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Respiratory > Physiology > Flashcards

Physiology Flashcards

1
Q

what is internal respiration

A

the internal mechanisms that consume O2 and produce CO2

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2
Q

what is external respiration

A

the sequence of events that leads to the exchange of O2 and CO2 between external environments and the cells of the body

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3
Q

identify the four steps of external respiration

A

ventilation, gas exchange between alveoli and blood, gas transport in the blood, gas exchange at the tissue level

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4
Q

describe ventilation

A

the mechanical process of moving gas in and out of the lungs- from atmosphere to alveolar sacs

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5
Q

what blood vessels involved in gas exchange with alveoli

A

pulmonary capillaries

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6
Q

what blood vessels involved in gas exchange with tissues

A

systemic capillaries

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7
Q

what is the first step of external respiration

A

ventilation

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8
Q

what is boyle’s law

A

at any constant temperature the pressure of the gas varies inversely with the volume of the gas

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9
Q

how does boyle’s affect ventilation

A

gases will move from higher to lower pressures

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10
Q

what two factors holds the lungs to the thoracic walls

A

intrapleural fluid cohesiveness (water molecules in intrapleural fluid are attracted to each other and resist bring separated), the negative intrapleural pressure (the sub-atmospheric intrapleural pressures create a transmural pressure gradient across lung and chest wall)

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11
Q

what is the significance of the transmural pressure gradient against the lung and chest walls (2)

A

holds them together, pushing lungs out and chest inwards, also pressure play role in ventilation

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12
Q

how can you calculate the transmural pressure gradient across lung wall (transpulmonary pressure)

A

intra-alveolar (intrapulmonary) pressure - intrapleural (intrathoracic) pressure

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13
Q

how can you calculate the transmural pressure gradient across thoracic wall

A

atmospheric pressure - intrapleural (intrathoracic) pressure

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14
Q

describe the three pressures in relation to each other before inspiration

A

intra-alveolar pressure equal to atmospheric pressure and greater than intra-pleural pressure

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15
Q

what must happen for air to flow into the lungs during inspiration?

A

the intra-alveolar pressure must be less than the atmospheric pressure

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16
Q

describe the process of inspiration

A

thorax and lungs expand as a result of contraction of inspiratory muscles decreasing the intra-alveolar pressure (air then enters lung until atmospheric pressure is regained)

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17
Q

explain the significance of the transmural pressure gradient across the lung and chest wall

A

allows lung expansion and prevents collapsing of the lung

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18
Q

describe the process of expiration

A

the relaxation of inspiratory muscles which causes the recoiling of the lungs and the intra-alveolar pressure to fall back to an atmospheric level

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19
Q

inspiration and (normal resting) expiration- passive or active processes

A

inspiration active

expiration passive

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20
Q

what is a pneumothorax

A

air in the pleural space

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21
Q

what does a pneumothorax abolish

A

the transmural gradient needed for lung expansion

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22
Q

what does a pneumothorax lead to and produce symptom wise

A

lung collapse, shortness of breath and chest pain

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23
Q

what are the physical signs of a pneumothorax (2)

A

hyperresonant percussion note, decreased/ absent breath sounds

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24
Q

what muscles are involved with normal resting breathing

A

diaphragm - major inspiratory muscle; increases vertically the volume of the thorax by contracting

external intercostal muscle- contraction lifts ribs out and moves out the sternum; bucket handle

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25
Q

what allows the lungs to recoil

A

their elastic nature

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26
Q

what gives the lungs their elastic nature (2)

A

elastic connective tissue and alveolar surface tension

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27
Q

what is alveolar surface tension made of

A

the attraction between water molecules at liquid air interface in alveoli produces a force that resists the stretching of the lungs

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28
Q

what is pulmonary surfactant

A

a complex mixture of lipids and proteins secreted by type 2 alveoli

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29
Q

what is the role of pulmonary surfactant

A

lowers alveolar surface by interspersing between the water molecules lining the alveoli

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30
Q

why is pulmonary surfactant so important

A

prevents smaller alveoli collapsing and releasing air into larger alveoli

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31
Q

describe the Law of LaPlace

A

refers to alveolar stability- smaller alveoli with smaller radii have higher tendency to collapse

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32
Q

describe alveolar interdependence

A

when an alveoli starts to collapse the surrounding alveoli are stretched then recoil exerting expanding forces in the collapsing alveolus to open it

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33
Q

what are the major inspiratory muscles

A

the diaphragm and external intercostal muscles

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34
Q

what are the accessory muscles of inspiration and when are they used

A

sternocleidomastoid, scalenus, pectoral - forceful inspiration

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35
Q

what are the muscles of active respiration

A

abdominal muscles and internal intercostal muscles

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36
Q

what is tidal volume (TV)

A

volume of air entering or leaving lungs in a single breath

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37
Q

what is inspiratory reserve volume (IRV)

A

extra volume of air that can be maximally inspired over and above the resting tidal volume

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38
Q

what is reserve volume (ERV)

A

extra volume of air that can be actively expired via maximal contraction beyond the normal volume of air after a resting tidal volume

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39
Q

what is residual volume (RV)

A

Minimum volume of air remaining in lungs after even a maximal expiration

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40
Q

what is inspiratory capacity (IC)

A

maximal volume of air that can be inspired after a normal resting expiration

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41
Q

how can inspiratory capacity be calculated

A

IRV + TV

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42
Q

what is functional residual capacity (FRC)

A

volume of air in lungs after normal passive expiration

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43
Q

how is functional residual capacity calculated

A

ERV + RV

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44
Q

what is vital capacity

A

maximal volume of air that can be moved out of the lungs during a single breath following a maximal expiration

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45
Q

how is vital capacity calculated

A

IRV + TC + ERV

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46
Q

what is total lung capacity

A

total volume of air the lungs can hold

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47
Q

how is total lung capacity calculated

A

VC + RV

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48
Q

what volume cannot be measured by spirometry

A

residual volume (and therefore total volume)

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49
Q

when does residual volume increase

A

when the elastic recoil of the lungs is lost

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50
Q

what curve is used in spirometry

A

volume time curve

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51
Q

what is a forced vital capacity

A

maximum volume of air that can be forcibly expelled from the lungs after a maximum inspiration

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52
Q

what is forced expiratory volume in one second (FEV1)

A

volume of air that can be expelled during the first second of a forced vital capacity determination

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53
Q

what is the FEV1/FVC ratio and its usual value

A

proportion of forced vital capacity that can be expired in the first second (>70%)

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54
Q

what are the dynamic lung volumes

A

FVC, FEV1

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55
Q

what are dynamic lung values useful in diagnosing

A

obstructive and restrictive lung disease

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56
Q

what is the usual value for the FEV1/FVC and curve in obstructive lung disease

A

<70%

curve; same maximal value (FVC) but less steep curve

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57
Q

what is the usual value for the FEV1/FVC in restrictive lung disease

A

normal (>70%)

curve; same steepness, lower maximal value

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58
Q

what is the primary determinant of airway resistance?

A

radius of the conducting airway

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59
Q

what does parasympathetic stimulation cause in the airways

A

bronchoconstriction

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60
Q

what does sympathetic stimulation cause in the airways

A

bronchodilation

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61
Q

what is more difficult, expiration or inspiration

A

expiration

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62
Q

during inspiration what pulls the airways open

A

the thorax

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63
Q

what happens to intrapleural pressure during inspiration

A

it decreases

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64
Q

what happens to intrapleural pressure during expiration

A

it increases

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65
Q

what do the lungs do during expiration

A

recoil

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66
Q

what is dynamic airway compression

A

when rising pleural pressure during active expiration compresses the alveoli and airway

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67
Q

what does dynamic airway compression result in

A

make expiration more difficult in patients with airway obstruction

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68
Q

does dynamic airway compression cause problems in normal people

A

nope

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69
Q

describe how dynamic airway compression is beneficial in healthy individuals

A

increased airway resistance increases the upstream airway pressure which helps open airways by increasing the driving pressure between the alveoli and airways

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70
Q

give two examples of airway obstructions

A

asthma, COPD

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71
Q

what happens to the driving pressure when there is an airway obstruction

A

driving pressure between alveolus and airway is lost over obstructed segment

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72
Q

what does the loss in driving pressure result in

A

a fall in the airway pressure downstream

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73
Q

what does a fall in airway pressure downstream lead to

A

airway compression by the rising pleural pressure during active expiration

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74
Q

are diseased airways more likely to collapse

A

yes

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75
Q

what makes airway obstruction worse

A

if the patient also has decreased elastic recoil of lungs

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76
Q

what causes reduced elastic recoil (2)

A

emphysema, obstructed airway caused by COPD

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77
Q

what is the peak flow meter used to measure and in what patients

A

peak flow rate in patients with obstructive lung disease

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78
Q

what is the compliance of the lungs

A

measure into the effect that has to go into stretching or distending of the lungs

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79
Q

what is pulmonary compliance measured in

A

volume change per unit of pressure change across the lungs

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80
Q

less compliant = more/less effort?

A

more

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81
Q

what can decrease lung compliance (5)

A

pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia, absence or surfactant

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82
Q

what symptoms can decreased lung compliance produce

A

shortness of breath

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83
Q

how can decreased pulmonary compliance show in spirometry

A

restrictive pattern of lung volume (restrictive lung disease)

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84
Q

what can cause increased pulmonary compliance

A

if the elastic recoil of the lungs is lost- emphysema

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85
Q

what does increased lung compliance result in for the patients

A

hyperinflation of the lungs- harder to get air out

86
Q

what is work of breathing

A

energy expended on breathing

87
Q

what four factors can increase work of breathing

A

decreased pulmonary compliance, increased airway resistance, decreased elastic recoil, need for increased ventilation

88
Q

what is pulmonary ventilation

A

the volume of air breathed in and out per minute

89
Q

what is alveolar ventilation

A

volume of air exchanged between the atmosphere and alveoli per minute (represents new air available for gas exchange with blood)

90
Q

what is anatomical dead space

A

parts of airways where the air is not available for gas exchange

91
Q

how do you calculate pulmonary ventilation

A

(in liters) tidal volume x respiratory

92
Q

is alveolar ventilation greater or smaller than pulmonary

A

less because of dead space

93
Q

how do you calculate alveolar ventilation

A

(tidal volume - dead space volume) x respiratory rate

94
Q

how do you increase pulmonary ventilation

A

increase depth and rate of breaths

95
Q

what method of increasing pulmonary ventilation is more advantageous, why?

A

depth because of dead space

96
Q

what is the definition of ventilation

A

rate at which gas is passing through the lungs

97
Q

what is the definition of perfusion

A

the rate at which blood is passing through the lung

98
Q

which part of the lung has better blood flow and ventilation

A

bottom

99
Q

what is alveolar dead space

A

ventilated alveoli that are not adequately perfused with blood

100
Q

what is physiological dead space

A

anatomical dead space and alveolar dead space

101
Q

when could alveolar dead space become significantly increased

A

during disease

102
Q

what matches airflow to blood supple in the lungs

A

local controls that act on the smooth muscles of airways

103
Q

increased perfusion leads to what which then causes what

A

accumulation of CO2 in alveoli

decreases airway resistance leading to increased airflow

104
Q

what does increased ventilation cause and then lead to

A

increase in alveolar O2 concentration

pulmonary vasodilation which increases blood flow

105
Q

what are the four factors that influence gas transfer across the alveolar membrane

A

partial pressure gradient of O2 and CO2,
diffusion coefficient of CO2 and O2,
Surface area of alveolar membrane,
thickness of alveolar membrane

106
Q

what does the partial pressure of a gas determine

A

the pressure gradient of that gas

107
Q

why is a partial pressure gradient important

A

how gases move (across membranes etc)

108
Q

what is partial pressure

A

the pressure that that gas would exert if it occupied the total volume in absence of all the other gases in the mixture (for non reactive mixtures)

109
Q

what is daltons law of partial pressures

A

the total pressure exerted by a gaseous mixture = the sum of all the partial pressures of the components of the mixture

110
Q

what is the alveolar gas equation

A

PAO2 = PiO2 - (PaCO2 /0.8)

111
Q

what does PAO2 represent

A

partial pressure of O2 in alveolar air

112
Q

what does PiO2 represent

A

partial pressure of O2 in inspired air

113
Q

what does PaCO2 represent

A

partial pressure of CO2 in arteriole blood

114
Q

what does 0.8 represent

A

respiratory exchange ratio (ratio of CO2 produced/ O2 consumed)

115
Q

do gases move from higher to lower/ lower to higher partial pressures

A

higher to lower

116
Q

why is the partial pressure gradient for CO2 much smaller than that of O2

A

CO2 more soluble in membranes

117
Q

what is the diffusion coefficient of a gas

A

measure of the solubility of a gas in a membrane

118
Q

is the diffusion coefficient of CO2 bigger or smaller than that of O2

A

bigger (20x)

119
Q

what is the difference between PAO2 and PaO2

A 
A = alveolar 
a = arterial
120
Q

why is there a gradient between PaO2 and PAO2 (is it normal)

A

small gradient normal as ventilation-perfusion not perfect

big gradient would indicate problems with gas exchange in the lungs or a right to left shunt in the heart

121
Q

what features of lungs facilitate effective gas exchange

A

large surface area and thin membranes

122
Q

how is surface area of airways increased

A

airways divide repeatedly

123
Q

where does the entire cardiac output go to

A

pulmonary circulation

124
Q

what is ficks law of diffusion

A

the amount of gas that moves across a sheet of tissue per unit time is proportional to the area of the sheet but inversely proportionate to its thickness

125
Q

describe alveoli

A

thin walled inflatable sacs, closely spaced

126
Q

what do alveolar walls consist of

A

a single layer of flattened type one alveolar cells

127
Q

what encircles each alveolus

A

pulmonary capillaries

128
Q

what are the 7 non respiratory functions of the respiratory system

A 
route for water and heat loss,
enhances venous return,
helps maintain normal acid-base balance,
enables vocalisations.
defends against inhaled foreign matter,
nose- organ of smell,
removes, modifies, activates or inactivates various materials passing through the pulmonary circulatory system
129
Q

what is Henry’s law

A

the amount of gas that dissolves in a liquid is proportional to the partial pressure of the gas at equilibrium with the liquid

130
Q

as a result of henry’s law if the partial pressure of the gas phase what would happen to the concentration of the gas in liquid phase

A

would increase proportionally

131
Q

how is oxygen carried in the blood (2)

A

dissolved in blood, bound to haemoglobin in red blood cells,

132
Q

when is haemoglobin considered fully saturated

A

when all Hb present is carrying maximum O2 load

133
Q

how many Hb units in one molecule of haemoglobin

A

4

134
Q

what is the primary factor that determines the percentage saturation of haemoglobin with O2

A

PO2

135
Q

describe the shape of the O2-Hb dissociation curve

A

sigmoid shape

136
Q

what is the significance of the sigmoid shape (2)

A

flatter upper proportions means that a moderate fall in alveolar PO2 will not much affect oxygen loading, sites become occupied

steep lower part means that the peripheral tissues get a lot of oxygen for a small drop in capillary PO2, cooperativity

137
Q

what is oxygen delivery to tissues a function of

A

oxygen content of arterial blood and cardiac output

138
Q

how to you calculate oxygen delivery index

A

DO2I = CaO2 x CI (cardiac index (cardiac output to body surface area))

139
Q

what determines the O2 content of the arterial blood

A

concentration of haemoglobin and percentage saturation of haemoglobin with O2

140
Q

what affects the delivery of O2 to the tissues

A

respiratory disease, heart failure or anaemia

141
Q

how do you calculate the oxygen content of arterial blood

A

CaO2 = 1.34 (one gram of Hb carries 1.34 ml of oxygen whenn fully saturated) x (conc of Hb) x SaO2 (Hb saturated with O2)

142
Q

how can respiratory disease decrease oxygen delivery

A

decrease arterial PO2 and therefore Hb saturation with O2

143
Q

how does heart failure impair oxygen delivery

A

decreases cardiac output

144
Q

how is the bohr effect seen on a O2-Hb dissociation curve

A

shift to the right

145
Q

what is the bohr effect

A

increased release of O2 by conditions at the tissues

146
Q

what conditions cause the bohr effect (4)

A

increases in carbon dioxide partial pressure in the blood, decrease in blood ph, increased in temperature, increase in 2,3-Biphosphoglycerate

147
Q

how is foetal haemoglobin (HbF) different to adult haemoglobin (HbA) (2)

A

in structure (two alpha and two beta subunits) and affinity (higher) for O2

148
Q

what does a foetal O2-Hb dissociation curve look like compared to normal

A

shifted to the left due to higher affinity

149
Q

why does HbF have a higher affinity for O2

A

as interactes with 2,3-Biphosphogylcerate

150
Q

what is the significance of HbF’s higher affinity for O2

A

allows transfer of of oxygen from mother to foetus even when the PO2 is low

151
Q

whats the difference between O2-Hb and O2-myoglobin dissociation curves

A

O2-myoglobin curve is hyperbolic

152
Q

explain the shape of the O2-myoglobin curve

A

only one haem group- no cooperation, releases O2 at very low PO2- short term storage during anaerobic conditions

153
Q

how is CO2 carried in the blood (give percentages for each carriage)

A

solution (10%), as bicarbonate (HCO3-) (60%), as carbamino-haemoglobin (30%)

154
Q

describe bicarbonate formation

A

CO2 diffuses into r.b.c. and reacts with water and is converted into carbonic acid by carbonic anhydrase. Carbonic acid then dissociates into hydrogen ions and bicarbonate (HCO3-). Chlorine shift replaces the HCO3- with chlorine from outside the cell resulting in the release of bicarbonate into blood.

155
Q

what are carbamino compounds made of

A

CO2 + terminal amine groups in blood proteins

156
Q

what is the amino group in carboamino-haemoglobin

A

globin

157
Q

what is the role of Hb in blood buffering

A

binds with the hydrogen ions forms in bicarbonate formation

158
Q

describe the CO2 dissociation curve

A

linear compared to O2-Hb dissociation

159
Q

what is the haldane effect

A

removing O2 from Hb increases Hb’s ability to pick up CO2 and CO2 generated H+

160
Q

how does the haldane affect show on CO2 dissociation curves

A

oxygen shifts the curve to the right

161
Q

how does the haldane effect work in synchrony with the Bohr effect and what is the result

A

as the bohr effect facillitates the removal of O2 from Hb at a tissue level and pushes the O2 disscoiation curve to the right. Thus Bohr liberates O2 and helps in the uptake of CO2

162
Q

how is the liberation of CO2 facilitated at the lungs

A

as where Hb binds to O2 thus weakening its ability to bind to CO2 and H+

163
Q

what generates the rhythm of breathing and where is it located

A

the pre-botzinger complex. located near upper end of medulla respiratory complex

164
Q

what is the pre-botzinger complex

A

a network of neurons

165
Q

what part of the medulla is thought to control the rhythm of breathing

A

the medulla oblongata

166
Q

what is excited when rhythm is generated by the pre-botzinger complex

A

the dorsal respiratory group neurons

167
Q

what happens when the dorsal respiratory group neurons fire in bursts

A

contraction of inspiratory muscles- inspiration

168
Q

what happens when firing of the dorsal neurons stops

A

passive expiration

169
Q

what does increased firing from the dorsal neurons excite

A

the ventral respiratory group neurons

170
Q

what does the excitation of the ventral respiratory neuron group lead to

A

stimulation of internal intercostals, abdominal = forceful expiration

171
Q

what is thought to modify the rhythm of breathing

A

neurons in the pneumotaxic centre of the pons

172
Q

what does stimulation of the pneumotaxic centre cause

A

terminates inspiration

173
Q

when is the pneumotaxic centre stimulated

A

when dorsal respiratory neurons fire

174
Q

name and describe the condition which would result from a lack of modification of rhythm

A

apneusis- breathing is prolonged inspiratory gasps with brief expiration

175
Q

what do impulses from the apneustic centre excite and result in

A

inspiratory area of medulla, prolonged expiration

176
Q

name the stimuli that influences respiratory centres from its description;
cerebral cortex, limbic system, hypothalamus

A

higher brain centres

177
Q

name the stimuli that influences respiratory centres from its description;
guard against hyperinflation

A

stretch receptors in the walls of the bronchioles and bronchi

178
Q

name the stimuli that influences respiratory centres from its description;
stimulated by pulmonary capillary congestion, pulmonary oedema and pulmonary emboli

A

Juxtapulmonary (J) receptors

179
Q

name the stimuli that influences respiratory centres from its description;
stimulated by joint movement

A

joint receptors

180
Q

name the stimuli that influences respiratory centres from its description;
increased respiratory rate due to drop in blood pressure

A

baroreceptors

181
Q

what is the hering-breuer reflex

A

activated during inspiration, afferent discharge inhibits inspiration

182
Q

how do impulses from moving limbs affect breathing

A

increase

183
Q

list the 5 factors that could increase ventilation during breathing

A

body movement reflexes, adrenaline, cerebral cortex impulses, increase in body temp, (later) accumulation of CO2 and H+ generated by muscles

184
Q

what is the cough reflex triggered by

A

irritations of airways or tight airways

185
Q

what does afferent discharge stimulate

A

short intake of breath, closure of the larynx, contraction o abdominal muscles, opening of larynx ans expulsion of air

186
Q

what is the chemical control of respiration an example of

A

negative feedback control system

187
Q

what are the controlled variables in the negative feedback system of the chemical control of respiration

A

blood gas tensions, especially CO2

188
Q

what do chemoreceptors sense

A

values of gas tension

189
Q

where are peripheral chemoreceptors located

A

in the carotid and aortic bodies

190
Q

what do peripheral chemoreceptors sense

A

tension of oxygen and CO2, and H+ conc in the blood

191
Q

where are the central chemoreceptors located

A

near the surface of the medulla in the brain stem

192
Q

what do central chemoreceptors respond to

A

H+ conc of the cerebrospinal fluid (CSF)

193
Q

how is the cerebrospinal fluid separated from the blood

A

via the blood brain barrier

194
Q

describe the relative permeability of CO2, H+ and HCO3-

A

impermeable to H+ and HCO3-

CO2 diffuses readily

195
Q

why is CSF less buffered than blood

A

as contains less proteins

196
Q

what does hypercapnia result in

A

an increase in ventilation

197
Q

at what level of PO2 are peripheral chemoreceptors stimulated and what does this result in

A

> 8 kPa increase in ventilation

198
Q

what does partial pressure of inspired oxygen depend on

A

total pressure and proportion of oxygen in gas mixture

199
Q

what is hypoxia at high altitudes caused by

A

decreased partial pressure of inspired oxygen

200
Q

what is the acute response to hypoxia

A

increased ventilation and cardiac output

201
Q

list the chronic adaptations to high altitude hypoxia (5)

A

increased RBC production, 2,3-Biphosphoglycerate produced within RBC (eases O2 offloading to tissues), increased number of capillaries, increased number of mitochondria (more efficient use of O2, kidneys conserve acid (increasing arterial pH)

202
Q

how to peripheral chemoreceptors adjust acidosis

A

via the addition of non carbonic acid H+ to the blood

203
Q

what are the physical effect of stimulation of the peripheral chemoreceptors by H+

A

hyperventilation to increase elimination of CO2

204
Q

can CO2 generate H+

A

yes

205
Q

what does the elimination of CO2 also result in

A

a reduction of the H+ load in the body

206
Q

what is the dominant control of ventilation

A

arterial PCO2

207
Q

when does arterial PO2 affect central chemoreceptors

A

severe hypoxia depresses respiratory centre

208
Q

why does arterial H+ only affect the peripheral not central chemoreceptors

A

as H+ cannot cross blood brain barrier

209
Q

hoe does 2,3 BPG affect an O2-Hb dissociation curve

A

shifts it to the right

210
Q

what might become important for people with chronic CO2 retention

A

hypoxic drive

Respiratory (26 decks)

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