Breathing Quantified Flashcards
What is a spirometer?
device that allows plotting lung volume against time (spirogram)
spirometer cannot measure all lung volumes/capacities (TLC and RV)
How many lung volumes and capacities are there?
there are 4 static lung volumes, and combination of these give rise to 4 lung capacities
What are the 4 static lung volumes?
- tidal volume (TV)
- inspiratory reserve volume (IRV)
- expiratory reserve volume (ERV)
- residual volume (RV)
What are the 4 lung capacities?
- inspiratory capacity (IC)
- functional residual capacity (FRC)
- vital capacity (VC)
- total lung capacity (TLC)
What is tidal volume (TV)?
volume of what you normally breathe in and out
What is inspiratory reserve volume (IRV)?
volume above what you normally breathe in
What is expiratory reserve volume (ERV)?
volume below what you normally breathe out
- after taking a single normal breath in, exhale all the way – ERV is what you can squeeze out
What is residual volume (RV)?
volume you couldn’t breathe out – still some air left in lungs
- maximum expiration
What is inspiratory capacity (IC)?
IC = TV + IRV
breathe all the way in, then exhale back to end of normal breath
What is functional residual capacity (FRC)?
FRC = ERV + RV
end of normal breath
What is vital capacity (VC)?
total volume of air that can be displaced from lungs by maximal expiratory effort
fill lungs completely, then empty completely
What is total lung capacity (TLC)?
TLC = IC + FRC
amount of air you breathe between total inspiration and total expiration possible
maximum inspiration
What are factors that influence static lung volumes? (4)
- height
- gender
- age
- ethnicity
How does height influence static lung volume?
taller = larger lung volume
How does gender influence static lung volume?
male = larger lung volume
How does age influence static lung volume?
- lung volumes increase with development until ages 20-25 year old
- older = higher RV and FRC
- older = lower VC, resulting in gas trapping
- changes are due to stiffening of chest wall with onset of senescence
- NOT due to increasing compliance in lungs
How does ethnicity influence static lung volume?
differences partly due to body build (ie. relative length or width of chest wall)
What do restrictive diseases do?
restrict inspiration
lung volumes reduced – difficulty getting air into lungs due to changes in mechanics of lungs or chest wall
What are some restrictive diseases?
- pulmonary fibrosis (stiff lungs)
- ankylosing spondylitis (stiff chest wall)
- kyphoscoliosis (stiff chest wall)
How does pulmonary fibrosis affect the lungs?
stiff lungs = elastance increases, compliance decreases → can’t stretch → problems getting air in
What do obstructive disease do?
limit air flow out of lungs during expiration
difficulty getting air out of lungs, due to resistance increasing or compliance increasing
What are some obstructive diseases?
- chronic obstructive pulmonary disease (COPD)
- asthma
- chronic bronchitis
- emphysema
Forced Vital Capacity (FVC) Maneuver
List the steps of the maneuver.
- breathing nicely
- fill lungs and exhale as fast/hard as you can
- volume breathed out is forced vital capacity
- measure what happens in first second – how much you can breathe out
- results: normal vs. obstructive vs. restrictive
Forced Vital Capacity (FVC) Maneuver
What is the result of the maneuver in a normal lung?
most people can breathe out within first second of the maneuver – 75% or more
Forced Vital Capacity (FVC) Maneuver
What is the result of the maneuver in an obstructive lung?
- cannot breathe as fast (expiration slower than normal)
- ratio of forced expired volume (amount breathed out in first second) relative to total amount they can breath (FVC) is < 70%
Forced Vital Capacity (FVC) Maneuver
What is the result of the maneuver in a restrictive lung?
vital capacity is lower than normal
but FEV1/FVC is normal or > 70% (higher than normal)
What are the mechanisms behind airway narrowing in obstructive diseases?
airway resistance increases, maximal expiratory flow decreases → hard time breathing out
- bronchoconstriction: COPD, asthma
- inflammation: COPD, asthma, chronic bronchitis, bronchiolitis
- excess mucus production: asthma, chronic bronchitis, cystic fibrosis
- reduced alveolar elastic recoil: emphysema (walls of airway destroyed, lung compliance increased)
Described the mechanism of reduced alveolar elastic recoil behind airway narrowing in obstructive diseases.
reduced alveolar elastic recoil: emphysema (walls of airway destroyed, lung compliance increased)
- reduced tethering, keeping neighbouring airways open
- cannot generate typical driving pressure for forced expiration – lower because you still have force of chest wall, but force of lung recoil
How is breathing quantified?
minute ventilation (VE) = VT x breathing frequency
What are the 3 kinds of ventilation?
- minute ventilation (VE)
- alveolar ventilation (VA)
- dead space ventilation (VDS)
Which type of ventilation is important (what we REALLY want to know)?
alveolar ventilation – because that’s where gas exchange occurs
Describe what happens to the 500 ml of tidal volume when you breathe in.
350 ml stays in conducting airways and enters respiratory zone to participate in gas exchange in alveoli
- this introduced fresh air is diluting what’s already in lungs
- at end of normal breath, there’s ~2400 ml sitting at FRC in alveoli
What type of breathing pattern has the most alveolar ventilation?
deep and slow > normal quiet breathing > shallow and fast (which is 0)
What type of breathing pattern has the most dead space ventilation?
shallow and fast > normal quiet breathing > deep and slow
What type of breathing pattern has the most minute ventilation?
normal quiet breathing = shallow and fast = deep and slow
What is anatomic dead space?
airways NOT participating in gas exchange – nose to terminal bronchioles
If more dead space is added, what do you need to do to get the same amount of air?
increase volume of air intake
What is alveolar dead space?
portion of breathing that reaches alveoli
does NOT participate in gas exchange because of inadequate perfusion to alveolus – could be partial or 0
When is alveolar dead space insignificant?
in healthy lungs
When is alveolar dead space significant?
in disease states – ie. in presence of pulmonary embolus (blood clot)
could be due to:
- partial obstruction by blood clot
- narrow vessel
either way, rate of perfusion is abnormal
- if some blood can pass through, it will have same values of O2 and CO2 by the time it reaches end of capillary
- end capillary partial pressure will reflect what was in alveoli
- ventilation/perfusion ratio will affect what alveolar gas values are, which are ultimately reflected in arterial blood – measure of arterial blood partial pressures indexes what’s going in alveolus (same as alveolus values)
What is alveolar ventilation
portion of breathing that reaches alveoli and participates in gas exchange
breathing pattern determines alveolar ventilation and amount of air available for gas exchange
What is the composition of end pulmonary capillary blood in steady state?
reflects alveolar PO2 and PCO2
What are the two key players in gas exchange?
relative rate of these changes:
- alveolar ventilation (how well alveolus is being ventilated)
- alveolar perfusion (how well alveolus is being perfused)
Describe the composition of deoxygenated blood coming from pulmonary artery.
- mixed venous – already seen by tissues and completed gas exchange
- low in O2, high in CO2
Describe the process of alveolar ventilation and perfusion.
- deoxygenated blood goes to capillaries of pulmonary circulation
- exchange O2 and CO2 with alveoli due to differences in partial pressures of these gases
- O2 moves into blood
- CO2 moves out of blood into alveoli - by the time you get to end of capillary, composition of CO2 and O2 in terms of partial pressure is the same as alveolus
- reached equilibrium
- no more driving pressure for gases to move
- gas exchange is complete
What does matching alveolar ventilation and perfusion do?
impacts partial pressures of O2 and CO2 in alveolar air and pulmonary capillary blood
What happens if blood flow is only partially obstructed?
PO2 and PCO2 vary depending on size of obstruction
different V/Q ratios give different amounts of arterial partial pressures
(what we’re really interested in, because arterial blood is what will be seen by tissue for gas exchange – take O2, and put some CO2 back)
What happens if blood flow is completely obstructed?
- partial pressures in alveoli reflects what is coming in
- no exchange
- ventilation/perfusion ratio is infinity – alveolar dead space is ventilated, but does not participate in gas exchange
What do O2 and CO2 levels impact?
airway and blood vessel size
partial pressures of O2 and CO2 have impact on smooth muscle of local airways and pulmonary vessels, regulating their size and minimizing ventilation perfusion inequality
Why do we try to match ventilation and perfusion?
to ensure proper gas exchange
When might homeostatic control of ventilation and perfusion not help with matching ventilation and perfusion?
if ventilation/perfusion goes off a lot – there is a limit to what extent homeostatic control can help balance the two
When Ventilation > Perfusion
If there is dead space ventilation (or V/Q ratio = infinity), what are the relative PCO2 and PO2 levels?
(obstruction in capillary)
low PCO2
high PO2
When Perfusion > Ventilation
What might cause the obstruction in the alveoli?
mucus production
smooth muscle narrowing
resistance
When Perfusion > Ventilation
What are the PCO2 and O2 values in the alveoli?
values in alveoli (which are then reflected in blood that completed gas exchange at level of lungs) will be same as mixed venous blood – nothing happens
- no fresh air coming
- CO2 can’t leave
- called ‘shunt’
Ventilation > Perfusion
Ventilation < Perfusion
see notes
