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PULMONARY SYSTEM
Dr. Nick Bhattacharya
STRUCTURES OF THE
PULMONARY SYSTEM
Composed of 2 lungs, their airways, the blood
vessels that serve them, and the chest wall or
thoracic cage.
3 lobes in the right lung and 2 lobes in the
left.
Each lobe is divided into segments and
lobules.
The MEDIASTINUM is the space between
the lungs which contains the heart, great
vessels, and esophagus.
CONDUCTING AIRWAYS
The conducting airways allow air into
and out of the gas exchange structures
of the lung.
The NASOPHARYNX, OROPHARYNX
are called the UPPER AIRWAY.
Lined with ciliated mucosa that
warms and humidifies inspired air and
removes foreign particles from it.
CONDUCTING AIRWAYS
The LARYNX connects the upper and lower
airways and consists of the endolarynx and its
surrounding triangular-shaped bony and
cartilaginous structures.
False vocal cords (supraglottis) and the true
vocal cords.
The slit-shaped space between the true cords
forms the glottis.
The laryngeal box is formed by the epiglottis,
thyroid, and cricoid cartilages and the
arytenoid, corniculate, cuneiform cartilages.
CONDUCTING AIRWAYS
The TRACHEA connects the larynx to
the BRONCHI.
Two main airways, or bronchi, branch
at the CARINA.
The right and left main bronchi enter
the lungs at the HILI, along with the
pulmonary blood and lymphatic vessels.
CONDUCTING AIRWAYS
Bronchial walls have three layers:
epithelial lining, smooth muscle layer,
and a connective tissue layer.
The epithelial lining of the bronchi
contains single-celled exocrine
glands, the mucus-secreting GOBLET
CELLS, and ciliated cells.
GAS-EXCHANGE AIRWAYS
The conducting airways terminate in gasexchange airways.
RESPIRATORY BRONCHIOLES,
ALVEOLAR DUCTS, and ALVEOLI.
Sometimes called the ACINUS.
The bronchioles from the sixteenth through
the twenty-third divisions are called the
RESPIRATORY BRONCHIOLES.
End in ALVEOLAR DUCTS, which lead to
ALVEOLAR SACS.
GAS-EXCHANGE AIRWAYS
The alveoli are the primary gasexchange units of the lung, where
oxygen enters the blood and carbon
dioxide is removed.
PORES OF KOHN allow some air to
pass through the septa from alveolus to
alveolus promoting collateral ventilation
and even distribution of air.
GAS-EXCHANGE AIRWAYS
Type I alveolar cells provide structure, and
type II alveolar cells secrete
SURFACTANT.
A lipoprotein that coats the inner
surface of the alveolus and facilitates its
expansion during inspiration.
ALVEOLAR MACROPHAGES ingest
foreign material and prepare it for removal
through the lymphatics.
CIRCULATION
The pulmonary circulation facilitates gas
exchange, delivers nutrients to lung
tissues, acts as a reservoir for the left
ventricle, and serves as a filtering
system that removes clots, air, and
other debris from the circulation.
Has a lower pressure and resistance
than the systemic circulation.
CIRCULATION
Usually one third of the pulmonary vessels are
perfused at any given time.
The arterioles divide at the terminal bronchioles
to form a network of pulmonary capillaries
around the acinus.
Capillary walls consist of an endothelial layer
and a thin basement membrane.
Very little separation exists between blood and
gas in the alveolus.
Gas exchange occurs across the
ALVEOLOCAPILLARY MEMBRANE.
CIRCULATION
Each pulmonary vein drains several
pulmonary capillaries.
The bronchial circulation is part of the
systemic circulation, and it supplies nutrients
to the conducting airways, large pulmonary
vessels, and membranes that surround the
lungs.
Does not participate in gas exchange but
warms and moistens inspired air and
provides airway nourishment.
CIRCULATION
Lung vasculature also includes
deep and superficial lymphatic
capillaries.
The lymphatic system plays an
important role in keeping the lung
free of fluid.
CHEST WALL AND PLEURA
The THORACIC CAVITY is contained by the chest
wall and encases the lungs.
The PLEURA adheres firmly to the lungs and then
folds over itself and attaches firmly to the chest wall.
The membrane covering the lungs is the
VISCERAL PLEURA.
That lining the thoracic cavity is the PARIETAL
PLEURA.
T he area between the two pleurae is the
PLEURAL SPACE, or PLEURAL CAVITY.
Pressure in the pleural space is usually negative.
VENTILATION
VENTILATION is the mechanical movement
of gas or air into and out of the lungs.
RESPIRATION is the exchange of oxygen
and CO2 during cellular metabolism.
GAS PRESSURE is a measurement of the
amount of collisions gas molecules have with
each other and the container in a confined
space.
The smaller the area or container, the
greater the pressure.
VENTILATION
Heat increases the speed of molecules, which
increases the number of collisions and therefore
the pressure.
BAROMETRIC PRESSURE (atmospheric
pressure) is the pressure exerted by gas molecules
at specific altitudes.
Sea level: 760 mm Hg.
Sum of the pressure exerted by each gas in the
air.
The portion of the total pressure exerted by any
individual gas is its PARTIAL PRESSURE.
VENTILATION
The amount of water vapor contained in a gas
mixture is determined by the temperature of the
gas and is unrelated to barometric pressure.
The partial pressure of water vapor must be
subtracted from the barometric pressure
before the partial pressure of other gases in
the mixture can be determined.
Gas that enters the lungs is humidified as it
passes through the upper airway.
(760-47) X 0.209 = 149 = pp O2 at sea level.
LUNG VOLUMES
TITAL VOLUME (Vt): Amount of gas inspired
and expired during normal breathing.
INSPIRED RESERVE VOLUME (IRV): Amount
of gas that can be inspired in addition to tidal
volume.
EXPIRATORY RESERVE VOLUME (ERV):
Amount of gas that can be expired after a
passive (relaxed) expiration.
RESIDUAL VOLUME (RV): Volume of gas that
cannot be expired and is always present in the
lung.
LUNG VOLUMES
TOTAL LUNG CAPACITY (TLC): Total gas
volume in the lung when it is maximally
inflated; sum of RV, ERV, Vt, and IRV.
VITAL CAPACITY (VC): Maximum amount
of gas that can be displaced (expired) from
the lung; sum of IRV, Vt, and ERV.
FUNCTIONAL RESIDUAL CAPACITY
(FRC): Amount of gas remaining in the lung
at the end of a passive expiration; sum of RV
and ERV; at this point the lungs are at rest.
LUNG VOLUMES
INSPIRATORY CAPACITY (IC): Amount of
gas that can be inspired after a passive
expiration (from FRC); includes Vt, and IRV.
DEAD-SPACE VENTILATION (D): Volume
of air that does not participate in gas
exchange.
ANATOMIC DEAD SPACE: Portion of tidal
volume that remains in conducting airways;
1/3 of each breath.
ALVEOLAR DEAD SPACE: Volume of gas in
unperfused alveoli.
LUNG VOLUMES
PHYSIOLOGIC DEAD SPACE: Sum of
normal anatomic dead space and alveolar
dead space.
ALVEOLAR VENTILATION (A): Portion of
tidal volume that reaches alveoli; during
expiration, part of this alveolar gas remains in
the conducting airways and moves back into
the alveoli with the next inspiration.
Lung capacities are always the sum of two or
more volumes.
CONTROL OF
VENTILATION
The RESPIRATORY CENTER in the brain
stem controls respiration by transmitting
impulses to the respiratory muscles, causing
them to contract and relax.
The basic rhythm of respiration is set by the
DRG (dorsal respiratory group) which
receives afferent input form PERIPHERAL
CHEMORECEPTORS in the carotid and
aortic bodies and from several different types
of receptors in the lungs.
CONTROL OF
VENTILATION
IRRITANT RECEPTORS are found in
the epithelium of all conducting
airways.
Sensitive to noxious aerosols, gases,
and particulate matter.
Initiates the cough reflex.
Causes bronchoconstriction and
increased ventilatory rate.
CONTROL OF VENTILATION
STRETCH RECEPTORS, located in the
smooth muscles of airways, and are sensitive
to increases in the size or volume of the
lungs.
Decrease ventilatory rate and volume when
stimulated.
J-RECEPTORS are located near the
capillaries in the alveolar septa.
Sensitive to increased pulmonary capillary
pressure, which stimulates them to
initiated rapid, shallow breathing.
CONTROL OF
VENTILATION
The parasympathetic and sympathetic
nervous systems control airway caliber.
Parasympathetic cause smooth muscle
to contract.
Sympathetic causes smooth muscle to
relax.
Parasympathetic division is the main
controller of airway caliber under normal
conditions.
CONTROL OF
VENTILATION
CHEMORECEPTORS monitor the pH, PaCO2, and
the PaO2 of arterial blood.
CENTRAL CHEMORECEPTORS monitor arterial
blood indirectly by sensing changes in the pH of
CSF.
PaCO2 regulates ventilation through its impact
on the pH (hydrogen ion content) of the CSF.
Sensitive to small changes in the pH and can
maintain a normal PaCO2 under many different
conditions.
Become insensitive if hypoventilation is longterm.
CONTROL OF
VENTILATION
PERIPHERAL CHEMORECEPTORS are
sensitive primarily to oxygen levels in arterial
blood (PaO2).
The PaO2 must drop well below normal (to
approximately 60 mm Hg) before they
have much influence on ventilation.
Become the major stimulus to ventilation
when the central chemoreceptors are
“reset” by chronic hypoventilation.
MECHANICS OF
BREATHING
The major muscles of inspiration are the
diaphragm and the external intercostal
muscles.
Inspiration at rest is usually assisted by the
diaphragm only.
The accessory muscles of inspiration are the
sternocleidomastoid and scalene muscles.
Assist inspiration when minute volume is
very high, or when the work of breathing is
increased because of disease.
MECHANICS OF
BREATHING
No major muscles of expiration because
normal, relaxed expiration is passive and
requires no muscular effort.
The accessory muscles of expiration, the
abdominal and internal intercostal
muscles, assist expiration when minute
volume is high, when expiration exceeds
FRC, or when airway obstruction is
present.
MECHANICS OF
BREATHING
SURFACE TENSION refers to the tendency
for liquid molecules that are exposed to air to
adhere to one another.
Alveolar ventilation is made possible by
SURFACTANT, which lowers surface tension
by coating the air-liquid interface in the
alveoli.
Normal alveoli are much easier to inflate at
low lung volumes than at high volumes.
Surfactant also keeps the alveoli free of fluid.
MECHANICS OF
BREATHING
The lung and chest wall have elastic properties
that permit expansion during inspiration and
return to resting volume during expiration.
The ELASTICITY of the chest wall is the result
of the configuration of its bones and
musculature.
ELASTIC RECOIL is the tendency of the lungs
to return to the resting state after inspiration.
Depends on an equilibrium between opposing
forces of recoil in the lungs and chest wall.
MECHANICS OF
BREATHING
COMPLIANCE is the measure of lung and
chest wall distensibility and is defined as
volume change per unit of pressure change.
Opposite of elasticity.
Determined by alveolar surface tension and
the elastic recoil of the lung and chest wall.
Increased in aging and emphysema,
decreased in ARDS, pneumonia, fibrosis.
MECHANICS OF
BREATHING
AIRWAY RESISTANCE is determined by
the length, radius, and cross-sectional area of
the airways and density, viscosity, and
velocity of the gas.
½ to 2/3 of total airway resistance occurs
in the nose.
Next highest resistance is in the
oropharynx and larynx.
Increases as the diameter of the airways
decreases.
MECHANICS OF
BREATHING
The work of breathing is determined by
the muscular effort required for
ventilation.
Increased considerably in diseases
that disrupt the equilibrium between
forces exerted by the lung and chest
wall.
GAS TRANSPORT
The delivery of oxygen to the cells of the body and
the removal of CO2.
Effective gas exchange depends on an approximately
even distribution of gas (ventilation) and blood
(perfusion) in all portions of the lungs.
The alveoli in the upper portions of the lungs
contain a greater residual volume of gas and are
larger and less numerous than those in the lower
portions.
During ventilation, most of the TV is distributed to
the bases where compliance is greater.
GAS TRANSPORT
The bases of the lungs are better perfused than
the apexes, thus, ventilation and perfusion are
greatest in the same lung portions, the lower
lobes, and depend on body position.
The lungs are divided into three zones on the
basis of relationships among all the factors
affecting pulmonary blood flow.
Zone I: alveolar pressure exceeds pulmonary
arterial and venous pressures. Capillary bed
collapses and normal blood flow ceases.
GAS TRANSPORT
Zone II: alveolar pressure is greater than venous
pressure but not arterial pressure. Blood flow
through but is impeded by alveolar pressure.
Zone III: both arterial and venous pressures are
greater than alveolar pressure and blood flow is
not affected. In the base of the lung.
Blood flow through the pulmonary capillary bed
increases in regular increments from the apex to the
base.
Perfusion exceeds ventilation in the bases and
ventilation exceeds perfusion in the apexes of the
lung.
GAS TRANSPORT
The relationship between ventilation and
perfusion is called the VENTILATIONPERFUSION RATIO (V/Q).
Normal is 0.8.
Oxygen is transported in the blood in two
forms: a small amount dissolves in plasma,
and the remainder binds to hemoglobin
molecules.
The alveolocapillary membrane has a large
total surface area.
GAS TRANSPORT
The PAO2 is much greater in alveolar gas than in
capillary blood which promotes rapid diffusion
down the concentration gradient from alveolus
into the capillary.
As the PaO2 increases, oxygen moves from the
plasma into the red blood cells and binds with
hemoglobin molecules.
O2 continues to bind with hemoglobin until
the hemoglobin binding sites are filled or
SATURATED.
GAS TRANSPORT
The total oxygen content of the blood depends
on the amount of oxygen chemically combined
with hemoglobin as well as that dissolved in the
blood.
Changes in hemoglobin concentration affect the
oxygen content of the blood.
Increased hemoglobin concentration is a
major compensatory mechanism in pulmonary
diseases that impair gas exchange.
GAS TRANSPORT
When hemoglobin molecules bind with
oxygen, OXYHEMOGLOBIN (HbO2) forms.
Oxyhemoglobin association or hemoglobin
saturation.
Hemoglobin desaturation occurs in the
tissues when oxygen is released.
Both processes are plotted on a graph:
OXYHEMOGLOBIN DISSOCIATION
CURVE.
GAS TRANSPORT
A shift to the right depicts hemoglobin’s
decreased affinity for oxygen.
A shift to the left depicts hemoglobin’s
increased affinity for oxygen.
The shift in the dissociation curve by
changes in CO2 and hydrogen ion
concentrations is called the BOHR
EFFECT.
GAS TRANSPORT
CO2 is carried in the blood in 3 ways:
Dissolved in plasma (PCO2)
As bicarbonate
As carbamino compounds.
Approximately 60% of the CO2 in venous blood
and 90% in arterial blood are carried in the form
of bicarbonate.
CO2 is 20 times more soluble than O2 and
diffuses quickly from the tissue cells into the
blood.
GAS TRANSPORT
Reduced hemoglobin (hemoglobin
that is dissociated from oxygen)
can carry more CO2 than
hemoglobin that is saturated with
O2.
HALDANE EFFECT
PULMONARY
CIRCULATION
The most important cause of pulmonary
artery constriction is low alveolar PO2
(PAO2).
Chronic alveolar hypoxia can result in
permanent pulmonary artery hypertension,
which eventually leads to right heart failure
(cor pulmonale).
Acidemia also causes pulmonary artery
constriction.