Respiration 1 Flashcards
1
Q
In mammals, the lungs are contained in the
A
thorax
2
Q
The conducting system of airways is composed of:
A
6 parts
- nose
- mouth
- pharynx
- trachea
- bronchi
- bronchioles
3
Q
__ divides into 2 bronchi
A
trachea
4
Q
Why is the conducting system known as non-respiratory
A
all the gas that is contained in the pathways- there is no opportunity for gas-exchange to occur
5
Q
___ leads to the respiratory surface
A
conducting system
6
Q
what is the respiratory surface
A
area where gas exchange takes place
7
Q
what are the components of the respiratory surface
A
3
- respiratory bronchiole (tiny bronchioles)
- alveolar sac
- alveolus
8
Q
can gas exchange occur in respiratory bronchioles?
A
yes, because they are very tiny and part of the respiratory surface
9
Q
terminal bronchioles lead to ___ bronchioles
A
respiratory
10
Q
respiratory bronchioles terminate into the
A
alveolar sac
11
Q
Tv stands for
A
tidal volume
aka quiet resting
12
Q
Tv is
A
normal resting
around .5litres
increases as you breathe in deeper and decreases as you exhale deeper
13
Q
residual volume is not equal to anatomical deadspace because ___
A
not equal to the anatomical deadspace because there is residual volume in the respiratory passages as well that cannot be completely collapsed when you breathe
14
Q
Expiratory reserve volume
A
difference between the lower value of the tidal breathe and the upper limit of the residual volume
15
Q
inspiratory reserve volume??
A
maximum lung capacity is around 6litres
16
Q
how much air is in the residual volume
A
more than 1 litre of air
17
Q
why is
A
max respiratory capacity is less than the total lung volume
18
Q
What do we need to add up to get our total lung
A
inspiratory reserve volume + tidal volume + expiratory reserve volume + residual volume
IRV + TV + ERV + RV = total lung volume
4.2 litres in females
6litres in males
19
Q
Breathing rate and tidal volume depend on __
A
the needs of the annimal (e.g metabolic and excercise needs)
20
Q
Define Eupnea
A
normal quiet breathing
21
Q
Define apnea
A
absence of breathing
22
Q
Define hyperpnea
A
increased lung ventilation by CO2
23
Q
Define Dyspnea
A
difficult or laboured breathing
24
Q
Define hypoventilation
A
decreased amount of air ventilated
25
Define hyperventilation
increased amount of air ventilated
26
People with _____ such as obesity, scoliosis, ___ have difficulty inflating their lungs
restrictive lung disease
muscle dystrophy
27
people with ___ such as ____ have difficulty emptying their lungs due to __
obstructive lung disease
asthma, emphysema
restricted airways
28
Why can obesity and pregnancy cause difficulty in breathing?
obesity => larger organ volume in the body cavity => limit the ability of the lungs to expand
pregnancy=> fetus taking up more room in the body cavity= less space for the lungs to expand
29
Why isn't all the air inhaled available for gas exchange?
because of the anatomical dead space
30
what is PVR
pulmonary ventilation rate
= tidal volume x frequency (f)
i.e PVR (ml per min)= ml of breath x breaths per min
31
What is alveolar ventilation rate?
AVR
= (tidal volume -dead space(ds)) x frequency
AVR (ml per min) = TV(min per breath) - DS(ml per breath) x f(breaths per min)
available for oxygen absorption
32
AVR stands for
alveolar ventilation rate
33
AVR is measured in
ml per min
34
DS is measured in
ml per breath
35
TV is measured in
ml per breath
36
frequency is measured in
breaths per min
37
How can you increase AVR ?
By increasing the tidal volume or frequency of breaths. However, increasing TV is more effective.
If we double the frequency then we must also double the ds volume.
E.g 2 x 500ml - 2x1150DSml = 700ml of air for gas exchange
However, if we double the tidal volume, we do not need to double the deadspace vol and therefore will have a larger volume available for gas exchange
E.g 100ml -150ml = 850ml for gas exchange
38
During exercise what do we do to increase AVR?
By increasing both TV and f.
39
amount of expired oxygen is roughly around
18% when resting
40
what happens to the expired oxygen volume when you exercise
it begins to decline from 18% at resting
41
What are the main differences between quiet breathing and forced breathing?
Quiet breathing:
- dorsal respiratory group inhibited
- inspiratory muscles relax
- passive expiration occurs
- DRG active
forced breathing:
DRG and inspiratory centre of ventral respiratory group inhibited
-inspiratory muscles relax and expiratory muscles contract
-active expiration occurs
-DRG and inspiratory center active and expiratory center od VRG inhibited
42
what are the similarities between quite breathing and forced breathing?
when inspiratory muscles contract this leads to inspiration
after inspiration the DRG are inhibited and the inspiratory muscles relax causing expiration which causes the DRG to become active
43
what are alveoli?
very small spheres
| -their walls form a boundary between air and fluid
44
the pressure difference across the fluid/air interface of the alveolar wall depends on ___
surface tension and the radius of the alveolar sphere according to the Young-Laplace Law
45
What is Young-Laplace Law?
the pressure difference at the boundary between air and fluid of the alveolar wall is equal to double the surface tension divided by the radius of the alveolar
delta P= 2gamma/ R
delta P = pressure difference across fluid/air interface at the alveolar boundary
gamma= surface tension
R= radius of the sphere
46
as the radius of the alveolar decreases the pressure difference ___
increases
47
surfactant increases/decreases surface tension depending on its concentration
decreases
48
in young-laplace law ___ doesn't change
surface tension is constant
between the fluid and air
49
What is a design disadvantage of the alveoli and why?
having 2 diff sized alveoli.
smaller radius = greater pressure tension, therefore, air will move from the smaller alveolar to the bigger one as it collapses.
As the lungs inflate and deflate, the individual alveoli will also inflate and deflate at different times depending on their size which influences pressure difference
this problem can be overcome by using surfactant
50
What can you use to overcome the problem of having smaller alveoli collapse as larger ones inflate?
having surfactant - that decreases the surface tension on the surface of a liquid.
cells that line the alveoli produce the surfactant - this lowers te surface tension which reduces the pressure in the alveoli.
the more surfactant you have the greater the decrease in surface tension
51
TLC stands for
total lung capacity
52
Why does the surface tension change depending on whether the lungs are full or deflated?
due to the amount of surfactant in the alveoli.
as lungs deflate, alveoli get smaller = surfactant becomes more concentrated
equalize the pressure on the 2 diff alveoli
53
Why is it important to have surfactant, in terms of 2 diff alveoli sizes
prevents alveoli from collapsing
to equalize the pressures between the alveoli by differences in the relative concentrations of surfactant
big alveolus = larger radius with a thin layer of surfactant= will have a greater surface tension
small alveolus = smaller radius with a more concentrated layer of surfactant = reduced surface tension
54
What happens to the alveoli if there is no surfactant present
the smaller alveoli will collapse as the pressure difference is too great and will diffuse into the larger alveoli
*issues for babies as they have a delayed production of surfactant
(starts production few weeks prior to birth)
55
what happens to the surfactant in the alveoli as the alveoli collapse or expand
the concentration of the surfactant increases in the alveoli
56
what happens to the pressure of the alveoli when the alveoli decrease in radius and increase in surfactant?
the pressure decreases
prevents the alveoli from collapsing, therefore, making it easier to fill them during inhalation - this decreases the pressure required to fill the lungs
57
what happens to the surfactant layer as the lungs fill with air and alveoli expand?
surfactant layer becomes thinner, increasing surface tension and intra-alveolar pressure- making exhalation easier
58
What is IRDs
- describe what it is
- how it affects the individual
- rate of affecting
- how it can be treated
IRDS = infant respiratory distress syndrome
-occurs in premature infants due to the lack of surfactant produced - leading cause of death in pre-term infants.
condition declines with gestational age from 50% at 26weeks to 25% at 30 weeks
infants can be treated with natural or artificial surfactant
59
What is surfactant?
surfactant is a phospholipid
produced within the alveolar cells
- made in the golgi apparatus
- once transported out of the cell, it forms a structure called tubular myelin which then breaks and forms a surface over the alveolar cells.
60
The production of surfactant in the lungs developed in __ therefore, it can still be found in __
fish
lungfishes, bonyfishes,
61
Why is there a period of no breathing after artifically hyperventilation?
LA
During hyperventilation by artificially increasing the ventilation within the alveoli, you are reducing the Co2 content in the alveolar gas.
quite breathing - you have a relatively high level of Ci2 within the lungs and if you increase the ventilation you are 'washing out' the CO2. By reducing the alveolar pCo2 you are also getting pCo2 out of the blood, reducing arterial pco2.
at the end of the hyperventilation period, you have v low blood pCO2 and since this drives inspiration you have to wait for the pCO2 levels to build up in the blood over a period of time before you get the chemosensory signal to excite the DRG to start inspiration again.
Therefore, this gives an intermitted pattern of tidal breathing + no breathing until enough CO2 builds up to continue normal breathing again
62
If a person who was artificially ventilating were to exercise at the end of the ventilation period, what would occur?
exercise would cause a build up of co2 through the increase in metabolism and this would cause a quicker return of ventilation followed by normal breathing.
63
How does the pCO2 and pO2 change after hyperventilation?
normal/resting arterial pCO2 is around 4ommHg , after hyperventilation it is 10-15mmHg
normal alveolar pO2 is around 75mmHg, after hyperventilation it is around 130mmHg (more similar to air 150mmHg).
Takes 1.5 mins to reduce to normal pO2. and nearly 3mins for pCo2 to return to normal
64
What is the relationship between alveolar pCO2 and pO2 with ventilation?
Co2 influence has been known for many years
O2 demonstrated by Heymans in 1920's
Blood low in O2/ high in Co2 around ventricle or aorta stimulated breathing (but only when vagus nerves intact) = aortic bodies - vagus nerve (afferent nerves to CNS) known as peripheral chemoreceptors
similarily, carotid arteries also had these zones = chemosensitive carotid bodies- glossopharyngeal nerve (afferent nerves to CNS)
65
Why would we want to measure the carotid artery?
it is the main arterial route for blood. so we want to make sure the blood brain oxygen conc is maintained.
66
What are the two main bodies located near the heart, responsible for homeostasis of O2 and Co2 ?
And what occurs under normal O2 conc
LA
cells within the carotid and aortic bodies (glomus cells).
glomus cells have afferent nerve endings (sensory).
carotid bodies send information via the glossopharyngeal nerves.
aortic bodies send infor via vagus nerve.
contain dopamine granules within the glomus cells. under normal O2 conc, dopamine is released from glomus cells and hyperpolarizes the sensory nerve ending preventing them from discharge.
glomus cells =releasing dopamine and inhibiting the post-synaptic neuron, therefore, there is no discharge for the post-synaptic neuron to send infor to the brain
67
What are the postulated mechanisms of action for the glomus cells
1. when pO2 conc normal
= dopamine release from glomus cell= hyperpolarises sensory nerve ending - prevents discharge
2. hypoxic conditions = dopamine release is now reduced - this release the post synpatic cell from inhibition and sensory nerve endings become active.
post-synpatic cell depolarised and now fires APs to the brain 'o2 conc too low'
when post-synpatic cell starts to discharge, AP that is sent to the brain contains positive feedback onto the glomus cells.
as they in turn, release acetylcholine onto glomus cells that further inhibits dopamine release
68
What are the chemoreceptors of the carotid and aortic bodies stimulated by?
3
1. lowered pO2
2. elevated pCo2
3. elevated [H+] (low blood pH)
particularly simulated by lowered pO2.
69
in terms of o2, chemoreceptors respond to?
o2 tension
-this can be demonstrated with carbon monoxide as it decreases the O2 carrying capacity of blood without changing the pO2 conc wiithin the blood.
since CO2 is replaced by Co on the heamoglobin there will be no effect on chemoreceptor activity.
70
What is the main driver of respiration?
CO2
71
What kind of O2 conc change do you need for chemoreceptors to be stimulated? Give an example
you need a relatively large change in O2 for the chemoreceptors to be stimulated.
The receptors are insensitive until a % of O2 inspired falls from normal 21% to 14% or less.
72
what is the primary mechanism used to respond to changing O2 levels?
chemoreceptors of carotid and aortic bodies
73
why is Co2 the main driver?
for a large change in pO2 in blood = there is no difference in the amount of oxygen carried by the hemoglobin
hemoglobin can still be relatively well saturated even at relatively low pO2 levels.
we need a relatively large change in o2 in order for the receptors to be stimulated. but it has to be sensitive as at low Po2 levels the hemoglobin levels decline drastically due to the hemoglobin saturation curve.
74
How do we measure Co2?
using central chemoreceptors which are sensitive to pCO2 and [H+]
75
where are the central chemoreceptors located? and what do they measure?
upper and lateral medulla oblongata measured the Co2 diffusion into the CSF
CSF = has no buffering capacity
CSF is basically saline solution, therefore, its pH will change drastically with a change in Co2.
Co2 = acid will dissociate in fluid to form carbonic acid
blood = full of protein = act well as pH buffers as they will soak up [H+], particularly hemoglobin.
Therefore, in order to get a huge change pH in blood, you have to change the Co2 by a huge amount.
76
How does co2 concentration affect ventilation?
Co2 within blood diffuses across the BBB, binds with water to form carbonic acid which dissociates into bycarbonate and [H+]. the protons change the pH = affect the chemoreceptors which will then change ventilation accordingly.
77
Co2 effects are much greater on ventilation than O2 T/F
T
increased Co2 = large change in alveolar ventilation
78
how can you increase one's breath-holding?
whats the down-side
decreasing alveolar Co2 you can increase the breath-holding quite dramatically.
however, it takes a while for Co2 conc to rise before it starts to stimulate breathing again
79
what is a known risk of forced hyperventilation?
| give an example
hyperventilate at the surface (wash off the CO2) and then hold breath for much longer
However, you can get to a point where you're exercising where the Co2 conc does not get up to the required point where it will start to stimulate the need to breathe before the blood o2 level drops to a point where you go unconscious.
= aka shallow water blackout
you can blackout before pCo2 reaches involuntary threshold
80
What happens if you hold your breath for a certain time?
and what happens if the pC02 involuntary threshold is 50mmHg
metabolism continues and pCo2 levels rise by ~5mmHg per min
50mmHg = can hold breath for 2 mins
2mins
5 x 2 = 10mmHg
81
Normally pCo2 is ___mmHg in arterial blood
40mmHg
82
If one hyperventilates and the pCo2 is driven to 30mmHg you can hold your breath for ?
4 mins
5 x 4 = 20
83
describe the pCo2 involuntary threshold of 50mmHg
50mmHg before you get an uncontrollable urge to breathe
