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Phol 480: Pulmonary Physiology Section,
Session 1: Pulmonary Mechanics
Instructor: Jeff Overholt
e-mail: [email protected]
phone: 8962
location: E616 Med. School
Text: Berne and Levy, Fourth Ed. Chapters 32
and 33
Other resources: Pulmonary
Physiology by Michael G. Levitzky
The major purpose of breathing is to supply O2 and to
remove CO2 from cells
Four major functions to achieve this goal:
1. Pulmonary ventilation: movement of air into and out
of lungs
2. Diffusion of O2 and CO2 between the alveoli and the
blood
3. Transport of O2 and CO2 in the blood to and from
cells
4. Control of ventilation
Once the O2 is transferred to the cells it is utilized to
metabolize various food molecules involving a
series of enzymatic reactions. During this process
there is release of energy which is stored in the
form of ATP-This process is called cellular
respiration.
From the time of birth until our death we
breath continuously at a rate of 12-15
breaths/min. However, breathing can
change in response to alterations in
blood chemistry.
-Breathing and gas exchange can
increase 20-fold to meet the body’s
energy demands during periods of
need such as exercise.
In unicellular organisms movement of O2
and CO2 occur through simple
diffusion. In multicellular organisms,
because of long diffusion distances
between cells and the environment.
Specialized organs for gas exchange
developed. In air breathing animals
these are the Lungs.
I. BASIC ANATOMY:.
The lungs are composed of 2 treelike structures:
1. Vascular tree: consists of arteries and veins
connected by capillaries
2. Airway tree: consists of hollow branching tubes that
conduct air from the environment to site of gas
exchange to the blood.
Conducting Zone: (in descending order): Nose (conchae)Pharynx-Larynx-Trachea-Bronchi-Bronchioles:
A. Functions to:
1. Warm and humidify the air
2. Distribute air to the lungs
3. Defense system (remove dust and bacteria)
B. Supplied by separate circulatory system bronchial
circulation-part of the systemic circulation.
C. Trachea and bronchi lined with ciliated, mucous coated
epithelium that aid in clearing passageway. Cilia beat
toward the pharynx.
-Epithelium rests on smooth muscle (can constrict or
dilate independent of the lung) and is supported by
cartilage.
D. Bronchioles: Lack cartilage, simple cuboidal
epithelium, volume depends on lung volume.
-have sensory cells sensitive to stretch and irritants
**NO GAS EXCHANGE TAKES PLACE IN THE
CONDUCTING ZONE-DEAD SPACE
Respiratory Zone: Alveolar duct and alveolar sacs.
A. SITE OF GAS EXCHANGE
B. Has it’s own circulation: the pulmonary circulation
-in order to match ventilation, follows and branches
along with the pulmonary tree.
-pulmonary artery from right ventricle supplies
nutrients to the alveolar walls
-capillary surface area nearly as great as the
alveolar surface area
-can increase from 70 ml (normal) to 200 ml
(exercise) recruitment
-capillaries also cover several alveoli, increase
time of exposure of red blood cells to alveolar
gas
C. Terminal Respiratory Unit: functional
exchange unit of lungs
Greatly increases surface area: 60,000
terminal respiratory units, each with
5000 alveoli and 250 alveolar ducts.
II. VENTILATION:
Main purpose is to maintain an optimal concentration
of O2 and CO2 in the alveolar gas.
How do we move air into and out of the lungs.
1. The lungs are housed in an airtight cavity, the
thoracic cavity, that is separated from the abdomen
by a large dome-shaped muscle, the diaphragm.
Lungs conform to the thoracic cavity by contact of
fluid lined pleura:
visceral pleura: covers the lungs
parietal pleura: lines the thoracic cavity
2. The anterior portion of the thoracic cavity is
bounded by the ribs. The external and internal
intercostal muscles lie between the ribs. The ribs
are hinged on one side to the vertebral column and
on the other to the sternum.
A. Inspiration:
The primary inspiratory muscle is the diaphragm. The
diaphragm is a skeletal muscle and is innervated by the
phrenic nerve. The diaphragm contracts during every
inspiration.
-contraction of the diaphragm increases the vertical
diameter of the thoracic cavity.
Voluntary muscles
The external intercostals raise the rib cage and increase the
anterior-posterior diameter of the thoracic cavity.
Accessory muscles
Active during forced breathing. These include the scalene
muscles of the neck. The sternocleidomastoids insert on
the top of the sternum. These muscles elevate the upper
rib cage during heavy breathing such as during exercise.
B. Expiration:
During normal tidal breathing at the end of inspiration
the diaphragm relaxes, and expiration is a passive
process. The natural recoil tendency of the lungs
and chest wall cause deflation of the lungs.
-elastic fibers
-surface tension
During forced expiration other expiratory muscles
become active
-internal intercostals oppose the external intercostals
and pull the rib cage down.
-abdominal muscles force the contents of the
abdominal cavity up against the diaphragm.
Especially important in coughing, vomiting, etc.
C. Pressures:
Airflow is due to changes in pressure in the thoracic
cavity that are transmitted to the alveoli.
Three important pressures associated with breathing and
airflow:
1. Pleural pressure (PPL): pressure in the pleural fluid
between the lung and chest wall.
2. Alveolar pressure (PA): pressure inside the alveoli.
3. Transmural pressure (PTM): the pressure difference
across the airway or across the lung wall.
-Transpulmonary pressure: alveolar pressurepleural pressure. Keeps the lungs from collapsing.
Is always positive during normal breathing.
-Transairway pressure: airway pressure-pleural
pressure. Transairway pressure is important in
keeping the airways open during expiration.
Pressures (cont’d)
Inspiration:
PPL is negative during quiet breathing and becomes
more negative during inspiration. This causes PA to
drop with respect to atmospheric pressure (very
little pressure needed, -1 mmHg)
Expiration:
PPL becomes less negative and PA becomes slightly
positive (+1 mmHg)
During heavy breathing PA can go from -80 to 100
mmHg
Pressures (cont’d)
Pneumothorax: hole in the thoracic cavity, PPL
becomes 0, can no longer generate (-)
pressures in the alveoli.
D. Compliance:
Compliance: the ease with which the lungs can be
distended.
-how well the lung inflates and deflates with a change in
transpulmonary pressure is a function of the elastic
properties of the lung.
Lung elastance: inverse of compliance, a measure of
the ability of the lungs to resist stretch.
Compliance (cont’d)
Pressure-volume relations: elastic properties of the
lungs can be determined by measuring changes in
lung volume that occur with changes in pressure.
Compliance=V/P: volume increase in lungs for each
unit increase in pressure
normal ~0.13L/cm (lungs alone are more
compliant than this, but part of energy must go
to expand the thoracic cage).
Compliance can be measured in human lungs by
measuring the pleural pressure and the volume of
the lungs with a spirometer.
Compliance depends on a number of things:
-elastic properties of lungs
-surface forces inside the alveoli
Inflation curve is different than deflation curve
-The inflation curve requires a higher
transpulmonary pressure than the
deflation curve at any given volume.
-This is possible if surface tension is different
during inflation and deflation. Variable
surface tension is responsible for
hysteresis.
E. Surface tension:
Within water the forces on water molecules attract one
another, at the surface, the attraction is stronger
from molecules under the surface.
The surface of the alveoli are moist, creating an airliquid interface in the alveoli, very high surface
tension would make lungs very non-compliant.
Compare to saline filled lung (no air-water interface)
that is much more compliant.
Surfactant: a special lipoprotein mixture coating the
surface of alveoli.
-synthesized in alveolar type II cells
-main ingredient is dipalmitoyl phosphatidylcholine
(DPPC)
Functions of Surfactant:
1. Reduces muscular effort of breathing (makes lungs
more compliant).
2. Reduces elastic recoil of the lungs at low volume
(prevents alveoli from collapsing)
3. Maintains the equality of size of alveoli during
inflation/deflation
-as alveoli become smaller decreases surface
tension more, makes smaller alveoli easier to
inflate. As alveoli become larger increases surface
tension, harder to inflate.
4. Responsible for difference in inflation vs deflation
curve.
-during deflation, surfactant molecules are
squeezed together lowering the surface tension.
Resistance:
Some of the work of breathing goes to
overcoming airflow resistance
-Resistance is a meaningful term only during
flow
Resistance 
PressureDifference (cmH 2O)
Flow (liters/sec)
1. Resistance is inversely proportional to the 4th
power of the radius, i.e. increase diameter
decreases the resistance. The main factor that
affects resistance is the radius.
2. Most of the airway resistance is in the upper
airways (large airways) because the flow
velocity is greater.
-large number of parallel pathways in the
small airways decreases the flow velocity
Resistances in parallel are added as
reciprocals:
1  1  1  ....
R tot R1 R 2
Forced Vital Capacity
The resistance to airflow can not be measured directly,
but must be calculated from the pressure gradient
and airflow during a breath.
One way of indirectly assessing resistance is to look at
the results of a forced expiration into a spirometer:
Forced Vital Capacity (FVC): Large breath from FRC
to TLC and breath out as hard and fast as
possible.
Dynamic compression:
1. Airways are not rigid, therefore they can be
compressed during forced expiration.
2. As pleural pressure rises above pressure in
airway opening, the airways are compressed
above the point where pleural pressure equals
airway pressure.
Dynamic compression therefore:
-limits expiratory airflow, any further increase in effort
(pressure) further closes airways.
-maximal expiratory flow is independent of effort and
becomes dependent on the recoil pressure of the
lung.
Note that during inspiration, pleural pressure is always
less than airway pressure, there is no dynamic
compression and inspiration is effort dependent.
III. PULMONARY VOLUMES AND CAPACITIES
Can be measured with a spirometer.(except RV)
A. Four different volumes
1. Tidal volume (TV): volume of air inspired and
expired with a normal breath (.500 ml).
2. Inspiratory Reserve Volume (IRV): extra volume of
air that can be inspired after a normal tidal
inspiration (.3000 ml).
3. Expiratory Reserve Volume (ERV): extra volume of
air that can be expired after a normal tidal
expiration (.1100 ml).
4. Residual Volume (RV): volume of air remaining
after a maximal expiratory effort (.1200 ml). *Can
not be removed from lungs.
III. PULMONARY VOLUMES AND CAPACITIES (cont’d)
B. Four different capacities relating the above volumes
1. Inspiratory Capacity (IC): TV + IRV
2. Functional Residual Capacity (FRC): ERV + RV
amount of air remaining in the lungs at the end of a
normal tidal expiration (lungs at rest). At FRC the
chest wall and lungs are recoiling in equal and
opposite directions.
3. Vital Capacity (VC): IRV + TV + ERV the maximal
amount of usable lung capacity.
4. Total Lung Capacity (TLC): All of the above, maximal
volume to which the lungs can be expanded.
* VC is one of most important of all clinical respiratory
measurements for assessing the progress of disease.
Decrease compliance=decrease VC.
-restrictive diseases (limited expansion)
-large residual volume (COPD)
IV. Alveolar Ventilation
The most important aspect of breathing is to maintain
an optimal concentration of O2 and CO2 in the
alveolar gas.
Minute respiratory volume: total amount of air moved
each minute
TV x Rate: 12 x 500=6000 ml (6L)
However, minute respiratory volume does not reflect
true alveolar ventilation. Part of the air goes to fill
the non-gas exchanging parts of the airways, the
anatomic dead space (150 ml).
Therefore alveolar ventilation=(TV-dead space)
x Rate; (500-150) x 12=4.2L
Physiological dead space: Due to non-functioning
alveoli. Is the ADS + non-functional alveoli.
-nearly equal in normal, but in disease PDS can be
10X greater than ADS
Alveolar Ventilation (cont’d)
O2 and CO2 in air and alveolar gas are different
and air is constantly moving in and out by
ventilation. This should lead to fluctuations in
alveolar gas causing fluctuations in blood O2
and CO2 levels (heart rate much faster than
respiratory rate).
1. The large FRC (.2.4 L) acts as a buffer to
maintain the O2 and CO2 in alveolar gas
constant.
2. Small volume of alveolar ventilation/breath (VTVD). The first part of gas is gas remaining in
the dead space after last expiration.