Physiology Flashcards
(135 cards)
1
Q
what is internal respiration
A
intercellular mechanisms which consume CO2 and produce O2
2
Q
what is external respiration
A
the sequence of events that lead to the exchange of CO2 and O2 between the external environment and the body cells
3
Q
how many steps are involved in external respiration and what are they
A
four:
- ventilation
- exchange of O2 and CO2 between air in alveoli and blood
- transport of O2 and CO2 between lungs and tissue
- exchange of O2 and CO2 between blood and tissues
4
Q
what type of blood is involved in the 4th step of external respiration
A
systemic (capillaries)
5
Q
what type of blood is used in the 3rd step of external respiration
A
circulating
6
Q
where is the blood is used in the 2nd step of external respiration
A
pulmonary capillaries
7
Q
what 3 pressures are important for ventilation
A
- atmospheric
- intra-alveplar
- intrapleural
8
Q
explain ventilation via pressures
A
air moves from high to low pressure (due to boyles law). During inspiration the muscles will contract resulting in an increased volume causing the gas pressure (and intra-alveolar pressure) to decrease, this causes the air to move into the lungs until the intra-alveolar pressure = atmospheric pressure
9
Q
what is boyles law
A
at any constant temperature the pressure exerted by a gas varies INVERSELY with the volume of the gas
“as the volume increases, the pressure will decrease”
10
Q
how do the lungs adhere to the chest wall, what does the adherence cause
A
- intrapleural fluid cohesiveness = water molecules in the intrapleural fluid are attracted to each other and resit being pulled apart
- negative intrapleural pressure = intrapleural pressure is lower than atmospheric and intra-alveolar this causes the lungs to push out and the chest wall to push in and results in them sticking together
these 2 factors result in the lungs expanding when the chest wall does
11
Q
identify the muscles used in inspiration (under normal conditions)
A
- diaphragm (main)
2. intercostal muscles
12
Q
what type of expansion do the intercostal muscles allow
A
horizontal
13
Q
what type of movement does the diaphragm allow
A
vertical
14
Q
is inspiration active or passive
A
active, energy is needed to contract the muscles
15
Q
is expiration active or passive
A
passive
16
Q
what causes the lungs to recoil
A
- elastic connective tissue
2. alveolar surface tension
17
Q
what is alveolar surface tension
A
attraction between the water molecules at liquid air interface, produces A LOT of force
18
Q
what is surfactant and what secretes it
A
mixture of lipid and proteins secreted by type 2 alveoli
19
Q
what is the role of surfactant
A
reduces surface tension by interspacing between water molecules, it acts more on smaller alveoli
20
Q
what alveoli are at risk of collapse, what law is this
A
smaller alveoli, LaPlace’s law
21
Q
what prevents collapse of alveoli (3)
A
- surfactant
- alveolar independence
- transmural pressure
22
Q
what is alveolar independence
A
if a alveoli begins to collapse then surrounding alveoli will stretch then recoil reopening the collapsed alveoli
23
Q
what is tidal volume (TV) and what is the average volume
A
volume of air entering or leaving the lungs during a single breath
0.5L
24
Q
what is inspiratory reserve volume (IRV) and what is the average volume
A
extra volume of air that can be MAXIMALLY inspired over and above the typical resting tidal volume
3L
25
what is expiratory reserve volume (RV) and what is the average volume
extra volume of air that can be ACTIVELY expired by maximal contraction beyond the normal volume of air after a resting tidal volume
1L
26
what is residual volume (RV) and what is the average volume
minimum volume of air remaining in the lungs even after a maximal expiration
1.2L
27
what is inspiratory capacity (IC) and what is the average volume
maximum volume of air that can be inspired at the end of a normal quiet expiration
3.5L
28
what 2 volumes make the inspiratory capacity
IC = IRV + TV
29
what is functional residual capacity (FRC) and what is the average volume
volume of air in lungs at the end of normal passive expiration
2.2.L
30
what 2 volumes make the functional residual capacity
FRC = ERV +RV
31
what is vital capacity (VC) and what is the average volume
maximal volume of air that can be moved out during a single breath following a maximal inspiration
4.5L
32
what 3 volumes make up vital capacity
VC = IRV + TV + ERV
33
what is total lung capacity (TLC) and what is the average volume
total volume of air that the lugs can hold
| 5.7L
34
what 2 volumes make up total lung capacity
TLC = VC + RV
35
what are the accessory muscles of inspiration
sternocleidomastoid
| scalenus
36
what are the muscles of active respiration
internal intercostal muscles
| abdominal muscles
37
what lung volumes & capacities can't be measured by spirometry
residual volume
| total lung capacity
38
what does the volume time curve in spirometry allow you to determine
forced vital capacity (FVC)
forced expiration in 1 second (FEV1)
FEV1/FVC ratio
together all three are known as "dynamic lung volumes"
39
what are the dynamic lung volumes in obstructive lung disease
FVC = normal
FEV1 = reduced
FEV1/FVC ratio = reduced (>70%)
40
what are the dynamic lung volumes in restrictive lung disease
FVC = reduced
FEV1 = reduced
FVC/FEV1 ratio = normal
41
what is "work of breathing"
the energy required to breathe (normally 3% of total energy expenditure)
42
when is work of breathing increased (4)
1. DECREASED pulmonary resistance
2. DECREASED elastic recoil
3. INCREASED airway resistance
4. INCREASED need for ventilation (e.g. exercise)
43
when is residual volume increased (give examples)
when elastic recoil of the lung is lost e.g emphysema, old age
44
what is forced vital capacity (FVC)
maximum volume that can be forcibly expelled from the lungs following a maximum inspiration
45
what is forced expiratory volume in 1 second (FEV1)
volume of air that can be expired during the first second of expiration in FVC
46
examples of OBSTRUCTIVE lung disease
asthma
| COPD
47
examples of RESTRICTIVE lung disease
fibrosis
| interstitial lung disease
48
what factors influence airway resistance
```
airway radius (primary determinant)
disease states (e.g. asthma, COPD)
```
49
how is airway radius altered
parasympathetic stimulation = bronchoconstriction
| sympathetic stimulation = bronchodilation
50
what is lung compliance
measure of the effort required to stretch or distend the lungs
aka volume change per unit of pressure across the lungs
51
low compliance results in _______ work required
High
52
high compliance results in _______ work required
low
53
what causes increased compliance
loss of elastic recoil (e.g emphysema)
| age
54
what causes decreased compliance
```
fibrosis
oedema
lung collapse
pneumonia
absence of surfactant
```
55
what does increased compliance result in
patients have to work harder to get the air out of their lungs
hyperinflation
56
what does decreased compliance result in
greater pressure change is needed to produce a change in volume
SOB on exertion
57
what type of spirometry pattern can decreased compliance cause
restrictive
58
what causes dynamic airway compression
rising pleural pressure during active expiration
59
what does dynamic airway compression cause in normal people
increased pressure upstream in the airway which helps to open the airway by increasing driving pressure between the alveolus and the airway
60
what does dynamic airway compression cause in an obstruction
driving pressure between the alveolus and airway is lost leading to a fall in airway pressure downstream. This results in airway compression causing airway collapse
61
what is pulmonary ventilation
the volume of air breathed in and out per min
= tidal volume x RR
62
what is alveolar ventilation
the volume of air exchanged between the atmosphere and alveoli permit
= (tidal volume - dead space volume) x RR
63
why is alveolar ventilation lower than pulmonary ventilation
because of the presence of anatomical dead space
64
what is anatomical dead space
airways which are not available for gas exchange but which still contain some inspired air
65
how is pulmonary ventilation increased. which method is more effective and why
increase depth (tidal volume) of breathing and rate of breathing (RR)
depth is more effective due to dead space
66
what does the transfer of gases between the body and the atmosphere depend on
ventilation and perfusion
67
what is ventilation
the rate at which GAS is passing through the lungs
68
what is perfusion
the rate at which BLOOD is passing through the lungs
69
what is alveolar dead space
ventilated alveoli which are not adequately perfused with blood
70
what is physiological dead space
alveolar dead space + anatomical dead space
71
what matches airflow to blood flow
local control of airway smooth muscle and arterioles
72
what is the result of increased perfusion
accumulation of CO2 in alveoli which will decrease airway resistance via airway dilatation leading to increased airflow (ventilation)
73
what is the result of increased ventilation
increase in alveolar O2 concentration which will cause pulmonary vasodilatation leading to increased blood flow (perfusion)
74
what is the effect of decreased and increased O2 on pulmonary arterioles
```
decreased = vasoconstriction
increased = vasodilation
```
75
what is the effect of decreased and increased O2 on systemic arterioles
decreased = vasodilation
| increased =vasoconstriction
76
what factors influence the rate of gas exchange across the alveolar membrane
1. partial pressure gradient of O2 and CO2
2. diffusion coefficient for O2 and CO2
3. surface area of alveolar membrane
4. thickness of alveolar membrane
77
what is partial pressure and what does it determine
it is the pressure that a gas would exert if it occupied the total volume of the mixture without the other gases
it determines the pressure gradient
78
what would a big gradient between the partial pressure of oxygen in the alveolar air and the oxygen in the arterial blood indicate
problems with gas exchange or a L to R shunt in the heart
79
what is the diffusion coefficient
solubility of a gas in membranes
80
compare the diffusion coefficient of CO2 and O2 and give an explanation for it
CO2>O2 by quite a bit to make up for the difference in partial pressure
81
compare the partial pressures of CO2 and O2
O2>CO2 by quite a bit
82
explain the effects of membrane surface area on gas transfer
Large surface area = fast transfer
83
explain the effects of membrane thickness on gas transfer
thick membrane = slow transfer
84
what are alveoli
thin-walled inflatable sacs
85
describe alveoli (walls & encirclement)
walls concept of a single layer of flattened type 1 alveolar cells each encircled by a pulmonary capillary with a narrow interstitial space
86
how is O2 carried in the blood
1. dissolved (tiny amount)
| 2. bound to haemoglobin
87
what is the MAIN method of O2 transport within the blood
bound to haemoglobin
88
describe the binding of O2 to haemoglobin
reversible
89
describe haemoglobin (Hb)
4 harm groups, each one can bind to a O2
90
what is the primary factor which determines % saturation of Hb with O2
partial pressure of O2 (PO2)
91
what type of curve is theO2-Hb dissociation curve
sigmoidal
92
what is oxygen delivery index due to
CO x O2 conc of arterial blood
93
what is O2 concentration of arterial blood determined by
concentration of Hb in the blood
| % saturation of Hb with O2
94
what is O2 delivery to the tissues affected by
1. DECREASED PO2
2. respiratory diseases
3. anaemia
4. Heart failure
95
what is the Bohr effect
RIGHT shift of Hb-O2 curve causing increased release of O2 at the tissues
96
what causes the Bohr effect
INCREASED:
1. PCO2
2. [H+]
3. temperature
4. 2,3-biphosphoglycerate
97
how does foetal Hb differ from adult Hb
structure: has 2 alpha units and 2 gamma units (instead of 4 alpha) causing less interaction with 2,3-biphosphoglycerate
affinity: has a higher affinity for O2
98
what effect does foetal Hb have on the dissociation curve
shifts to the LEFT
99
why does foetal Hb have a higher affinity for O2 than adult Hb
to allow O2 transfer from the mother to the foetus even if the PO2 is low
100
describe the myoglobin curve
hyperbolic
101
what does the presence of myoglobin indicate
muscle damage
102
what does myoglobin do
it releases O2 at a very LOW PO2
| it provides short term storage for O2 at anaerobic conditions
103
how is CO2 carried in the blood
1. in solution (10%)
2. as bicarbonate
3. carbamino compounds
104
describe the process of CO2 transport through the blood as a bicarbonate
this process occurs in RBC
| water reacts with CO2 to from carbonic acid which dissociates into a H+ ion and a bicarb ion
105
describe the process of CO2 transport through the blood as a carbamino compound
formed by the combination of CO2 with terminal amine groups in blood proteins
very RAPID formation (even without enzymes)
106
how is the MAJORITY of CO2 transported in the blood
as a bicarbonate
107
what is the Haldane effect
removing O2 from Hbincreases the ability of Hb to pick up CO2 and H+ generated by CO2
108
how does the Bohr and Haldane effect work together
they work in SYNCHRONY to facilitate O2 liberation and uptake of CO2 and H+ generated by CO2 at tissues
109
How is CO2 liberation at the lungs facilitated
Hb picks up O2 at the lungs which WEAKENS its ability to bind to CO2 and H+ generated by CO2
110
state the location of the respiratory centres and their function
```
medulla = major rhythm generator
pons = neurones here modify the rhythm
```
111
what happens when the pneumatic centre is stimulated
inspiration is terminated
112
what causes pneumatic centre stimulation
dorsal respiratory neurones firing
113
what is the role of the pneumatic centre
prevents breathing becoming prolonged inspiratory gasps with brief expiration
114
how is inspiration terminated
pneumatic centre is stimulated by dorsal neurones firing
115
how is inspiration prolonged
apneustic centre is stimulated leading to excitement of inspiratory area of the medulla
116
what does apneustic centre stimulation cause
excitement of inspiratory are of medulla causing prolonged inspiration
117
where is the rhythm of breathing generated
medulla
118
where is the rhythm of breathing modified
pons
119
how is active breathing established (role that neurones play)
increased firing from dorsal neurones excites a second group of ventral respiratory group neurones which excites the internal intercostal and abs to create forceful expiration
120
how is tidal breathing established (role that neurones play)
pre-botzinger complex generates the rhythm, dorsal respiratory group neurones are excited and fire in bursts which causes contraction of inspiratory muscles. (inspiration)
when firing stops, the muscle relaxes (passive expiration)
121
what is the rhythm generated by (_____ complex)
pre-botzinger complex
122
what external stimuli are capable of influencing the respiratory centres
higher brain centres = cerebral cortes, limbi system, hypothalamus
stretch/joint/baro- receptors
123
what role do stretch receptors play in breathing
prevent over-inflation of lungs
124
what role do joint receptors play in breathing
detect change in movement which will cause a change in ventilation required
125
what role do baroreceptors play in breathing
decreased BP results in increased ventilatory rate
126
where are the peripheral chemoreceptors located
on carotid bodies at carotid bifurcation
| on aortic bodies on the superior aspect of the arch of the aorta
127
where are the central chemoreceptors located
near the surface of the medulla
128
what are the central chemoreceptors stimulated by
[H+] of the cerebrospinal fluid
129
what are the peripheral chemoreceptors stimulated by
tension of O2 and CO2 in blood
| [H+] in blood
130
what are the acute responses to hypoxia
hyperventilation
| increased CO2
131
what are the chronic adaptions to hypoxia
```
increased RBC production
increased2,3-BPG production
increased number of capillaries
increased number of mitochondria
kidneys conserve acid
```
132
how would a rise in arterial [H+] effect ventilation
ventilation would increase (acid-base balance)
133
how would a drop in arterial [H+] effect ventilation
ventilation would decrease (acid-base balance)
134
how would a severe drop in arterial PO2 effect ventilation
severe hypoxia depresses respiratory centre causing decreased ventilation
135
how would a drop in arterial PCO2 effect ventilation
ventilation would increase (acid-base balance)
