Phol 480: Pulmonary Physiology Section, Session 1: Pulmonary Mechanics

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Phol 480 Pulmonary Physiology Section, Session
1 Pulmonary Mechanics Instructor Jeff
Overholt e-mail jxo2_at_po.cwru.edu phone
8962 location E616 Med. School Text Berne and
Levy, Fourth Ed. Chapters 32 and 33 Other
resources Pulmonary Physiology by Michael G.
Levitzky
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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.
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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
bodys 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.
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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-T
rachea-Bronchi-Bronchioles A. Functions to 1.
Warm and humidify the air 2. Distribute air to
the lungs 3. Defense system (remove dust and
bacteria)
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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
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Respiratory Zone Alveolar duct and alveolar
sacs. A. SITE OF GAS EXCHANGE B. Has its 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
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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.
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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.
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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.
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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.
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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
pressure-pleural 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.
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Pressures (contd) 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
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Pressures (contd) Pneumothorax hole in the
thoracic cavity, PPL becomes 0, can no longer
generate (-) pressures in the alveoli.
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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.
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Compliance (contd) 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
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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.
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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
air-liquid 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)
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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.
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Resistance Some of the work of breathing goes
to overcoming airflow resistance -Resistance is a
meaningful term only during flow
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
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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.
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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.
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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.
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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.
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III. PULMONARY VOLUMES AND CAPACITIES (contd)
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
compliancedecrease VC. -restrictive diseases
(limited expansion) -large residual volume (COPD)
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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 5006000 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 124.2L
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
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Alveolar Ventilation (contd) 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 (VT-VD). The first part of gas
is gas remaining in the dead space after last
expiration.