The Respiratory System
Anatomy and Mechanics
Pulmonary volumes and capacities
(a capacity is the sum of two or more volumes)
The system can be divided into
conducting and respiratory
zones
The airway undergoes
about 16 generations of
branching between
trachea and respiratory
bronchioles. This is a
situation where each
generation of branches
has a lower flow
resistance than the
previous one.
The basic functional unit
of the lung is an acinus
(pl. acini) – a group of
alveoli served by a single
terminal bronchiole.
Each alveolus is a thinwalled sac that is densely
surrounded by pulmonary
capillaries.
The airway is under autonomic control
• The airway is lined with smooth muscle that is
dually innervated by the ANS:
– Psymp – constricts
– Symp – dilates
However, other chemical mediators may play
important roles, including prostaglandins and
NO
The thoracic cavity is a box whose volume changes over the respiratory
cycle
The thoracic cavity is a box
with one opening – the
thoracic outlet - through
which the trachea passes to
connect the lungs with the
atmosphere. The volume of
the box can be increased by
contraction of the external
intercostals, which lift the
ribs and swing them
outward, and by contraction
of the diaphragm, which
takes a domed shape when
relaxed and a flatter shape
when contracted.
Both chest wall and lung have elastic recoil
properties
Lung-Chest
Mechanics
The chest
wall elastic
recoil can
be thought
of as a stiff
spring that
wants to
pull the
chest out
Intrapleural fluid connects lung and chest wall –
the two opposing forces of chest elastic recoil and
lung elastic recoil cause intrapleural pressure to be
negative relative to atmospheric pressure. The
coupling ensures that the lungs do not collapse at
any stage of the respiratory cycle.
The lung elastic
recoil is a
relatively weak
spring that wants
to collapse the
lung on itself.
When respiratory muscles are
relaxed, the tendency of the
chest wall to spring out is
balanced by the tendency of the
lung to collapse. If the two
elastic components become
uncoupled, as when the chest
wall is breached, the lung
collapses and the chest wall
springs out.
Pulmonary surfactant
• The major source of lung elastic recoil is the surface
tension of the thin layer of water on the alveolar surface
• If the water were pure, there would be two bad
consequences
– Inflating the lung against the resistance of the surface tension
would require a lot of effort, and respiratory work would be much
greater
– Small alveoli would tend to merge into larger ones, reducing lung
surface area
These problems are prevented by pulmonary surfactant, a
phospholipid detergent secreted by type B alveolar cells.
How surfactant
preserves the frothlike structure of the
lung
Without surfactant, large alveoli
have smaller pressures than
smaller ones and tend to grow at
the expense of small ones
With surfactant, large alveoli
tend to become smaller and
smaller ones tend to become
larger
Lack of surfactant causes
respiratory distress syndromes
• Premature infants: ordinarily a rise in
levels of the adrenal cortical hormone
cortisol induces production of surfactant
before birth.
• In some adults with lung trauma from
smoke inhalation or toxic gas, surfactant
production is impaired
Pressure and volume changes over the respiratory cycle
Note that pressure changes at
the level of the alveoli are what
drive movement of air in
ventilation – alveolar pressure
is negative to atmospheric
during inspiration and positive
during expiration. In contrast,
intrapleural pressures are
always negative and simply
become more negative as the
chest is expanded during
inspiration.
Some thought questions
• What changes would you expect in the
intrapleural pressure values in the case of
each of the following:
– Increased ventilation during exercise
– An increase in airway resistance, as in
asthma
– A decrease in lung compliance (i.e. an
increase in stiffness), as in respiratory
distress syndrome or fibrotic lung disease?
Well, don’t say I never give anything away…
This is the answer to the first thought question, showing a
TV of 500 ml and one of 1000 ml
The next slide should help some with questions 2 and 3
Respiratory work can be divided into two
components: elastic work and flow resistance work
The alveolar pressure trace
reflects only the force needed
to move a tidal volume of air
– overcoming the flow
resistance of the airway
The intrapleural pressure trace
includes both the flow-resistive
component and an additional one
– the force needed to overcome
the lung’s elastic recoil.
1-second forced expiratory volume
Classically, FEV1.0 was used as a one measure of lung health
– currently, the maximum flow velocity a patient can achieve
during an expiration is used, because it is simpler to measure
and can be done by patients with an at-home device.
Another thought question or two…
• How would FEV1.0 (or peak flow velocity)
change with an increase in airway
resistance, as with asthma? How about
with an increase in lung compliance, as in
emphysema? Or a decrease in lung
compliance, as in fibrotic disease or
respiratory distress syndrome?
Alright, now I’m giving away the whole candy
store…
emphysema
asthma
Pulmonary edema
System ventilation, alveolar ventilation and
deadspace ventilation
• System: Vtotal =TV x RR
– about 5 L/min at rest
• Alveolar: Valv = (TV – DSV) x RR
What is dead space and why does it matter? This is the volume of the
airway that must be ventilated in order to bring air to the alveoli.
Anatomically, it corresponds to the entire conducting system.
At the end of an expiration, the last of the gas that leaves the alveoli
passes into the conducting system. This gas then is the first to enter the
alveoli in the next inspiration. Thus, for all practical purposes, this dead
space gas never left the alveoli and could not contribute to alveolar
ventilation during the next breath. Similarly, air from the atmosphere that
was drawn into the conducting system at the end of an inspiration simply is
returned to the atmosphere at the beginning of the next expiration without
ever reaching the alveoli.
Alveolar ventilation vs pulmonary volume
DS ventilation is about 25-30% of system ventilation at
rest. For a person whose respiratory rate is 12
breaths/min, dead space volume is 150 ml and tidal
volume is 500 ml, Valv is 4200 ml/min. This sounds like
a nice large number. However, for a single breath of 500
ml, with 350 ml of actual alveolar ventilation, the 350 ml
is added to a lung volume (the functional residual
volume) that is already 2300 ml. As a result of this, a
single breath has very little impact on the composition of
alveolar gas, and alveolar gas will always have a lower
O2 content and a higher CO2 content than atmospheric
air.
Ventilation overbalances perfusion
Alveolar ventilation
and perfusion are
regulated at the level
of single acini
Pulmonary arterioles respond to
changes in oxygen and carbon
dioxide exactly the opposite of
the way systemic ones do.
Perfusion overbalances ventilation
Bronchioles constrict in response
to decreased carbon dioxide and
increased oxygen - they dilate
when the opposite changes
occur. These responses tend to
optimize the ventilation/perfusion
ratio throughout the lung.