusitis: inflamed sinuses
– Since the nasal mucosa is continuous with the sinuses infections
can easily spread to the sinuses
• Sinus headache: when the passageways connecting the
sinuses to the nasal cavity are blocked with mucus or
infectious material, the air in the sinus cavities is absorbed
resulting in a partial vacuum (localized over the inflamed
areas)
THE PHARYNX
• The pharynx connects the
nasal cavity and mouth
superiorly to the larynx
and esophagus inferiorly
• Commonly called the
throat
• Muscular pharynx is
composed of skeletal
muscle
Nasopharynx
• Serves as only an air
passageway
• During swallowing, the soft
palate and its pendulous
(hanging loosely) uvula move
superiorly, an action that closes
off the nasopharynx and
prevents food from entering the
nasal cavity
• Contains the pharyngeal
tonsil (adenoids), which traps
and destroys airborne
pathogens
HOMEOSTATIC IMBALANCE
• Infected and swollen
adenoids (pharyngeal
tonsils) block air passage
in the nasopharynx,
making it necessary to
breathe through the
mouth
– Air is not properly
moistened, warmed, or
filtered before reaching the
lungs
HOMEOSTATIC IMBALANCE
•
•
The pharyngotympanic
(auditory) tubes, which drain the
middle ear cavities and allow ear
pressure to equalize with
atmospheric pressure, open into
the lateral walls of the nasopharynx
A ridge of pharyngeal mucosa,
referred to as a tubal tonsil, arches
over each of these openings
– Help protect the middle ear
against infections likely to
spread from the nasopharynx
– The pharyngeal tonsil also
plays this protective role
NASOPHARYNX
OROPHARYNX
•
Is an air and food passageway
that extends inferiorly from the
level of the soft palate to the
epiglottis
– Air and food mix
– Both swallowed food and inhaled
air pass through
•
•
Epithelium is adapted for increased
frictional and greater chemical
trauma accompanying food passage
Two kinds of tonsils lie embedded
in the mucosa:
– Paired palatine tonsils lie in the
lateral walls
– Lingual tonsil covers the base of
the tongue
LARYNGOPHARYNX
• Is an air and food passageway
that lies directly posterior to
the epiglottis, extends to the
larynx, and is continuous
inferiorly with the esophagus
• The esophagus conducts food
and fluids to the stomach
• Air enters the larynx anteriorly
• During swallowing, food has
the “right of way”, and air
passage temporarily stops
MIDSAGITAL SECTION OF THE
HEAD AND NECK
UPPER RESPIRATORY TRACT
THE LARYNX
BASIC ANATOMY
• The larynx (or voice box)
attaches superiorly to the hyoid
bone, opening into the
laryngopharynx, and attaches
inferiorly to the trachea
– From 4th to 6th vertebra
• Three functions:
– Provide an open airway
– Switching mechanism to route
air and food into the proper
channels
– Because it houses the vocal
cords. The 3rd function is voice
production
THE LARYNX
• The larynx consists of
hyaline cartilages:
– Thyroid:shield-shaped
• Midline laryngeal
prominence (Adam’s
Apple)
– Cricoid: ring shaped
– Paired arytenoid,
corniculate, and cuneiform
– Epiglottis, which is elastic
cartilage
• Covered by mucosacontaining taste buds
LARYNX
POSTERIOR ASPECT OF
LARYNX
CARTILAGINOUS FRAMEWORK
OF LARYNX
• During swallowing,
the larynx is pulled
superiorly and the
epiglottis tips to
cover the laryngeal
inlet
VOCAL CORDS
• Vocal ligaments attach the
arytenoid cartilages to the
thyroid cartilage
– These ligaments composed
largely of elastic fibers form
the core of mucosal folds,
called the vocal folds (true
vocal cords)
• Which vibrate as air passes
over them to produce sound
• Superior to the vocal cords
are the false vocal cords
– No part in sound production
but help to close the glottis
when we swallow
VOCAL CORDS
VOCAL CORDS
• Below the vocal folds the epithelium is a
pseudostratified ciliated columnar type that acts as
a dust filter
• The power stroke of its cilia is directed upward
toward the pharynx so that mucus is
continually moved away from the lungs
• We help to move mucus up and out of the
larynx when we “clear our throats”
VOICE PRODUCTION
•
•
•
Voice production involves the
intermittent release of expired air
and the opening and closing of the
glottis
The length of the true vocal cords and
the size of the glottis change with the
action of the intrinsic laryngeal muscles
that clothe the cartilage
As the length and tension of the cords
change, the pitch (depends on the
frequency and loudness: height of
wave) of the sound varies
–
The tenser the cords, the faster they
vibrate and the higher the pitch
•
–
(b) the glottis is wide when we produce
deep tones and narrows to a slit for
high-pitched sounds
Male larynx enlarges during puberty
•
Vocal cords become longer and thicker
causing them to vibrate slower (voice
becomes deeper)
VOICE PRODUCTION
•
•
Loudness of the voice depends on the force with which the airstream
rushes across the vocal cords:
– The greater the force, the stronger the vibration and the louder the sound
– The power source for creating the airstream is the muscles of the chest,
abdomen, and back
Vocal folds actually produce buzzing sounds
– The perceived quality of the voice depends on the coordinated activity
of many structures above the glottis
• The entire length of the pharynx acts as a resonating chamber, to
amplify and enhance the sound quality
• Oral, nasal, and sinus cavities also contribute to vocal resonance
• Good enunciation depends on the shaping of sound into
recognizable consonants and vowels by muscles in the pharynx,
tongue, soft palate, and lips
HOMEOSTATIC IMBALANCE
• Laryngitis
– Inflammation of the vocal folds
– Vocal folds swell, interfering with their
vibrations
– Produces a change in the voice tone,
hoarseness, or in severe cases inability to speak
above a whisper
THE LARYNX
• The vocal folds and the medial space between
them are called the glottis
• Under certain conditions, the vocal folds act as a
sphincter that prevents air passage
– Valsalva’s maneuver is a behavior in which the glottis
closes to prevent exhalation and the abdominal muscles
contract, causing intra-abdominal pressure to rise
• Defecation: helps empty the rectum and can also stabilize the
body trunk when one lifts a heavy load
THE TRACHEA
• The trachea, or
windpipe, descends from
the larynx through the
neck into the
mediastinum, where it
terminates by dividing
into the two primary
bronchi at midthorax
• Cilia continually propel
debris-laden mucus
toward the pharynx
Cross-sectional view of the trachea, illustrating its relationship to the
esophagus and the position of the supporting cartilage rings
TRACHEA
• 16-20 C-shaped
cartilage rings:
– Prevents the trachea
from collapsing despite
the pressure changes in
breathing
HOMEOSTATIC IMBALANCE
• Smoking inhibits and ultimately destroys
cilia, after which coughing is the only
means of preventing mucus from
accumulating in the lungs
– For this reason, smokers with respiratory
congestion should avoid medications that
inhibit the cough reflex
HOMEOSTATIC IMBALANCE
• Tracheal obstruction is life threatening
• Heimlich maneuver, a procedure in which
air in the victim’s lungs is used to “pop
out”, or expel, an obstructing piece of food
– Cracked ribs are a distinct possibility when
done incorrectly
BRONCHIAL TREE
BRONCHI and SUBDIVISIONS
• Site where conducting
zone structures give
way to respiratory
zone structures
THE BRONCHIAL TREE
• The conducting zone consists
of right and left primary
bronchi that enter each lung and
diverge into secondary bronchi
that serve each lobe of the lungs
• The right primary bronchus
is wider, shorter, and more
vertical than the left and is
the more common site for an
inhaled foreign object to
become lodged
• By the time incoming air
reaches the bronchi, it is warm,
cleansed of most impurities,
and saturated with water vapor
Conducting Zone Structures
• Once inside the lungs, each primary bronchus subdivides into
secondary (lobar) bronchi—three on the right and two on the left—
each supplying one lung lobe
• Secondary bronchi branch into several orders of smaller tertiary
bronchi, which ultimately branch into bronchioles
– Cilia are sparse, and mucus-producing cells are absent in the
bronchioles
• Thus, most airborne debris found at or below the level of the bronchioles
is removed by macrophages in the alveoli
• Amount of smooth muscle in the walls increases as the passageways
become smaller
– A complete layer of circular smooth muscle in the bronchioles and the
lack of supporting cartilage (which would hinder constriction) allows the
bronchioles to provide substantial resistance to air passage under certain
conditions
CONDUCTING RESPIRATORY
PASSAGES
THE BRONCHIAL TREE
RESPIRATORY TREE
• The respiratory zone begins
as the terminal bronchioles
feed into respiratory
bronchioles that terminate in
alveolar ducts within clusters
of alveolar sacs, which consist
of alveoli
• Approximately 300 million gasfilled alveoli in the lungs
account for most of the lung
volume and provide a
tremendous surface area for gas
exchange
RESPIRATORY ZONE
STRUCTURES
ALVEOLI
• Consists of a single layer
of squamous epithelium,
type-I cells, surrounded
by a basal lamina:
– The thinness of their walls
is hard to imagine, but a
sheet of tissue paper is
much thicker
• External surfaces of the
alveoli are densely
covered with pulmonary
capillaries
RESPIRATORY MEMBRANE
THE RESPIRATORY MEMBRANE
• The alveolar and
capillary walls and
their fused basal
laminae form the
respiratory
membrane, an airblood barrier that has
gas on one side and
blood flowing past on
the other
THE RESPIRATORY MEMBRANE
• Gas exchanges occur readily
by simple diffusion across the
respiratory membrane—O2
passes from the alveolus into
the blood, and CO2 leaves the
blood to enter the gas-filled
alveolus
• The type I cells also are the
primary source of angiotensin
converting enzyme, which plays
a role in blood pressure
regulation
RESPIRATORY MEMBRANE
RESPIRATORY MEMBRANE
• Interspersed among
the type-I cells are
cuboidal type-II cells
that secrete
surfactant:
– Reduces the surface
tension of the alveolar
fluid
RESPIRATORY MEMBRANE
• Alveoli have 3 other
significant features:
– They are surrounded by
elastic fibers
– They contain open alveolar
pores connecting adjacent
alveoli allowing air pressure
throughout the lung to be
equalized and provide
alternate air routes to any
alveoli whose bronchi have
collapsed
– They have remarkably
efficient alveolar
macrophages
RESPIRATORY MEMBRANE
THE LUNGS AND PLEURAE
GROSS ANATOMY
•
•
•
The lungs occupy all of the
thoracic cavity except for the
mediastinum; each lung is
suspended within its own pleural
cavity and connected to the
mediastinum by vascular and
bronchial attachments called the
lung root
Because the apex of the heart is
slightly to the left of the median
plane, the two lungs differ
slightly in shape and size
The left lung is smaller than the
right, and the cardiac notch—a
concavity in its medial aspect—is
molded to and accommodates the
heart
THORACIC CAVITY
THE LUNGS AND PLEURAE
GROSS ANATOMY
• The left lung is
subdivided into upper
and lower lobes by
the oblique fissure
• The right lung is
partitioned into upper,
middle, and lower
lobes by then oblique
and horizontal
fissures
THE LUNGS AND PLEURAE
GROSS ANATOMY
• Each lobe contains a
number of pyramidshaped
bronchopulmonary
segments (9-10)
separated from one
another by connective
tissue septa
BRONCHIAL TREE
LOBULES
• Smallest subdivisions of
the lung
• Appear at the lung surface
as hexagons
• Each is served by a large
bronchiole and its
branches
• In most city dwellers and
in smokers, the
connective tissue that
separates the individual
lobules is blackened with
carbon
THORACIC CAVITY
THE LUNGS AND PLEURAE
GROSS ANATOMY
• Each lobe contains a number of
bronchopulmonary segments, each served
by its own artery, vein, and tertiary
bronchus
LUNGS
GROSS ANATOMY
• Lung tissue consists largely of air spaces,
with the balance of lung tissue, its
stroma, comprised mostly of elastic
connective tissue
• Soft, spongy, elastic organs that together
weigh just over 1 Kg (2.5 pounds)
Blood Supply and Innervation of the Lungs
• There are two
circulations that
serve the lungs:
– Pulmonary
circulation
– Bronchial
circulation
TRANSVERSE SECTION OF
THORAX
Blood Supply and Innervation of the Lungs
• The pulmonary
network:
– Carries systemic venous
blood (pulmonary arteries)
to the lungs for
oxygenation
– Freshly oxygenated blood
is conveyed from the
respiratory zones of the
lungs to the heart by
pulmonary veins
– Large-volume, low pressure
Blood Supply and Innervation of the Lungs
• The bronchial arteries provide systemic blood to the
lung tissue:
– Arise form the aorta
– Run along the branching bronchi, supplying all lung tissues except
the alveoli (these are supplied by the pulmonary circulation)
– Small-volume, high pressure
• Although some systemic venous blood is drained from the
lungs by the tiny bronchial veins, there are multiple
anastomoses between the two circulations, and most
venous blood returns to the heart via the pulmonary veins
Blood Supply and Innervation of the Lungs
• The lungs are innervated by parasympathetic
and sympathetic motor fibers, and visceral
sensory fibers
• These nerve fibers enter each lung through the
pulmonary plexus on the lung root and run along
the bronchial tubes and blood vessels in the lungs
• Parasympathetic fibers constrict the air tubes
• Sympathetic fibers dilate the airways
PLEURAE
• Thin, double-layered serosa
• Parietal pleura covers the
thoracic wall, superior face of
the diaphragm, and continues
around the heart between the
lungs, forming the lateral walls
of the mediastinal enclosure and
snugly encloses the lung root
• Visceral pleura covers the
external lung surface,
following its contours and
fissures
PLEURAE
PLEURAE
• Produces pleural fluid, which fills the
slitlike pleural cavity between the parietal
and visceral pleurae
• Lubricating secretion allows the lungs to
glide easily over the thorax wall during our
breathing movements
HOMEOSTATIC IMBALANCE
• Pleurisy: inflammation of the pleurae
– Often results from pneumonia
– Less pleural fluid
• Pleural surfaces become dry and rough, resulting in friction
and stabbing pain with each breath
– Conversely, excessive fluid might be produced
• Exerts pressure on the lungs
• Hinders breathing movements, but is much less painful than
the dry rubbing type
• Pleural effusion:
– Blood fluid accumulation
MECHANICS OF BREATHING
• Breathing (pulmonary ventilation)
consists of two phases:
– Inspiration: period when air flows into the
lungs
– Expiration: period when gases exit the lungs
Pressure Relationship in the
Thoracic Cavity
• Respiratory pressures are always described relative to
atmospheric pressure (Patm), which is the pressure exerted by the
air (gases) surrounding the body
– At sea level: 760mm Hg (pressure exerted by a column of
mercury 760mm high)
• Can also be expressed in atmosphere units: 760mm Hg = 1
atm
– A negative respiratory pressure, such as -4mm, indicates
that the pressure in that area is lower than atmospheric
pressure
» 760-4= 756mm Hg
– A positive respiratory pressure is higher than atmospheric
pressure
– Zero respiratory pressure is equal to atmospheric pressure
Intrapulmonary Pressure (P pul)
• Is the pressure in the
alveoli, which rises
and falls during
respiration, but always
eventually equalizes
with atmospheric
pressure
Intrapleural Pressure (P ip)
• Is the pressure in the pleural cavity
– It also rises and falls during respiration, but is always
about 4 mm Hg less than intrapulmonary pressure
• The pressure in the pleural cavity, the
intrapleural pressure (Pip), also fluctuates with
breathing phases
• It is always about 4 mm Hg less than Ppul
• Hence, Pip is negative relative to both the
intrapulmonary and atmospheric pressures
Intrapleural Pressure (P ip)
• How is this negative pressure established and
maintained?
– There are opposing forces acting
– Forces act to pull the lungs (visceral pleura) away from the thorax
wall (parietal pleura) and cause lung collapse:
• The lungs’ natural tendency to recoil
– Always assumes the smallest size possible
• The surface tension of the alveolar fluid
– Constantly acts to draw the alveoli to their smallest possible
dimension
– These lung-collapsing forces are opposed by the natural
elasticity of the chest wall, a force that tends to pull thorax
outward and to enlarge the lungs
Intrapleural Pressure (P ip)
• WHO WINS????
– Neither in a healthy person, because of the strong
adhesive force (attraction between unlike molecules)
between the parietal and visceral pleura
• Pleural fluid secures the pleurae together in the same way a
drop of water holds two glass slides together
• The pleurae slide from side to side easily, but they remain
closely apposed, and separating them requires extreme force
• Net result of the dynamic interplay between these forces is a
negative Pip
Intrapleural Pressure (P ip)
• The importance of negative pressure in the
intrapleural space and the tight coupling of the
lungs to the thorax wall cannot be
overemphasized
– Any condition that equalizes Pip with the
intrapulmonary (or atmospheric) pressure causes
immediate lung collapse
– It is the transpulmonary pressure—the difference
between the intrapulmonary and intrapleural
pressures ( Ppul – Pip ) –that keeps the air spaces of
the lungs open (keeps them from collapsing)
INTRAPULMONARY and INTRAPLEURAL
PRESSURE RELATIONSHIPS
HOMEOSTATIC IMBALANCE
• Atelectasis: lung collapse
– Commonly occurs when air enters the pleural cavity through a
chest wound, but it may result from a rupture of the visceral pleura,
which allows air to enter the pleural cavity from the respiratory
tract
– Common sequel to pneumonia
• Pneumothorax: presence of air in the intrapleural space
– Reversed by closing the “hole” and drawing air out of the
intrapleural space with chest tubes, which allow the lung to
reinflate and resume its normal function
• Because the lungs are in separate cavities, one lung can
collapse without interfering with the function of the
other
Pulmonary Ventilation: Inspiration and Expiration
• Pulmonary ventilation is a mechanical process causing
gas to flow into and out of the lungs according to
volume changes in the thoracic cavity
• Volume changes lead to pressure changes—pressure
changes lead to the flow of gases to equalize the pressure
• Boyle’s law states that at a constant temperature,
the pressure of a gas varies inversely with its
volume: P1V1 = P2V2
– Where P is the pressure of the gas in millimeters of
mercury, V is its volume in cubic millimeters, and
subscripts 1 and 2 represent the initial and resulting
conditions respectively
INSPIRATION
• Gases always fill their container
• During quiet inspiration, the diaphragm and
intercostals contract, resulting in an increase in
thoracic volume, which causes intrapulmonary pressure
to drop below atmospheric pressure, and air flows into
the lungs
• Ppul drops about 1mm Hg relative to Patm
– Anytime the intrapulmonary pressure is less than the atmospheric
pressure (Ppul < Patm, air rushes into the lungs along the pressure
gradient
– Inspiration ends when Ppul = Patm
– During the same period Pip declines to about -6 mm Hg relative to
Patm
Changes in thoracic cavity during
Inspiration and Expiration
INSPIRATION
• During forced inspiration, accessory
muscles of the neck and thorax contract,
increasing thoracic volume beyond the
increase in volume during quiet inspiration
EXPIRATION
• Quiet expiration is a passive process that relies mostly
on elastic recoil of the lungs as the thoracic muscles
relax
– As the inspiratory muscles relax and resume their resting length,
the rib cage descends and the lungs recoil
• Thus, both the thoracic and intrapulmonary volume decreases
compressing the alveoli
• Ppul rises to about 1 mm Hg above atmospheric pressure
• Ppul > Patm, the pressure gradient forces gases to flow out of the lungs
• Forced expiration is an active process relying on
contraction of abdominal muscles to increase intraabdominal pressure and depress the ribcage
Changes in thoracic cavity during
Inspiration and Expiration
Changes in Intrapulmonary and Intrapleural Pressures during Inspiration
and Expiration
Notice that normal atmospheric pressure (760mmHg) is given a value of 0
on the scale
Physical Factors Influencing
Pulmonary Ventilation
• Lungs are stretched during inspiration and
recoil passively during expiration
• Inspiratory muscles consume energy to enlarge the
thorax
• Energy is also used to overcome various factors
that hinder air passage and pulmonary
ventilation:
– Airway resistance
– Alveolar surface tension forces
– Lung compliance (elasticity)
Airway Resistance
• Major nonelastic source of resistance to gas flow is
friction, or drag, encountered by air in the airways
• Gas flow is reduced as airway resistance increases
• The relationship between gas flow (F), pressure (P),
and resistance (R) is given by the following equation:
– F = ∆P/R
• The amount of gas flowing into and out of the alveoli is
directly proportional to ∆P, the difference in pressure, or
the pressure gradient, between the external atmosphere and
the alveoli
Airway Resistance
• Gas flow changes inversely with resistance
– Gas flow decreases as resistance due to friction
increases:
• As with the cardiovascular system, resistance in the respiratory
tree is determined mostly by the diameters of the conducting
tubes
• However, as a rule, airway resistance is insignificant for
two reasons:
– 1. Airway diameters in the first part of the conducting zone are
huge
– 2. Gas flow stops at the terminal bronchioles ( where small
airway diameters might start to be a problem) and diffusion takes
over as the main force driving gas movement
Airway Resistance
• Airway resistance
peaks in the mediumsized bronchi and then
declines sharply as the
total cross-sectional
area of the airway
increases rapidly
Resistance of the various segments
of the Respiratory Passageways
HOMEOSTATIC IMBALANCE
• Inhaled irritants and inflammatory chemicals
(histamine, bronchoconstrictors) activate a reflex of the
parasympathetic division of the nervous system causing
vigorous constriction of the bronchioles and
dramatically reduce air passageways
– Example: acute asthma attack can stop pulmonary ventilation
almost completely, regardless of the pressure gradient
• Conversely, epinephrine released during sympathetic
nervous system activation or administered as a drug dilates
bronchioles and reduces airway resistance
• Local accumulations of mucus, infectious material, or solid
tumors in the passageways are important sources of airway
resistance in those with respiratory disease
Alveolar Surface Tension Forces
• Alveolar surface tension due to water in the alveoli acts to draw
the walls of the alveoli together, presenting a force that must be
overcome in order to expand the lungs
• At any gas-liquid boundary, the molecules of the liquid are more
strongly attracted to each other than to the gas molecules
– This unequal attraction produces a state of tension at the liquid
surface, called surface tension
• Draws the liquid molecules closer together and reduces their
contact with the dissimilar gas molecules
• Resists any force that tends to increase the surface area of the
liquid
Alveolar Surface Tension Forces
•
•
Water is composed of highly polar molecules and has a very high surface
tension
Because water is the major component of the liquid film that coats the
alveolar walls, it is always acting to reduce the alveoli to their smallest
possible size
– If the film was pure water, the alveoli would collapse between breaths
– But the alveolar film contains surfactants, a detergent-like complex of
lipids and proteins produced by the type II alveolar cells
• Surfactant decreases the cohesiveness of water molecules, much the
way a laundry detergent reduces the attraction of water for water,
allowing water to interact with and pass through fabric
• As a result, the surface tension of alveolar fluid is reduced, and
less energy is needed to overcome those forces to expand the lungs
and discourage alveolar collapse
HOMEOSTATIC IMBALANCE
• Infant respiratory Distress Syndrome (IRDS)
– Condition peculiar to premature babies
– Since inadequate pulmonary surfactant is produced
until the last two months of fetal development, babies
born prematurely often are unable to keep their alveoli
inflated between breaths
• Treated by:
– Positive-pressure respirators that force air into the alveoli ,
keeping them open between breaths
» Bronchopulmonary dysplasia: damage to delicate lungs by
use of respiators
– Spraying natural or synthetic surfactant into the newborn’s
respiratory passageways also helps
Lung Compliance
• Healthy lungs are unbelievably stretchy, and
this distensibility (swell, expand) is referred to
as lung compliance
• Lung compliance (CL) is a measure of the change
in lung volume (∆VL) that occurs with a given
change in the transpulmonary pressure [∆(PpulPip)]
– CL = ∆VL / ∆(Ppul – Pip)
Lung Compliance
• Lung compliance is determined by:
– Distensibility of lung tissue and the surrounding
thoracic cage
– Alveolar surface tension
• Because lung (and thoracic) distensibility is
generally high and alveolar surface tension is kept
low by surfactant, the lungs of healthy people tend
to have high compliance, which favors efficient
ventilation
Lung Compliance
• Compliance is diminished by factors with any
of the following effects:
– 1.Reduce the natural resilience of the lungs as fibrosis
• E.g., development of nonelastic scar tissue in tuberculosis
– 2.Block the smaller respiratory passages
• E.g., with fluid (pneumonia) or mucus (chronic bronchitis)
– 3.Reduce the production of surfactant
– 4.Decrease the flexibility of the thoracic cage or its
ability to expand
• The lower the lung compliance, the more
energy is needed just to breathe
HOMEOSTATIC IMBALANCE
• Deformities of the thorax, ossification of the
costal cartilages (common during old age),
and paralysis of the intercostal muscles all
reduce lung compliance by hindering
thoracic expansion
Respiratory Volumes and Pulmonary
Function Tests
• Respiratory volumes and specific
combinations of volume, called
respiratory capabilities, are used to gain
information about a person’s respiratory
status
• The four respiratory volumes of interest
are: tidal, inspiratory, expiratory reserve,
and residual
Respiratory Volumes and Capacity
• The values recorded represent normal values for a
healthy 20 year old male weighing about 70 Kg
(155 pounds)
Respiratory Volumes and Capacities
Tidal Volume
• Tidal volume is the amount of air that
moves in and out of the lungs with each
breath during normal
• About 500 ml of air (quiet breathing)
Inspiratory Reserve Volume (IRV)
• The inspiratory reserve volume is the
amount of air that can be forcibly
inspired beyond the tidal volume
• 2100 to 3200 ml of air
Expiratory Reserve Volume (ERV)
• The expiratory reserve volume is the
amount of air that can be evacuated from
the lungs after tidal expiration
• Normally 1,000 to 1,200 ml of air
Residual Volume (RV)
• Residual volume is the amount of air that
remains in the lungs after maximal
forced expiration
• About 1,200 ml of air remains in the lungs
• Helps to keep the alveoli open and to
prevent lung collapse
Respiratory Volumes and Capacity
Respiratory Capacities
• Include inspiratory capacity, functional
residual capacity, vital capacity, and total
lung capacity
• Respiratory capacities always consist of two
or more lung volumes
Respiratory Volumes and Capacities
Inspiratory Capacity (IC)
• Inspiratory capacity is the sum of tidal volume
and inspiratory reserve volume, and represents
the total amount of air that can be inspired after a
tidal expiration
• Sum of TV and IRV
Functional Residual Capacity (FRC)
• Functional residual capacity is the
combined residual volume and expiratory
reserve volume, and represents the amount
of air that remains in the lungs after a tidal
expiration
• Sum of RV and ERV
Vital Capacity (VC)
• Vital capacity is the sum of tidal volume,
inspiratory reserve and expiratory reserve
volumes, and is the total amount of
exchangeable air
• Sum of TV,IRV, and ERV
• In healthy young males approximately 4800
ml
Total Lung Capacity (TLC)
• Total lung capacity is the sum of all lung
volumes
• Normally around 6000 ml in males
Respiratory Volumes and Capacities
Dead Space
• Some of the inspired air fills the conducting respiratory
passageways and never contributes to gas exchange in the alveoli
• The volume of these conducting zone conduits, which make up the
anatomical dead space, typically amounts to about 150 ml
– 1 ml per pound of body weight
• In a healthy young adult of 150 pounds
– TV is 500 ml, only 350 ml is involved in alveolar ventilation
– The remaining 150 ml of tidal breath is in the anatomical dead
space
– The anatomical dead space is the volume of the conducting
zone conduits, which is a volume that never contributes to gas
exchange in the lungs
Respiratory Volumes and Pulmonary
Function Tests
• The measuring device, a spirometer, is a simple
instrument utilizing a hollow bell inverted over water
– The bell moves as the patient breathes into a connecting
mouthpiece, and a graphic recording is made on a rotating drum
– Cannot provide a specific diagnosis, it can distinguish between
obstructive pulmonary disease involving increased airway
resistance (chronic bronchitis) and restrictive disorders involving
a reduction in total lung capacity resulting from structural or
functional changes in the lungs (tuberculosis, fibrosis due to
exposure to certain environmental agents such as asbestos)
– Pulmonary function tests evaluate losses in respiratory function
using a spirometer to distinguish between obstructive and
restrictive pulmonary disorders
Respiratory Volumes and Pulmonary
Function Tests
•
More information can be obtained about a patient’s ventilation status by
assessing the rate at which gas moves into and out of the lungs
– Minute Ventilation: total amount of gas that flows into or out of the
respiratory tract in 1 minute
• Normal quiet breathing: 6L/min (500 ml per breath multiplied by 12
breaths per minute)
• Vigorous exercise: 200L/min
– Alveolar Ventilation Rate (AVR): better index of effective ventilation
• Takes into account the volume of air wasted in the dead space and
measures the flow of fresh gases in and out of the alveoli during a
particular time interval
– AVR (ml/min) = frequency (breaths/min) X (TV – dead space)
(ml/breath)
– In a healthy person:
» AVR = 12 breaths/minute X (500-150 ml/breath)
» AVR = 4200 ml/min
Nonrespiratory Air Movements
• Cause movement of air into or out of the
lungs, but are not related to breathing:
(coughing, sneezing, crying, laughing,
hiccups, and yawning)
• Most result from reflex activity, but some
are produced voluntarily
BASIC PROPERTIES OF GASES
DALTON’S LAW
• Dalton’s law of partial pressure states that the total
pressure exerted by a mixture of gases is the sum of the
pressures exerted independently by each gas in the
mixture
– PN2 is 78.6% X 760 mm Hg = 597 mm Hg
– PO2 is 20.9 % X 760 mm Hg = 159 mm Hg
• At higher altitudes, pressure decreases (each partial
pressure decreases proportionally to the values at sea level)
• Below sea level (under water), pressure increases
– Pressure increases 1 atm (760 mm Hg) for each 33 feet of descent
• Thus at 99 feet below sea level, the total pressure is 4 atm ( 3040 mm
Hg) (partial pressure for each gas is also quadrupled)
BASIC PROPERTIES OF GASES
HENRY’S LAW
• Henry’s law states that when a mixture of gases is in
contact with a liquid, each gas will dissolve in the liquid
in proportion to its partial pressure
• How much of a gas will dissolve in a liquid at any given
partial pressure also depends on the solubility of the gas in
the liquid and on the temperature of the liquid
– Carbon dioxide is most soluble
– Oxygen is only 1/20 as soluble as CO2
– Nitrogen is practically insoluble
• The effect of increasing the liquid’s temperature is to
decrease gas solubility
BASIC PROPERTIES OF GASES
HENRY’S LAW
• Hyperbaric oxygen chambers: provide
clinical applications of Henry’s Law
– Chambers contain O2 at pressures higher than 1
atm and are used to force greater-than-normal
amounts of O2 into the blood of patients
suffering from carbon monoxide poisoning,
circulatory shock, gas gangrene, tetanus
poisoning from anaerobic bacteria, or
asphyxiation (lack of O2 or excess CO2)
HOMEOSTATIC IMBALANCE
• Although breathing O2 gas at 2 atm is not a
problem for short periods, oxygen toxicity
develops rapidly when PO2 is greater than
2.5-3 atm
• Excessively high O2 concentrations
generate huge amounts of harmful free
radicals, resulting in profound CNS
disturbances, coma, and death
COMPOSITION OF ALVEOLAR GAS
• The gaseous makeup of the atmosphere is quite
different from that in the alveoli
– The atmosphere is almost entirely O2 and N2
– The alveoli contain more CO2 and water vapor and
much less O2
• The relative proportions of gases in the alveoli
reflect gas exchange occurring in the lungs,
humidification of air by conducting passages, and
mixing of alveolar gas that occurs with each
breath
External Respiration
Pulmonary Gas Exchange
• Three factors influencing the movement of
oxygen and carbon dioxide across the
respiratory membrane are:
– 1. Partial pressure gradients and gas solubilities
– 2.Matching of alveolar ventilation and pulmonary blood
perfusion
– 3.Structural characteristics of the respiratory membrane
• External respiration involves O2 uptake and CO2 unloading
from hemoglobin in red blood cells
External Respiration
Partial Pressure Gradients and Gas Solubilities
• Because the PO2 of venous
blood in the pulmonary
arteries is only 40 mm Hg,
as opposed to a PO2 of
approximately 104 mm
Hg in the alveoli, a steep
oxygen partial pressure
gradient exists, and O2
diffuses rapidly from the
alveoli into the pulmonary
capillary blood
Partial Pressure Gradients Promoting
Gas Movements In The Body
External Respiration
Partial Pressure Gradients and Gas Solubilities
• Equilibrium—that is, a
PO2 of 104 mm Hg on both
sides of the respiratory
membrane—usually
occurs in 0.25 second,
which is about 1/3 the
time a red blood cell is in
a pulmonary capillary
• Blood can flow through
the pulmonary capillaries
3x as quickly and still be
adequately oxygenated
Oxygenation of Blood in the
Pulmonary Capillaries
External Respiration
Partial Pressure Gradients and Gas Solubilities
• Carbon dioxide moves in the opposite direction
along a much gentler partial pressure gradient of
about 5 mm Hg ( 45 mm Hg to 40 mm Hg) until
equilibrium occurs at 40 mm Hg
• Carbon dioxide is then expelled gradually from
the alveoli during expiration
• Even though the O2 pressure gradient for oxygen
diffusion is much steeper than the CO2 gradient,
equal amounts of these gases are exchanged
because CO2 is 20 times more soluble in plasma
and alveolar fluid than O2
External Respiration
Partial Pressure Gradients and Gas Solubilities
• The difference in the degree of the partial pressure
gradients of oxygen and carbon dioxide reflects he
fact that carbon dioxide is much more soluble than
oxygen in the blood
• A steep partial pressure gradient exists between
blood in the pulmonary arteries and alveoli, and O2
diffuses rapidly from the alveoli into the blood, but
carbon dioxide moves in the opposite direction
along a partial pressure gradient that is much less
steep
External Respiration
Ventilation-Perfusion Coupling
• For gas exchange to be
efficient, there must be a close
match, or coupling, between
ventilation (the amount of gas
reaching the alveoli) and
perfusion (the blood flow in
pulmonary capillaries
• Ventilation-perfusion coupling
ensures a close match between
the amount of gas reaching the
alveoli and the blood flow in
the pulmonary capillaries
External Respiration
Ventilation-Perfusion Coupling
• In alveoli where
ventilation is inadequate,
PO2 is low:
– The terminal arterioles
constrict, and blood is
redirected to respiratory
areas where PO2 is high and
oxygen pickup may be
more efficient
– In alveoli where ventilation
is maximal, pulmonary
arterioles dilate, increasing
blood flow into the
associated pulmonary
capillaries
VENTILATION-PERFUSION
COUPLING
External Respiration
Ventilation-Perfusion Coupling
•
While changes in alveolar PO2
affect the diameter of pulmonary
blood vessels (arterioles), changes
in alveolar PCO2 cause changes in
the diameters of the bronchioles
– Passageways servicing areas where
alveolar CO2 levels are high dilate,
allowing CO2 to be eliminated
from the body more rapidly, while
those serving areas where PCO2 is
low constrict
•
As a result of modifications made
by these two systems, alveolar
ventilation and pulmonary
perfusion are synchronized
VENTILATION-PERFUSION
COUPLING
Partial Pressure Gradients Promoting
Gas Movements In The Body
External Respiration
Thickness and Surface Area of the Respiratory Membrane
• The respiratory membrane is normally very
thin (0.5 to 1 um), and presents a huge
surface area for efficient gas exchange
HOMEOSTATIC IMBALANCE
• If the lungs become waterlogged and
edematous (excess amount of fluid) as in
pneumonia:
– The exchange membrane thickens dramatically
– Under such conditions, even the total time (0.75
s) that red blood cells are in transit through the
pulmonary capillaries may not be enough for
adequate gas exchange, and body tissues begin
to suffer from oxygen deprivation
HOMEOSTATIC IMBALANCE
• In certain pulmonary diseases, the
alveolar surface area actually functioning
in gas exchange is drastically reduced:
– Emphysema
• The walls of adjacent alveoli break through and the
alveolar chambers become larger with a loss in
elasticity
– Tumors, mucus, or inflammatory material
blocks gas flow into the alveoli
Internal Respiration: Capillary Gas
Exchange in the Body Tissues
– The diffusion gradients for oxygen and carbon
dioxide are reversed from those for external
respiration and pulmonary gas exchange
– The partial pressure of oxygen in the tissues is always
lower than the blood, so oxygen diffuses readily into
the tissues, while a similar but less dramatic gradient
exists in the reverse direction for carbon dioxide
– Gas exchange that occur between the blood and the
alveoli and between the blood and the tissue cells take
place by simple diffusion driven by the partial pressure
gradients of O2 and CO2 that exist on the opposite sides
of the exchange membranes
Partial Pressure Gradients Promoting
Gas Movements In The Body
TRANSPORT OF RESPIRATORY GASES
BY BLOOD
• Oxygen Transport:
– Since molecular oxygen is poorly soluble in the blood,
only 1.5 % is dissolved in plasma, while the remaining
98.5% must be carried on hemoglobin
• Up to four oxygen molecules can be reversibly bound to a
molecule of hemoglobin– one oxygen on each iron
• The affinity of hemoglobin for oxygen changes with each
successive oxygen that is bound or released, making oxygen
loading and unloading very efficient
GAS EXCHANGES AT THE BODY
TISSUES
GAS EXCHANGES IN THE
LUNGS
Association of Oxygen and
Hemoglobin
• The hemoglobin-oxygen combination,
called oxyhemoglobin, is written HbO2
• Hemoglobin that has released oxygen is
called reduced hemoglobin, or
deoxyhemoglobin (HHb)
»
Lungs
• HHb + O2 ↔ HbO2 + H+
» Tissues
Influence of PO2 on Hemoglobin Saturation
• The relationship between the
degree of hemoglobin
saturation and the PO2 of
blood is not linear
• This S-shaped curve has a steep
slope between 10 and 50 mm
Hg PO2 and then flattens out
between 70 and 100 mm Hg
• Remember, PO2 measurement
indicates only the amount of O2
dissolved in plasma, not the
amount bound to hemoglobin
OXYGEN-HEMOGLOBIN
DISSOCIATION CURVE
Influence of PO2 on Hemoglobin Saturation
• A hemoglobin saturation curve reveals important facts:
– Hb is almost completely saturated at a PO2 of 70 mm Hg, and
further increases in PO2 produce only small increases in O2 binding
– The adaptive value of this is that O2 loading and delivery to the
tissues can still be adequate when the PO2 of inspired air is well
below its usual levels, a situation common at higher altitudes and
in those with cardiopulmonary disease
– Most O2 unloading occurs on the steep portion of the curve, where
the partial pressure changes very little, only 20-25% of bound
oxygen is unloaded during one systemic circuit, and substantial
amounts of O2 are still available in venous blood (venous reserve)
• Thus, if O2 drops to very low in the tissues, as might occur during
vigorous exercise, much more O2 can dissociate from hemoglobin to
be used by the tissue cells without any increase in respiratory rate or
cardiac output
OXYGEN-HEMOGLOBIN
DISSOCIATION CURVE
Influence of Other Factors on
Hemoglobin Saturation
• The rate at which Hb reversibly binds or releases O2 is
regulated by PO2 , temperature, blood pH, PCO2, and
blood concentration of an organic chemical called BPG
(2,3-bisphosphoglycerate)
– BPG is produced by red blood cells (RBCs) as they
break down glucose by the anaerobic process called
glycolysis
– These factors interact to ensure adequate deliveries of
O2 to tissue cells
– All these factors influence Hb saturation by modifying
its three-dimensional structure, and thereby its affinity
for O2
Influence of Other Factors on
Hemoglobin Saturation
• Increase in temperature,
PCO2, H+ content of the
blood, or BPG levels in
blood decreases Hb’s
affinity for O2 and causes
the oxygen-hemoglobin
dissociation curve to shift
to the right
• This enhances oxygen
unloading from the blood
Effects of Temperature, PCO2, and Blood pH on the
Oxygen-Hemoglobin Dissociation Curve
Influence of Other Factors on
Hemoglobin Saturation
• A decrease in in
temperature, PCO2, H+
content of the blood,
or BPG levels in blood
increases
hemoglobin’s affinity
for oxygen and shifts
the dissociation curve
to the left
Effects of Temperature, PCO2, and Blood pH on the
Oxygen-Hemoglobin Dissociation Curve
The Hemoglobin-Nitric Oxide Partnership in
Gas Exchange
• Nitric oxide (NO), secreted by lung and vascular endothelial cells,
is a well-known vasodilator that plays an important role in blood
pressure regulation
• Hemoglobin, on the other hand, has a formidable reputation as a
vasoconstrictor because it is a NO scavenger—its iron-containing
heme group destroys NO
– Yet, there is a PARADOX: local vessels dilate where gases are
being unloaded and loaded:
• It appears that as O2 is unloaded so is NO, which dilates the
local vessels and aid oxygen delivery
• Then as deoxygenated hemoglobin picks up CO2, it also picks
up any circulating NO in the area and carries these gases to the
lungs where they are unloaded
Effects of Temperature, PCO2, and Blood pH on the
Oxygen-Hemoglobin Dissociation Curve
HOMEOSTATIC IMBALANCE
• Hypoxia: any conditions in which there is inadequate
oxygen delivery to body tissues
• Anemic hypoxia: reflects poor O2 delivery resulting from
too few RBCs or from RBCs that contain abnormal or too
little Hb
• Ischemic (stagnant) hypoxia: results when blood
circulation is impaired or blocked
– Congestive heart (pumping efficiency depressed) circulation may
cause body-wide ischemic hypoxia
– Emboli (mass of undissolved matter transmitted in the blood to a
location) or thrombi (blood clot that obstructs a vessel) block
oxygen delivery only to tissues distal to the obstruction
HOMEOSTATIC IMBALANCE
• Histotoxic hypoxia: occurs when body cells are
unable to use O2 even though adequate amounts
are delivered
– Consequence of metabolic poisons, such as cyanide
• Hypoxemic hypoxia: indicated by reduced
arterial PO2
– Possible causes include imbalances in the ventilationperfusion coupling mechanism
– Pulmonary diseases that impair ventilation
– Breathing air that containing scant (barely sufficient)
amounts of Oxygen
HOMEOSTATIC IMBALANCE
• Carbon Monoxide Poisoning: unique type
of hypoxemic hypoxia:
– Leading cause of death from fire
– CO is an odorless, colorless gas that competes
vigorously with O2 for heme binding sites
• Affinity for CO is more than 200 times greater than
its affinity for oxygen
Carbon Dioxide Transport
• Blood transports CO2 from
the tissue cells to the lungs in
three forms:
• 1. Dissolve in plasma (7-10%):
dissolved in plasma
• 2. Chemically bound to
hemoglobin (20%): carried as
carbaminohemoglobin
– CO2 + Hb ↔ HBCO2
(carbaminohemoglobin)
• Does not require an enzyme
• CO2 binds directly to the
amino acids of globin (not to
the heme)
– Does not compete with the
oxyhemoglobin (or NO)
transport mechanism
GAS EXCHANGES AT THE BODY
TISSUES
GAS EXCHANGES IN THE
LUNGS
Carbon Dioxide Transport
• 3. As bicarbonate ion in
plasma (70%):
– Most carbon dioxide molecules
entering the plasma quickly
enter RBCs, where most of the
reactions that prepare carbon
dioxide for transport as
bicarbonate ions (HCO3-) in
plasma occur
– When CO2 diffuses into the
RBCs, it combines with water,
forming carbonic acid (H2CO3)
– H2CO3 is unstable and quickly
dissociates into hydrogen ions
and bicarbonate ions:
• CO2 + H2O ↔ H2CO3 ↔
H+ + HCO3-
GAS EXCHANGES AT THE BODY
TISSUES
Carbon Dioxide Transport
– Although this reaction also occurs in plasma,
it is thousands of times faster in RBCs
because they (and not plasma) contain
carbonic anhydrase, an enzyme that
reversibly catalyzes the conversion of carbon
dioxide and water to carbonic acid
• Hydrogen ions released during the reaction bind to
Hb, triggering the Bohr ( alters the structure of
hemoglobin and release of oxygen) effect; thus, O2
release is enhanced by CO2 loading (as HCO3-)
Carbon Dioxide Transport
• Once generated, HCO3- diffuses quickly
from the RBCs into the plasma, where it
is carried to the lungs:
– To counterbalance this chloride ions (Cl-) move
from the plasma into the RBCs
• This ion exchange is called the chloride shift
Carbon Dioxide Transport
•
•
In the lungs the process is
reversed
As blood moves through the
pulmonary capillaries
– PCO2 declines from 45 mm Hg to
40 mm Hg
• For this to occur, CO2 must first
be freed from its bicarbonate state
–
HCO3- renters the RBCs (Clmoves into the plasma) and
binds with H+ to form carbonic
acid, which is then split by
carbonic anhydrase to release
CO2 and water
– This CO2, along with that released
from hemoglobin and from
solution in plasma, then diffuses
along its partial pressure gradient
from the blood into the alveoli
GAS EXCHANGES IN THE
LUNGS
GAS EXCHANGES AT THE BODY
TISSUES
HALDANE EFFECT
•
•
•
The lower the PO2, and the lower
the extent of Hb saturation with
oxygen, the more CO2 that can be
carried in the blood
Reflects the greater ability of
reduced hemoglobin to form
carbaminohemoglobin and to
buffer H+ by combination with it
As CO2 enters the systemic
bloodstream, it causes more oxygen
to dissociate from Hb (Bohr effect),
which allows more CO2 to combine
with Hb and more HCO3- to be
formed (Haldane effect)
HALDANE EFFECT
The lower the degree of Hb saturation, the greater the amount
of CO2 that can be transported by the blood
HALDANE EFFECT
• In the pulmonary
circulation, the situation is
reversed—uptake of O2
facilitates release of CO2
• As Hb becomes saturated
with O2, the H+ released
combines with HCO3-,
helping to unload CO2
from the pulmonary blood
• The Haldane effect
encourages CO2 exchange
in both the tissues and
lungs
GAS EXCHANGES IN THE
LUNGS
Influence of CO2 on Blood pH
• The H+ released during carbonic acid dissociation is
buffered by Hb or other proteins within the RBCs or in
plasma
• The HCO3- generated in the red blood cells diffuses into
the plasma, where it acts as the alkaline reserve part of
the blood’s carbonic acid-bicarbonate buffer system
– This system is very important in resisting shifts in blood pH
– Example:
• If hydrogen ion concentration in blood begins to rise, excess H+ is
removed by combing with HCO3- to form carbonic acid ( a weak acid
that dissociates very little at either physiological or acidic pH)
• If H+ concentration drops below desirable levels in blood, carbonic
acid dissociates, releasing hydrogen ions and lowering the pH again
Influence of CO2 on Blood pH
• Changes in respiratory rate or depth can produce
dramatic changes in blood pH by altering the amount
of carbonic acid in the blood
– Slow, shallow breathing allows CO2 to accumulate in the blood
• Carbonic acid levels increase and blood pH drops
– Rapid, deep breathing quickly flushes CO2 out of the blood,
reducing carbonic acid levels and increasing blood pH
• Respiratory ventilation can provide a fast-acting
system to adjust blood pH (and PCO2) when it is
disturbed by metabolic factors
• Respiratory adjustments play a major role in the acidbase balance of the blood
Control Of Respiration
Neural Mechanisms and Generation of Breathing
Rhythm
• Medullary Respiratory
Centers
– The medulla oblongata
contains:
• The dorsal respiratory group,
or inspiratory center
– With neurons that act as the
pacesetting group
– Neurons mostly involved in
inspiration
• And the ventral respiratory
group
– Which functions mostly
during forced breathing
– Contains a more even mix
of neurons involved in
inspiration and expiration
NEURAL PATHWAYS
Dorsal Respiratory Group (DRG)
• Appears to be the pacesetting respiratory center
• Inspiratory center
• When its neurons fire, impulses travel along the phrenic and intercostal
nerves to excite the diaphragm and external intercostal muscles
– The thorax expands and air rushes into the lungs
– The DRG becomes dormant
• Expiration occurs passively as the inspiration muscles relax and the lungs
recoil
• This cyclic on/off activity of the inspiratory neurons repeats
continuously and produces a respiratory rate of 12-15 breaths per
minute, with inspiratory phases lasting for about 2 seconds followed by
expiratory phases lasting about 3 seconds
NEURAL PATHWAYS
Ventral Respiratory Group (VRG)
• A network of neurons that extends in the ventral
brain stem from the spinal cord to the ponsmedulla junction
• Contains a more even mix of neurons involved in
inspiration and expiration
• Which functions mostly during forced breathing
(especially forced expiration) when more
strenuous breathing movements are needed
Pons Respiratory Centers
• Appears to smooth out the
transitions from inspiration to
expiration, and vice versa
• The pontine respiratory group
(PRG) continuously transmits
inhibitory impulses to the
inspiratory center of the
medulla
• The pons modifies the breathing
rhythm and prevents
overinflation of the lungs
through an inhibitory action on
the medullary respiration
centers
NEURAL PATHWAYS
Genesis of the Respiratory Rhythm
• Origin of the Normal Respiratory
Rhythm ????????????
• It appears to be the result of reciprocal
inhibition of interconnected neuronal
networks in the medulla
– On the part of the different respiratory centers
• The medullary centers maintain the normal
rhythm of breathing
Factors Influencing Breathing Rate and Depth
• The respiratory centers
in the medulla and
pons are sensitive to
both excitatory and
inhibitory stimuli
Pulmonary Irritant Reflexes
• Lungs contain receptors that respond to
an enormous variety of irritants
• Accumulated mucus, dust, noxious
fumes:
– Reflex constriction when present in the
bronchioles
– Cough when present in the trachea
– Sneeze when present in the nasal cavity
The Inflation Reflex
Hering-Breuer Reflex
•
•
•
•
The visceral pleurae and
conducting passages in the lungs
contain numerous stretch receptors
(baroreceptors) that are vigorously
stimulated when the lungs are
inflated
These receptors signal the
medullary respiratory centers,
sending inhibitory impulses that
end inspiration and allow
expiration to occur
As the lungs recoil, the stretch
receptors become quiet, and
inspiration is initiated once again
Is a protective response (prevents
excessive stretching of the lungs)
rather than a normal regulatory
mechanism
Influence of Higher Brain Centers
Hypothalamic Controls
• Acting through the limbic system, strong emotions, and
pain activate sympathetic centers in the hypothalamus,
that can modify respiratory rate and depth by sending
signals to the respiratory centers:
–
–
–
–
–
–
Touch something cold and gaped
Breath holding when we are angry
Increased respiratory rate when excited
Rise in body temperature increases respiratory rate
Drop in body temperature decreases respiratory rate
Dip in cold water causes cessation of breathing or gasping
Influence of Higher Brain Centers
Cortical Controls
• The cerebral cortex
can exert voluntary
control over
respiration by
bypassing the
medullary centers
and directly
stimulating the
respiratory muscles
Influence of Higher Brain Centers
Chemical Factors
• The most important are
changing levels of CO2,
O2, and H+ in arterial
blood
• Central chemoreceptors
located bilaterally in the
ventrolateral medulla and
peripheral chemoreceptors
found in the great vessels
of the neck respond to
these chemicals
Excitatory influences (+) increases the frequency
of impulses sent to the muscles of respiration and
result in deeper, faster breathing
Inhibitory influences (-) decrease the frequency of
impulses to the muscles of respiration and result
in shallow, slower breathing
Impulses may be excitatory or inhibitory (+/-)
depending on which receptors or brain regions
are activated
Influence of Higher Brain Centers
Influence of PCO2
• Of all the chemicals
influencing
respiration, CO2 is
the most potent and
the most closely
controlled
Influence of Higher Brain Centers
Influence of PCO2
• CO2 diffuses easily from the blood into the
cerebrospinal fluid, where it is hydrated and forms
carbonic acid
– As the acid dissociates, H+ is liberated:
• This same reaction occurs when CO2 enters RBCs
• Unlike RBCs or plasma, cerebrospinal fluid contains no proteins that
can buffer the added H+
• Thus, as PCO2 levels rise, a condition referred to as hypercapnia
– Cerebrospinal fluid pH drops, exciting the central chemoreceptors
– Causes an increase in rate and depth of breathing
» This breathing pattern is called hyperventilation which enhances
alveolar ventilation and quickly flushes CO2 out of the blood,
increasing blood pH
Influence of Higher Brain Centers
Influence of PCO2
• Notice that while rising
CO2 levels act as the
initial stimulus, it is
rising H+ levels that prod
the central
chemoreceptors into
activity
• In the final analysis,
control of breathing
during rest is aimed
primarily at regulating
the H+ concentration in
the brain
NEGATIVE FEEDBACK
MECHANISMS
HOMEOSTATIC IMBALANCE
• A person experiencing an anxiety attack may
hyperventilate involuntarily to the point where
he or she becomes dizzy or faints
• This happens because low CO2 levels in the blood
(hypocapnia) cause cerebral blood vessels to
constrict, reducing brain perfusion and producing
cerebral ischemia
• Such attacks may be averted by breathing into a
paper bag because then the air being inspired is
expired air, rich in carbon dioxide, which causes
carbon dioxide to be retained in the blood
HOMEOSTATIC IMBALANCE
Hypoventilation
• When PCO2 is abnormally low, respiration is
inhibited and becomes slow and shallow
HOMEOSTATIC IMBALANCE
Hyperventilation
• Sometimes swimmers voluntarily hyperventilate so that
they can hold their breath longer during swim meets
• This is incredibly dangerous for the following reasons:
– Blood O2 content rarely drops below 60% of normal during regular
breath-holding, because as PO2 drops, PCO2 rises enough to make
breathing unavoidable
– However, strenuous hyperventilation can lower PCO2 so much that
a lag period occurs before it rebounds enough to stimulate
respiration again
– This lag may allow oxygen levels to fall well below 50 mm Hg,
causing the swimmer to black out (and perhaps drown) before he
or she has the urge to breathe
Influence of PO2
• Cells sensitive (oxygen
sensors) to arterial O2
levels are found in the
peripheral
chemoreceptors of the
aortic arch and carotid
arteries
• Blood PO2 affects
breathing indirectly by
influencing
chemoreceptors sensitivity
to changes in PCO2
OXYGEN CHEMORECEPTORS
Influence of PO2
• Peripheral chemoreceptors monitor plasma
PO2 and stimulate an increase in ventilation
when PO2 drops below 60 mm Hg
HOMEOSTATIC IMBALANCE
• In people who retain CO2 because of pulmonary disease
(e.g., emphysema and chronic bronchitis), arterial PCO2 is
chronically elevated and, as a result, chemoreceptors
become unresponsive to this chemical stimulus
• In such cases, a declining PO2 acting on the oxygensensitive peripheral chemoreceptors provides the principal
respiratory stimulus, the hypoxic drive
• Thus, gas mixtures administered to such patients during
respiratory distress are only slightly enriched with O2
because inspiration of pure oxygen would stop their
breathing by removing their respiratory stimulus (low PO2
levels)
Influence of Arterial pH
• As arterial pH declines, the respiratory
system attempts to compensate by causing
an increase in rate and depth of breathing
– Attempt to compensate and raise the pH by
eliminating CO2 (and carbonic acid) from the
blood
– Mediated by the peripheral chemoreceptors
SUMMARY
• Rising CO2 levels are the most powerful
respiratory stimulant
– As CO2 is hydrated in cerebrospinal fluid,
liberated H+ acts directly on the central
chemoreceptors, causing a reflexive increase
in breathing rate and depth
– Low PCO2 levels depress respiration
SUMMARY
• Under normal conditions, blood PO2
affects breathing only indirectly by
influencing chemoreceptor sensitivity to
changes in PCO2
• Low PO2 augments PCO2 effects
• High PO2 levels diminish the effectiveness
of CO2 stimulation
SUMMARY
• When arterial PO2 falls below 60 mm Hg, it
becomes the major stimulus for respiration,
and ventilation is increased via reflexes
initiated by the peripheral chemoreceptors
• This may increase O2 loading into the blood,
but it also causes hypocapnia (low PCO2 blood
levels) and an increase in blood pH, both of
which inhibit respiration
SUMMARY
• Changes in arterial pH resulting from
CO2 retention or metabolic factors act
indirectly through the peripheral
chemoreceptors to promote changes in
ventilation, which in turn modify arterial
PCO2 and pH
• Arterial pH does not influence the central
chemoreceptors directly
RESPIRATORY ADJUSTMENTS
Adjustments During Exercise
• During vigorous exercise, deeper and more vigorous respirations,
called hyperpnea, ensure that tissue demands for oxygen are met
• The respiratory changes seen in hypernea match metabolic demands
and so do not lead to significant changes in blood O2 and CO2 levels
– By contrast, hyperventilation may provoke excessive ventilation, resulting
in low PCO2 and alkalosis
– The abrupt increase in ventilation that occurs as exercise begins reflects
interaction of three neural factors:
• 1. Psychic stimuli: our conscious anticipation of exercise
• 2. Simultaneous cortical motor stimulation of skeletal muscles and respiratory
centers
• 3. Excitatory impulses to the respiratory areas from proprioceptors in active
muscles, tendons, and joints
• The small but abrupt decrease in ventilation that occurs as exercise
ends reflects the shutting off of the neural control mechanisms
RESPIRATORY ADJUSTMENTS
Adjustments at High Altitude
• Acute mountain sickness (AMS) may result from a
rapid transition from sea level to altitudes above 8000
feet
– Air density and PO2 are lower
– Headache, shortness of breath, nausea, and dizziness
– In severe cases of AMS, lethal pulmonary and cerebral edema may
occur
• A long-term change from sea level to high altitudes
results in acclimatization of the body, including an
increase in ventilation rate, lower than normal
hemoglobin saturation, and increased production of
erythropoietin
SCUBA GEAR
• Self-contained underwater breathing apparatus
– Has freed divers to explore the ocean depths
• Heavy pressurized suits permits continual
equalization of the air pressure (produced by the
mixture of compressed air in the tank) with the
water pressure
– Air enters the lungs at a higher-than-normal pressure
– Descent is not usually a problem, unless below 100 feet
SCUBA GEAR
•
•
Nitrogen ordinarily has little effect on body functioning
– Hyperbaric (being exposed to gas pressure greater than atmospheric pressure)
conditions for an extended time force so much nitrogen into solution in the blood
that it provokes a narcotic effect called nitrogen narcosis
• Nitrogen is far more soluble in lipids than in water, so it tends to concentrate
in lipid-rich tissues such as the central nervous system, bone marrow, and fat
deposits
• Divers become dizzy, giddy, and appear to be intoxicated
• Most ascend to the surface gradually
– Dissolved nitrogen gas can be driven out of the tissues and eliminated by
the lungs without problems
• Ascent is too rapid, the PN2 decreases abruptly and the poorly soluble
nitrogen gas appears to “boil” from the tissue and out of solution in the
body
– Gas bubbles in the blood (lethal emboli): bends
Decompression sickness can also strike at high altitudes
– Unpressurized aircraft flying above 18,000 feet
DECOMPRESSION
HOMEOSTATIC IMBALANCES
OF
THE RESPIRATORY SYSTEM
• Chronic obstructive pulmonary diseases
(COPD):
– Seen in patients that have a history of
smoking
• Result in progressive dyspnea
– Difficult or labored breathing
• Coughing and frequent pulmonary infections
• Respiratory failure
– Accompanied by hypoxemia (low oxygen levels), CO2
retention, and respiratory acidosis
PATHOGENESIS OF COPD
HOMEOSTATIC IMBALANCES
OF
THE RESPIRATORY SYSTEM
• Obstructive emphysema is characterized by
permanently enlarged alveoli and deterioration of
alveolar walls
– Chronic inflammation leads to lung fibrosis, and invariably the
lungs lose their elasticity
• Airways collapse during expiration and obstruct the outflow of air
– Bronchioles open during inspiration but collapse during expiration
– Surprisingly gas exchange remains adequate until late in the disease
• Chronic bronchitis: inhaled irritants
– Results in excessive mucus production, as well as inflammation
and fibrosis of the lower respiratory mucosa
• Pulmonary infections are frequent because bacteria thrive in the
stagnant pools of mucus
PATHOGENESIS OF COPD
HOMEOSTATIC IMBALANCES
OF
THE RESPIRATORY SYSTEM
• Asthma is characterized by coughing, dyspnea
difficult or labored breathing), wheezing, and
chest tightness—alone or in combination
– Brought on by active inflammation of the airways
• Immune response under the control of TH2 cells (subset of
lymphocytes) that recruit eosinphils to the site
• Bronchoconstriction
• Common triggers: allergens
– Mites, cockroaches, cats, dogs, and fungi
– Marked by acute exacerbations (more violent)
followed by symptom-free periods
HOMEOSTATIC IMBALANCES
OF
THE RESPIRATORY SYSTEM
• Tuberculosis (TB) is an infectious disease caused by the
bacterium Mycobacterium tuberculosis and spread by
coughing and inhalation
– Mostly affects the lungs but can spread through the lymphatics to
affect other organs
– TB test depends on detecting anti-TB antibodies in the patient
• 1/3 of the world’s population is infected, but most people never
develop active TB because a massive inflammatory and immune
response usually contains the primary infection in fibrous, or
calcified, nodules (tubercles) in the lungs
– However, the bacteria survive in the nodules and when the person’s
immunity is low, they may break out and cause symptomatic TB,
involving fever, night sweats, weight loss, a racking cough, and spitting
up blood
HOMEOSTATIC IMBALANCES
OF
THE RESPIRATORY SYSTEM
• Lung Cancer:
– In both sexes, lung cancer is the most common type of malignancy, and is
strongly correlated with smoking
• 90% of lung cancer patients were smokers
– Because lung cancer is aggressive and metastasizes rapidly and widely,
most cases are not diagnosed until they are well advanced
– Squamous cell carcinoma arises in the epithelium of the bronchi, and
tends to form masses that hollow out and bleed
– Adencarcinoma originates in peripheral lung areas as nodules that develop
from bronchial glands and alveolar cells
– Small cell carcinoma contains lymphocyte-like cells that form clusters
within the mediastinum and rapidly metastasize
– Some small cell carcinomas cause problems beyond their effects on the
lungs because they become ectopic sites of hormone production
• Some secrete ACTH (leading to Cushing’s disease) or calcitonin
(hypocalcemia)
DEVELOPMENTAL ASPECTS
OF
THE RESPIRATORY SYSTEM
•
•
•
•
•
•
•
By the fourth week of development, the olfactory placodes are present and
give rise to olfactory pits that form the nasal cavity
The nasal cavity extends posteriorly to join the foregut, which gives rise to an
outpocketing that becomes the pharyngeal mucosa
By the eighth week of development, mesoderm forms the walls of the
respiratory passageways and stroma of the lungs
As a fetus, the lungs are filled with fluid, and vascular shunts are present that
divert blood away from the lungs; at birth, the fluid drains away, and rising
plasma PCO2 stimulates respiratory centers
Respiratory rate is highest in newborns, and gradually declines to adulthood;
in old age, respiratory rate increases again
As we age, the thoracic wall becomes more rigid, the lungs lose elasticity, and
the amount of oxygen we can use during aerobic respiration decreases
The number of mucus glands and blood flow in the nasal mucosa decline with
age, as does ciliary action of the mucosa, and macrophage
EMBRYONIC DEVELOPMENT
OF THE RESPIRATORY SYSTEM
HOMEOSTATIC IMBALANCE
•
Cystic fibrosis
–
Most common lethal genetic disease in the U.S.
•
–
–
–
–
Oversecretion of a viscous mucus that clogs the respiratory passages, providing a breeding
ground for airborne bacteria that predisposes the child to fatal respiratory infection that can be
treated only by a lung transplant
Impairs food digestion by clogging ducts that deliver pancreatic enzymes and bile to the small
intestine
Sweat glands produce an extremely salty perspiration
Conventional therapy:
•
•
•
–
1 out of 2400 births
Mucus-dissolving drugs
Clapping the chest to loosen thick mucus
Antibiotics to prevent infection
Cause: faulty gene that codes for a cystic fibrosis transmembrane conductance regulator protein
•
•
Lacks an essential amino acid
Enzyme remains stuck in the endoplasmic membrane and does not reach the plasma membrane to
perform its function
–
–
Consequently less Cl- is secreted and less water follows, resulting in the thick mucus typical of CF
Unable to reach the bacteria embedded in the mucus, immune cells begin to attack the lung
tissue, turning the air sacs into bloated cysts
DECOMPRESSION