Pulmonary 3: Lung Mechanics B

Question 1

What causes air to flow?

Answer 1

pressure gradient

Question 2

What two things determine air flow at a given pressure gradient?

Answer 2

1. pattern of gas flow

2. resistance to air flow by airways

Question 3

Describe three main patterns of gas flow. What determines which pattern will be?

Describe how dense and viscous gases influence flow.

Answer 3

flow through slow rate-laminar, particles of gas moving parallel to sides of tube, pressure at upstream end of tube must be greater than downstream end or no flow (fully developed laminar flow, flow rate in center higher than elsewhere. velocity profile that turns out to be parabola and flow in center is twice mean flow rate. spike of flow going down center of the tube) flow proportional to pressure difference.

if increase flow rate then flow can become transitional, seen where tube divides to 2 daughter branches. laminar flow upper part, then flow separation partially at junction of where tube divides and is called transitional flow

increase flow rate even more then movement of gas becomes random, get turbulence, occurs at high flow rates. flatter velocity profile. flow proportional to pressure difference.

whether flow turbulent or laminar depends on Reynolds number. R= 2rvD/viscosity. flow likely to be turbulent if Reynolds exceeds 2000. if high density gas more likely to get turbulent flow, if very viscous gas likely to get laminar flow.

Question 4

What determines flow rate? Give equation.

How is resistance related to radius?

What happens if you cut the size of a tube in half? When is this important clinically?

Answer 4

F= (P1-P2)pi r^2 divided by 8viscosityL.

R= 8Lviscosity/pi r^4
inversely proportional to r^4
directly proportional to airway length and viscosity

if half tube… resistance increases 16 fold. (important in asthma) Resistance to breathing increases tremendously

Question 5

At what Reynolds number are turbulences likely to occur?

Answer 5

at Re > 2000

Question 6

Draw a graph of airway generation against total cross sectional area. Label conducting zone and respiratory zone and terminal bronchioles. Show how flow changes…

Describe the rate air is inhaled in trachea and early airways. Describe velocity and diameter and thus the type of airflow. How does airflow change in the higher airway generations? How does it change as it continues toward the respiratory bronchioles? What is gas flow like there?

Answer 6

Slide 6.

Air is inhaled at a rate of about 1L/s. In the trachea and the early airway generations (1-5), average velocity is very high and diameter is large (Re> 2000); airflow is turbulent

Airflow becomes laminar in the higher airway generations and slows continuously until the respiratory bronchioles are reached. Here, gas transport occurs only via diffusion.

(at level of terminal bronchioles around 50,000 terminal bronchioles in lung… airways = to 2^n (where n is airway generation) each airway divides into 2 daughter airways. important is that there is very large number of very small airways)

Question 7

Graph airway resistance. Airway generation (0-20) against resistance (0 to .08) Label the conducting zone and the respiratory zone.

Where is highest resistance found on the graph? Why is it highest here?

Answer 7

Slide 7.

In general, airway resistance is proportional to 1/r^4 - so the smaller the radius the more the resistance… however, as airways get smaller they also multiply in number by bifurcation as the generations get larger in number. So resistance at any one generation of the airway system is really a parallel resistance.

The highest resistance is found at generation 4 within the medium sized bronchi of short length and frequent branching. Here the inspiratory airflow is highly non-laminar and turbulent which translates into higher than expected generational resistance.

very small airways down at bottom contribute v small amount of resistance.

Question 8

What is the difference between airways in parallel versus airways in series? Where are there airways in parallel?

Answer 8

Airways in parallel
1/Rtot =
1/R1+1/R2+1/R3

airways in parallel as airway generations get higher in number

Airways in series
Rtot=
Rlarge+Rmed+Rsmall

Question 9

Where are pollutants most likely to deposit? Why?

Answer 9

very small airways down at bottom contribute v small amount of resistance. has important implications, region where resistance is small in small airways is called silent zone- bc its difficult to pick up changes in resistance in this region of the lung, would like to do that bc many of changes in early disease occur in the small airways…

pollutants tend to deposit in the small airways bc they have slow diffusion and cant diffuse to terminal alveoli bc of their high mass. so they deposit in region of terminal and respiratory bronchioles…

Question 10

What is the “silent zone”?

Answer 10

intrinsic resistance of the very small resistance airways at higher generations- airways so small that that region constitutes silent zone and not able to measure pressure in it.

Question 11

Describe the resistances found in respiratory zone vs conducting zone. High/low?

Describe the 3 types of inspiratory air flows into the lung by generation number.

Answer 11

Measurable resistances are found in the conducting zone (Generations 1 to 15-16).
In the respiratory zone, where alveoli reside, the resistance is very low.

3 types of inspiratory airflow profiles as air flows into lung:

1. turbulent (generations 0-9)
2. laminar (generations 10-16)
3. diffusive (generations 17-23)

Question 12

How does diffusion affect O2 and CO2 movement in the respiratory zone?

Answer 12

Bc oxygen and CO2 move by diffusion in the respiratory zone, O2 diffuses continuously into and CO2 diffuses continuously out of the alveolocapillary blood independent of timing of the respiratory cycle (inspiration vs expiration vs pause)

Question 13

What does total airway resistance depend on?

How can you estimate total resistance?

Answer 13

summed resistances of each generation as well as resistances of nasal air passage ways

As resistance in the upper airways is 50 percent of the total airway resistance, Rtot can be estimated to be 1.6cm H2O/L/sec at FRC.
This resistance comes from summing the serial resistances in generations 1-16 which comes to 0.8 cm H2O/L/sec and then doubling this number to account for the resistance of the upper airways.

Question 14

Describe how airway resistance (AWR) changes as volume increases. Graph.
(Why this change?)

How do conductance/AWR change at low lung volumes? High lung volumes?

Why?

What about extra-alvelolar structures?

Answer 14

Slide 8.
Airway resistance (or airway conductance) is a function of lung volume. At low lung volumes when the entire lung and airways are shrunken down and much smaller, the total airway resistance is high (or conductance is low). At high lung volumes when the entire lung and airways are stretched out and much larger, the total airway resistance is low (or airway conductance is high).

AWR decreases as lung volume increases. Happens bc airways are tethered by alveoli and they are pulled open by radial traction of alveoli as lungs expand.

dependency of airway resistance on lung volume is bc of airway tethering. Negative intrapleural pressure is expressed only on the external surfaces of each lung lobe. The more negative the intrapleural pressure, the more the surface lung structures are stretched. But each lung unit (small airways to alveoli) and all connected (thethered) together through the lung parenchyma. That is, one outer alvelous pulls on its deeper neighbor who pulls on its deep neighbor, etc.

this is same w extra-alveolar blood vessels pulled open by radial traction of lung parenchyma- as expand the lung the tension in alveolar walls increases as lung expands and thats why resistance falls with increasing lung volume

Question 15

What is conductance? Graph a conductance line on this graph (slide 8).

Answer 15

conductance=1/R. inverse relationship with resistance and linear relationship with lung volume.

Slide 8.

Question 16

During inhalation from FRC to Vt above FRC, how does AWR change? How does this affect inhalation.

What does sympathetic activation lead to?
Vagal stimulation? Edema?

Answer 16

AWR decreases making it easier to inhale as the breath progresses. While sympathetic activation also leads to bronchodilation (=resistance decreases), vagal stimulation smooth muscle contraction and mucus or edema increase airway resistance?

Question 17

Why do patients with severe lung disease breath at high volumes?

Answer 17

See graph on slide 8.
Bc their resistance is less in those conditions.
COPD cannot breath at normal volume bc resistance would be too great… so tend to breath with high volume.

Question 18

How is bronchiole smooth muscle in airway walls controlled? What causes dilation? Give specific receptors.

What kind of a drug might you provide to someone with asthma?

Answer 18

bronchiole smooth muscle in airway walls is controlled by autonomic ANS. adrenergic stimulation dilates the airways. both beta 1 and beta 2 adrenergic receptors. beta 2 in airways, stimulate these can get increase in caliber of airways. relaxation. beta 2 receptor drugs v important in treatment of asthma. v important in treating airway disease

Question 19

How does cigarette smoke affect airways?

How does a diver breathe at high densities?

Answer 19

other factors- can be reflex constriction of airways.. if people inhale cigarette smoke- reflex constriction of airways that occurs

density of the gas.. in turbulent flow, density is one of factors (not in laminar flow tho) but in turbulent flow it is. diver that goes down deep into water, increase density of gas causes increase work of breathing. so use helium oxygen mixture which reduces work of breathing. helium oxygen mixture sometimes used in treatment of patients with lung disease.

Question 20

How can one test the mechanical properties of the pulmonary system?

Answer 20

spirometery.

Question 21

Graph forced vital capacity, forced expiratory volume in 1 second on spirogram graph and also time vs volume graph (label RV, TLC, FEF25-75, FEV1, FVC)

What is a normal ratio of FEV1/FVC?

What would a small FEV1 indicate?

What is FEF25-75?

What might an FEV1 look like in someone who had asthma?

Answer 21

Slide 9.

FEV1 is a measure of airway resistance. The smaller the FEV1, the higher the resistance to expiratory airflow (ex: asthma), trapping the air within the lungs.

FEF25-75 =average midmaximal expiratory flow

FEV1/FVC ratio is most important PFT measurement. It normalizes the expired volume in the first second to the total volume exhaled in the test. Clinically ratios greater than 75% are considered normal. Less than 75% are considered obstructive

Question 22

When you inspire as hard as you can, is intrapleural pressure high or low? Is flow rate high or low?

Expire at high volume?

What about at midvolume?

Answer 22

harder you inspire, the lower inter-pleural pressure, the higher the flow rate… harder you inspire, higher inspiratory flow rate… would expect that more you try to inhale the faster the air pulled into lung

also true of expiration at high lung volume, at high lung volume, higher you raise interplueral pressure, the higher the expiratory flow rate.

at midvolume- as you increase the inter-pleural pressure during exhalation, initially flow rate increases a bit then remains absolutely constant. no matter how much you try to exhale, contract expiratory muscles, you can’t raise the flow rate… more striking at low lung volume, over almost all expiration the flow rate is independent of inter-pleural pressure. so during much of expiration, expiratory flow is independent of effort.

Question 23

Draw a flow-volume loop for inspiration and expiration. Label TLC, RV, FEF25, FEF50, PEFR, and FEF75.

Describe what is happening when a patient undergoes this clinical test.

Answer 23

PEFR= peak expiratory flow rate
PIFR= peak inspiratory flow rate
FEF25/50/75= forced expiratory flow rates when 25/50/75 percent of VC has been exhaled

Subject slowly inhales up to TLC, holds his breath. With the nose clipped (to avoid loss of air through nasal air passages) the subject then forcefully exhales through a flow/volume sensor all the way down to RV. He again pauses to insure expiratory airflow is zero. Finally he forcefully inhales all the way up to TLC. again.

Flow is plotted on vertical axis. Expiratory flows are positive and inspiratory flows are negative. No flow is 0. Volume is plotted on horizontal axis with TLC to the L and RV to the R. The expiratory and inspiratory half cycles combine to form a continuous loop. Most positive flow is peak expiratory.

Question 24

Describe how the following factors change when lung volume increases:

• force of inspiratory muscles
• lung recoil pressure
• airway resistance

When does max. inspiratory flow occur?

Answer 24

force of inspiratory muscles decreases

lung recoil pressure increases

airway resistance decreases

max. inspiratory flow occurs half way between TLC and RV

Question 25

During expiration:

When does PEFR occur?
What happens to flow rate?

Answer 25

PEFR occurs early (first 20% of cycle)

Flow rate decreases toward RV= expiratory flow limitation.

Question 26

Draw a flow volume loop with maximal, moderate, and minimal effort. Label effort independent region. Label TLC and RV, TV and FRC, and volume exhaled.

Answer 26

Slide 12.

At high lung volumes (early expiration) airflow is effort dependent

At lower lung volumes (late expiration) airflow is limited and not dependent on breathing effort
= effort independent region
- flow is limited = expiratory flow limitation

Question 27

In the flow-volume loop, why does flow gradually decrease over the effort-independent region of expiration?

Answer 27

flow rate w dynamic compression of airways:
flow rate is caused by the difference in intrapleural and alveolar pressure. alveolar pressure exceeds intrapleural pressure and that pressure difference is responsible for flow, this gradually decreases and that’s why get flow decreasing down lung.
(important in patients with lung disease).

start inspiring… to inspire, inter-pleural pressure has to fall. alveolar pressure falls (if it doesn’t fall, no flow)

Question 28

What causes flow limitation?

Why is expiratory flow limited?

Answer 28

flow limitation is caused by the dynamic compression of airways when pressure outside airways is greater than pressure inside airways.

Flow limitation occurs when airways, which are intrinsically floppy, distensible tubes, become compressed. The airways become compressed when pressure outside the airway exceeds pressure inside airway.

Question 29

Describe pressure in alvelous, pleural pressure, and transpulmonary pressure at the start of exhalation before any gas flow occurs.

What holds the alveoli and airways open?

Answer 29

At start of exhalation, before any gas flow occurs, pressure inside alvelous (PA) is zero (no airflow), and pleural pressure (in example) is -30cmH2O.

So transpulmonary pressure is +30cm H2O. Bc there is no flow, the pressure inside the airways is zero and the pressure across the airways (transairway pressure) is +30 cmH2O (transairway = Pairway-Ppluera)
the positive transpulmonary and transairway pressure holds the alveoli and airways open.

Question 30

Describe how pleural pressures, alveolar pressure change in response to exhalation beginning. What causes the change in alveolar pressure?

Why does gas begin to flow? (What pressure differences cause this) What is the driving pressure for expiratory gas flow?

What happens to transmural pressure across the airways as gas flows out of alveoli? Provide 2 reasons why this happens.

Answer 30

When exhalation begins and expiratory muscles contract, pleural pressures rise to +60cm H2O (in this example).

Alveolar pressure also rises, in part because of the increase in pleural pressure (+60cm H2O) and in part because of the elastic recoil pressure of the lung at that volume (here is 30cmH2O).

Alveolar pressure is the sum of pleural pressure and elastic recoil pressure. This is the driving pressure for expiratory gas flow.

Bc alveolar pressure exceeds atmospheric pressure, gas begins to flow from alveolus to the mouth when the glottis opens. As gas flows out of the alveloi, the transmural pressure across the airways decreases.
Why?
Bc:
there is a resistive pressure drop caused by the frictional pressure loss associated with flow (expiratory airflow resistance)
also, as cross-sectional area of the airways decreases toward the trachea, gas velocity increases. This acceleration of gas flow further decreases the pressure.

Question 31

Why is expiratory gas flow decreasing?

What is equal pressure point? How will transairway pressure change? How does the relationship between airflow and total driving pressure change? Where does equal pressure point in normal lungs occur?
What happens at smaller lung volume to location of equal pressure point?
What will happen in lung disease?

Answer 31

p 440 book
This acceleration of gas flow further decreases the pressure.
So as air moves out of lung, the driving pressure for expiratory gas flow decreases.
The mechanical tethering that holds the airways open at high lung volumes diminishes as lung volume decreases.

equal pressure point- point between alveoli and the mouth at which pressure inside the airways equals the pressure that surrounds the airways.
(airflow becomes independent of total driving pressure)
(normal lung: equal pressure point in airways with cartilage)
(moves downward with smaller lung volume)
(altered in lung disease-obstruction…leading to premature airway closure (air trapping)

Airways toward the mouth become compressed because the pressure outside is greater than the pressure inside (dynamic airway compression). As a consequence, transairway pressure now becomes negative (ex: Paw-Ppl= 58-60=-2cmH2O just beyond the equal pressure point.

Question 32

When transairway pressure becomes negative right beyond the equal pressure point, no amount of effort will increase the flow further. Why?

Answer 32

Bc the higher pleural pressure tends to collapse the airway at the equal pressure point just as it also tends to increase the gradient for expiratory gas flow.

under these conditions airflow is independent of total driving pressure. Hence the expiratory flow is effort independent and flow limited

(it is also why the airway resistance is greater during exhalation than during inspiration)

Question 33

Where is the equal pressure point normally in lungs without disease?

Answer 33

equal pressure point occurs in airways that contain cartilage, and thus they resist collapse.

Equal pressure point is not static. As lung volume decreases and as elastic recoil pressure decreases, the equal pressure point moves closer to the alveoli.

Question 34

What happens to equal pressure point in individuals with lung disease?

Answer 34

Imagine an individual with airway obstruction secondary
to a combination of mucus accumulation and
airway inflammation. At the start of exhalation, the
driving pressure for expiratory gas flow is the same as
in a normal individual; that is, the driving pressure is
the sum of the elastic recoil pressure and pleural pressure.

As exhalation proceeds, however, the resistive
drop in pressure is greater than in the normal individual
because of the greater decrease in airway radius
secondary to the accumulation of mucus and the
inflammation. As a result, the equal pressure point now occurs in small airways that are devoid of cartilage.
These airways collapse. This collapse is known
as premature airway closure.

Premature airway
closure results in a less than maximal exhalation
that is known as air trapping and produces an increase
in lung volume. The increase in lung volume initially
helps offset the increase in airway resistance
caused by the accumulation of mucus and inflammation
because it results in an increase in airway
caliber and elastic recoil. As the disease progresses,
however, inflammation and accumulation of mucus
increase further, there is a greater increase in expiratory
resistance, and maximal expiratory flow rates
decrease.

Question 35

Graph FEV1 and FEV on a time/volume curve (measuring forced expiratory flow- spirogram). Show normal, obstructive lung disease (asthma, COPD), and restrictive lung disease (fibrosis)

Answer 35

Slide 15

FEV1 is reduced in
obstructive lung diseases,
such as Asthma, COPD.

FVC is reduced in
restrictive lung diseases,
such as fibrosis

Question 36

Describe 3 ways in which a patient with COPD tends to exaggerate the mechanism of dynamic compression.

Answer 36

if increase in resistance of the small airways near alveoli, will increase rate at which pressure is lost as we go up airway, as resistance increases, lose pressure more rapidly and this compression point will occur earlier. consequence- as go from high lung volume to low, point of collapse (equal pressure point), moves peripherally down lung bc of increase of resistance of small airways

increase in resistance of small airways-lost a lot of lung parenchyma and lost small airways so increase in airway resistance

another factor is pt with COPD have increased lung compliance… means difference between inter-pleural and alveolar pressure is reduced- lost some elastic recoil bc of destruction of the lung parenchyma, architecture of lung destroyed so diff. in pressure is less and since diff in pressure responsible for flow, flow rate is less

radial traction in these patients is reduced- bc of destruction of lung parenchyma, the tethering of airways not as strong, don’t have radial traction they should and are therefore more likely to collapse.

Question 37

Draw a time/volume graph showing how FVC and FEV1 changes in untreated asthma and after albuterol inhalation. (What is albuterol?)

Answer 37

albuterol is a beta 2 agonist

Slide 16.

Question 38

Draw a flow-volume loop showing normal, obstructive lung disease, and restrictive lung disease curves…how do the curves shift?

Answer 38

Slide 17.

Question 39

How do the following factors change in obstructive disorders?
FEV1/FVC
FEV1
FVC
TLC
RV

Answer 39

FEV1/FVC- decreased
FEV1-decreased
FVC-decreased or normal
TLC-normal or increased
RV-normal or increased

COPD is a general term that includes emphysema and chronic bronchitis. W emphysema the elastic tissue in the alveolar and capillary walls is progressively destroyed, which results in increased lung compliance and destroyed elastic recoil. The decrease in elastic recoil results in movement of the equal pressure point toward the alveolus and premature airway closure. This produces air trapping and increases in RV, FRC, and TLC. Airway resistance is also increased.
These increases in lung volumes increase the work of breathing by stretching the respiratory muscles and decreasing their efficiency.
(chronic bronchitis have same thing w equal pressure point and premature airway closure and increases in RV FRC and TLC but lung compliance is normal)

Question 40

How do the following factors change in restrictive disorders?
FEV1/FVC
FEV1
FVC
TLC
RV

Answer 40

FEV1/FVC- normal or increased
FEV1-decreased, normal or increased
FVC-decreased
TLC-decreased
RV-decreased

In restrictive lung diseases like pulmonary fibrosis, lung compliance is decreased. lung volumes are decreased but flow rates are relatively normal.

Question 41

How do the following factors change in mixed disorders?
FEV1/FVC
FEV1
FVC
TLC
RV

Answer 41

FEV1/FVC-decreased
FEV1-decreased
FVC-decreased or normal
TLC-decreased, normal, or increased
RV-decreased, normal, or increased

Question 42

Draw a graph that shows respiratory rate against mechanical work. Draw a line for total work, elastic work, and nonelastic work.

What is elastic work?
Non-elastic work?

Answer 42

Elastic work:
work to overcome lung elastic recoil, work to expand the thoracic cage, work to displace abdominal organs.
proportional to tidal volume

Non-elastic work (flow-resistive):
work to overcome airflow resistance
proportional to breathing frequency

Question 43

In normal lungs about how much total energy is required for breathing?

What changes in the following factors will lead to an increase in work? 
pulmonary compliance
airway resistance
elastic recoil
exercise

Answer 43

3% of total energy req. for breathing

Work is increased when:

Pulmonary compliance is reduced

Airway resistance is increased
Elastic recoil is decreased
Exercise, however total energy is also increased, proportion remains at ~5%

Question 44

Describe how work is affected in pulmonary fibrosis and COPD.

Answer 44

Pulmonary fibrosis:
increased elastic work: breathing becomes 
more shallow and rapidly

COPD:
increased flow-resistive work: breathing becomes more slowly and deeply

Question 45

Describe oxygen consumed by respiratory muscles and how this changes in exercise.

Answer 45

oxygen consumed by respiratory muscles is a small fraction of the oxygen flowing into the blood across alveolar-capillary membrane.

In severe exercise, this fraction can increase so far as to be inefficient in oxygenating the other working muscles of the body. That is, any increases in ventilation at this point simply go solely to those respiratory muscles moving the oxygen in the first place.

Question 46

How can you ensure that sufficient oxygen is delivered?

Why is combined work U-shaped?

When is lowest work of breathing?

Answer 46

elastic work can be increased (increase in tidal volume) or flow resistive work (frequency of breathing) can be increased.
(so combined work is U-shaped

lowest work of breathing is required for the frequency-volume combination at a normal tidal volume ventilation.

Question 47

What is elastic work proportional to? What is flow-resistive work proportional to?

Answer 47

Elastic work is proportional to tidal volume and flow resistive work is proportional to the frequency of breathing

Question 48

In the third trimester of pregnancy the enlarged uterus increases intrabdominal pressure and restricts movement of diaphragm. How does this affect FRC? Compliance? Airway resistance?

Answer 48

FRC decreases

change in lung volume results in decreased lung compliance and increased airway resistance

Question 49

What three factors are responsible for max. inspiratory flow? When is max. inspiratory flow?

Answer 49

Three factors are responsible for the maximum
inspiratory flow.

First, the force that is generated by
the inspiratory muscles decreases as lung volume
increases above RV.

Second, the recoil pressure of the lung increases as the lung volume increases above RV.
This opposes the force generated by the inspiratory
muscles and reduces maximum inspiratory flow.

However, airway resistance decreases with increasing
lung volume as the airway caliber increases. The combination
of inspiratory muscle force, recoil of the lung,
and changes in airway resistance causes maximal
inspiratory flow to occur about halfway between TLC
and RV