Tidal Volume

- Volume of air moving in and out of the lungs with each normal quiet breath
- Typically 500mL of air for an adult

Inspiratory reserve volume (IRV)

- Volume that we can inspire forcibly beyond the tidal volume
- Going from normal quiet breath to taking as much as you can into the
lungs

Expiratory Reserve volume

- How much you can push out of your lungs beyond normal tidal expiration

Residual Volume
- Volume remaining at the end of a forced expiration
- Never fully enter respiratory system, always something left behind
essentially because the lungs don’t collapse
Vital capacity

Forced Vital capacity:

- Measures from peak of maximal inspiration and trough of a maximal
expiration – total amount of exchangeable air during a forced breathing
maneuver
- There are standard range values for men and women and children
- The main determinant of vital capacity is height, the larger you are, the
larger your vital capacity tends to be

Forced maximal inspiration

Forced maximal expiration

Forced vital capacity – measures from peak of maximal inspiration and
trough of a maximal expiration – total amount of exchangeable air during a
forced breathing maneuver
- When we take a breath of air during inspiration, not all of it is going to be
involved in gas exchange, some will sit in conducting zones
- This is referred to as dead space
- Every breath of air we take à some of it becomes dead space
- The anatomical dead space we have includes nasal cavity, pharynx, larynx,
trachea, larger bronchial branches
- Anatomical dead space is about 150mL (for adult)
- Anatomical dead space wont change as an adult
- Alveolar dead space can develop because of some sort of pathology à
causes functional regions of the alveoli to be no longer capable of gas
exchange, may be because of build up of inflammatory material, a tumor,
anything that prevents alveoli from doing their purpose
- Less gas exchange occurs if there is alveolar dead space
FEV1 - Forced expiratory volume in one second
- Forced inspiration and forced maximal expiration, measures how much of
that exchangeable air are you getting out in that forced expiration
- Over 75% should be the amount you get out
- FEV1:FVC ratio expect to be around 80%
- Any obstructive airway disorder, that ratio will decrease because more
resistance to airflow because airways narrowed
- Might get the same volume out, but it will take longer, so within one
second, you are getting a smaller portion of forced vital capacity out
- FEV1:FVC is a good indicator of airway obstruction, it doesn’t help to
diagnose specific obstruction disorder but tells you if onbstruction is
present
- Minute ventilation – total amount of air moving out of respiratory system
every minute
- AVR: Teells you efficiency of gas exchange because takes into account dead
space
- If dead space increases, subtracting higher volume from TV so the AVR
decreases
- Our pO2 will decrease because there is less oxygen delivered, if there’s less
 gas exchange occurring, and less CO2 removed, so partial pressure of O2 and CO2
are altered in our arterial blood as a result, less o2 more co2 present
- When there is not enough gas exchange happening, we need to increase
frequency of breathing or increase tidal volume
- When there is dead space, breathing more deeply will fill additional regions of the
lung with air so you get more gas exchange occurring
- Normal healthy respiratory system
- Airway resistance is determined by diameter of the airways
- The smaller the diameter, the more resistance there is
- The greatest resistance to airflow is in the bronchi closest to trachea
(upper regions of bronchial tree)
- Even tho they have larger diameters
- The cross sectional area of the branches that branch of terminal
bronchioles greater than the tube that supplied them
- Typically quite little resistance to air flow entering the lungs
- Resistance in smaller bronchioles is important in disease states, when you
have things that cause inflammation (mucus build up, bronchoconstriction,
bronchospasm) causes major obstruction in these smaller vessels where
there is usually little resistance. Reduction in the diameter of those smaller
bronchiole branches leads to a big increase in resistance

- Flow rate is inversely proportional to resistance, if you increase resistance,

reduction in airflow
What is the role of the respiratory control center?
Alter the rate and depth of breathing appropriately to match the body’s
requirements for gas exchange to make sure that everything stays in balance.
It alters ventilation by changing either inspiratory depth (volume of air moving
in with each breath) or inspiratory rate (

- Inspiration determined by contraction of respiratory muscles, for control

center to bring about respiration it has to send an impulse to respiratory
muscles to make them contract giving volume and pressure change
- How deeply we breathe in inspiration is determined by how actively the
respiratory control centre stimulates the respiratory muscles and a forceful
contraction is generated as a result
- If muscles contract more forcefully, bigger change in V and P, and deeper
breath moving in
- Respiratory rate is determined by how long the respiratory control centre
is active for during those cycles of inspiration and expiration, how long the
impulses last for
- Change rate and depth of breathing to meet bodys demands for gas
 exchange
- The main stimuli for altering ventilation are chemical stimuli in arterial blood
(levels of CO2, O2, H+)
- Present in medulla and PONS
- VRG: Responsible for generating the rhythm of breathing (frequency that
we take our breaths)
- Also integrates sensory information being received from all areas of the
body

- DRG: Receives the sensory information and communicate that to the VRG
that then either brings about an inc. in rate and depth of breathing that is
appropriate to the sensory information that is being received from the
body about things like level of O2, CO2, how physically active we are etc
from receptors

- PRC: Smoothing effect over cycles of inspiration and expiration so it is not

so abrupt
- It allows to change breathing patterns so you can sing, sleep etc
- Sensory information being sent to Respiratory control centre
- Some stimulate an increase in ventilation
- Some always stimulate decrease in ventilation or both

Proprioceptors in muscles and joints that relay information about how

active we are (sitting at rest or in gym etc) à send sensory information to
RCR, if the receptors are suddenly more active it is because we are more
active

+ - tells RCR to increase ventilation to match to increased requirements for

gas exchange

Central Chemoreceptors
- Monitor CO2 primarily
- Monitoring H+ in CSF
- Mediate about 70% of ventilatory response to CO2
- If there is too much CO2, it is above normal range, the RCR when it detects
it is increase ventilation
- If there is too much CO2, have to increase ventilation to get rid of it
- Process of ventilation is to get rid off CO2 and get in oxygen
- Increasing ventilation would blow off excess CO2 levels

Peripheral Chemoreceptors
- Enlarged blood vessels in similar location to baroreceptors
- Monitor PO2, PCo2, pH
- If O2 is low, CO2 is increased, or pH has decresed à all of these changes require
ventilation to increase, to get more oxygen in, blow off CO2 and help to adjust pH
- PCo2 is main controller of ventilation (generally)
- CO2 is more tightly regulated than oxygen levels are
- WHY? – because it can have a big effect on pH
- Too much CO2 can make u acidic, vice versa, therefore needs to be tightly
regulated
- So resp. system is important for trying to maintain acid base balance
- Normally arterial PCo2 is 40mmHG, maintained very tightly +/- 3mmHg
- When it increases or decreases beyond that, it brings a change in
ventilation
- If arterial pCO2 increases, have to increase ventilation to blow off CO2
- If it decreases, have to reduce Co2

- Once it leaves pulmonary circuit, what is the composition à this is what is

monitored
- Venous blood composition is not monitored in same way, it can vary
substantially, there could be lots of CO2 if we are exercising but lungs
should take care of that and arterial blood should be normal
- When arterial pCO2 increases, the AVR should increase
- Our response to changes in CO2 can be altered by different things, anesthetic
agents depress the response of chemoreceptors
- Acidosis enhances it
- What is looking at composition of arterial blood?
- Central – the most sensitive to changes in CO2
- They are stimulated when co2 from cerebral capillaries diffuse into CSF
- Cerebral capillaries are carrying blood with high CO2 (abnormal)
- Gases can freely pass across BBB into CSF
- This same reaction that we saw in RBC catalyzed by carbonic anhydrase can
also happen in CSF when CO2 diffuses in
- In capillary, CO2 increases, and more H+ present, but these H+ can not
pass across BBB, but CO2 can
- WHAT is stimulating central chemoreceptors: NOT CO2 gas, H+ produced
in CSF as a result of CO2 coming in
- Central chemoreceptor stimulated by H+, info is sent to respiratory control
centre
- Monitor arterial o2, co2, and pH
- PO2 in venous blood: 40mmHg, hemoglobin is 75% saturated when it is 40
- Top of O2 hemoglobin saturation curve is quite steep, don’t see much of a
change in saturation of hemoglobin until you get below 60mmHg
- There is sufficient saturation of haemoglobin above 60mmHg
- High altitude is where O2 saturation drops, it can also happen with
pathology when ventilation has been inadequate
- Usually changes in CO2
- If your inspiratory depth is too great and could potentially damage lungs
due to over inflation, those stretch receptors will detect that and send an
inhibitory influence to the control centre to reduce inspiration

- Irritant receptors detect noxious substances, help reduce inspiration to

help reduce these substances getting into alveoli