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Respiratory > Physiology > Flashcards

Physiology Flashcards

1
Q

what is internal respiration?

A

refers to the intercellular mechanisms which consumes O2 and produces CO2.

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2
Q

what is external respiration?

A

refers to the sequence of events that lead to the exchange of O2 and CO2 between external environment and the cells of the body.

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3
Q

what are the four steps of external respiration?

A

1) ventilation - process of moving gas in and out the lungs
2) gas exchange between alveoli and blood in the pulmonary capillaries
3) gas transport in the blood between lungs and tissues
4) gas exchange at the tissue level

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4
Q

what is Boyle’s Law?

A

at any constant temperature the pressure exerted by a gas varies inversely with the volume of the gas. Gases move from a higher to lower pressure.

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5
Q

what happens during ventilation?

A

air flow down a pressure gradient from a region of a high pressure to a region of low pressure. during inspiration the thorax and lungs expand as a result of contraction of inspiratory muscle. as the volume of the gas increases the pressure by the gas decreases.

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6
Q

what two forces hold the thoracic wall and the lungs in close opposition?

A

1) the intrapleural fluid cohesiveness - water molecules in the intrapleural fluid are attracted to each other and resist being pulled apart. So the pleural membranes tent to stick together.
2) the negative intrapleural pressure - the sub-atmospheric intrapleural pressure create a transmural pressure gradient across the chest wall. so the lungs are forced to expand outwards while the chest is forced to squeeze inwards.

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7
Q

what is the atmospheric pressure?

A

760mm Hg at sea level

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8
Q

what is the intra-alveolar (intrapulmonary) pressure?

A

760mm Hg at sea level - it is the pressure within the lung alveoli.

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9
Q

what is intrapleural (intrathoracic) pressure?

A

pressure exerted outside the lungs within the pleural cavity - usually less than atmospheric pressure.

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10
Q

what is inspiration?

A

an active process brought about by contraction of inspiratory muscles

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11
Q

what does the increase in size of the lungs do to the intra-alveolar pressure?

A

causes it to fall

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12
Q

what does air do during inspiration?

A

enters lungs down its pressure gradient until the intra-alveolar pressure becomes equal to atmospheric pressure

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13
Q

what is expiration?

A

Normal expiration is a passive process brought about by relaxation of inspiratory muscles

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14
Q

What does the recoil of the lungs do to the intra-alveolar pressure?

A

causes it to rise

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15
Q

what happens to air during expiration?

A

leave the lungs down its pressure gradient until the intra-alveolar pressure becomes equal to atmospheric pressure

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16
Q

what does pneumothorax do to the pressure gradient?

A

abolishes the transmural pressure gradient

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17
Q

what causes the lungs to recoil during expiration?

A
  • elastic connective tissue in the lungs

- alveolar surface tension

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18
Q

what is alveolar surface tension?

A

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

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19
Q

what would happen if the alveoli were lined with water alone?

A

the surface tension would be too strong so the alveoli would collapse

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20
Q

what is the law of LaPlace?

A

the smaller alveoli have a higher tendency to collapse

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21
Q

what is pulmonary surfactant?

A

complex mixture of lipids and proteins secreted by type II alveoli

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22
Q

what does pulmonary surfactant do?

A

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

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23
Q

How is respiratory distress syndrome caused?

A

developing fetal lungs cant make surfactant until late in pregnancy so premature babies may not have enough pulmonary surfactant, this causes respiratory distress syndrome as the baby makes very strenuous inspiratory efforts in an attempt to overcome the high surface tension and inflate the lungs.

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24
Q

what us alveolar interdependence?

A

if an alveolus start to collapse the surrounding alveoli are stretched and then recoil exerting expanding forces in the collapsing alveolus to open in.

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25
Q

what forces keep the alveoli open?

A
  • transmural pressure gradient
  • pulmonary surfactant
  • alveolar interdependance
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26
Q

which forces promote alveolar collapse?

A
  • elasticity of stretched lung connective tissue

- alveolar surface tension

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27
Q

what are the major inspiratory muscles?

A

diaphragm and external intercostal muscles

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28
Q

what are the accessory muscles of inspiration?

A

sternocleidomastoid, scalenus and pectoral

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29
Q

when do accessory muscles of inspiration contract?

A

during forceful inspiration

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30
Q

what are the muscles of active expiration?

A

abdominal muscles and internal intercostal muscles

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31
Q

what is tidal volume (TV)?

A

volume of air entering or leaving lungs during a single breath

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32
Q

what is inspiratory reserve volume (IRV)?

A

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

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33
Q

what is expiratory reserve volume (ERV)?

A

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

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34
Q

what is residual volume (RV)?

A

minimum volume of air remaining in the lungs even after a maximal expiration

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35
Q

what is inspiratory capacity (IC)?

A

maximum volume of air that can be inspired at the end of a normal quiet expiration (IC = IRV + TV)

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36
Q

What is functional residual capacity (FRC)?

A

volume of air in lungs at end of normal passive expiration (FRC = ERV + RV)

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37
Q

What is vital capacity (VC)?

A

maximum volume of air that can be moved out during a single breath following a maximal inspiration (VC = IRV + TV + ERV)

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38
Q

What is total lung capacity (TLC)?

A

total volume of air the lungs can hold (TLC = VC + RV)

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39
Q

When does residual volume increase?

A

when the elastic recoil of the lungs is lost e.g. in emphysema

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40
Q

what is FVC?

A

forced vital capacity - maximum volume that can be forcibly expelled from the lungs following a maximum inspiration

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41
Q

what is FEV1?

A

forced expiratory volume in one second - volume that can be expired during the first second of expiration in an FVC.

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42
Q

what is the FEV1/FVC ratio?

A

the proportion of the forced vital capacity that can be expired in the first second = (FEV1/FVC) x 100

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43
Q

what is the primary determinant of airway resistance?

A

radius of the conducting airway

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44
Q

what does parasympathetic stimulation cause?

A

bronchoconstriction

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45
Q

what does sympathetic stimulation cause?

A

bronchodilatation

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46
Q

what happens to intrapleural pressure during inspiration and expiration?

A

falls during inspiration, rises during expiration

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47
Q

what is dynamic airway compression?

A

the rising pleural pressure during active expiration compresses the alveoli and airway, this helps push the air out the lungs

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48
Q

what is pulmonary compliance?

A

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

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49
Q

what is pulmonary compliance decreased by?

A

pulmonary fibrosis, pulmonary oedema, lung collapse, pneumonia and absence of surfactant

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50
Q

when might pulmonary compliance be increased?

A

if elastic recoil of lungs is lost e.g. in emphysema. this results in patients having to work harder to get air out of lungs. compliance may also increase with age

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51
Q

when is work of breathing increased?

A
  • pulmonary compliance decreased
  • airway resistance increased
  • elastic recoil decreased
  • when there is a need for increased ventilation
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52
Q

how is pulmonary ventilation (L) calculated?

A

= tidal volume x respiratory rate

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53
Q

why is alveolar ventilation less than pulmonary ventilation?

A

because of anatomical dead space

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54
Q

how do you calculate alveolar ventilation?

A

= ( tidal volume - dead space volume) x respiratory rate

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55
Q

what is pulmonary ventilation?

A

volume of air breathed in and out per minute

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56
Q

what is alveolar ventilation?

A

volume of air exchanged between the atmosphere and alveoli per minute

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57
Q

why is more advantageous to increase depth of breathing rather than rate?

A

because of anatomical dead space

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58
Q

what does the transfer of gases between body and atmosphere depend on?

A

ventilation and perfusion

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59
Q

what is ventilation?

A

rate at which gas is passing through the lungs

60
Q

what is perfusion?

A

rate at which blood is passing through the lungs

61
Q

what is alveolar dead space?

A

ventilated alveoli which are not adequately perfused with blood

62
Q

what could happen to alveolar dead space in disease?

A

it could increase

63
Q

what is accumulation of CO2 in alveoli a result of? what does it do?

A

result of increased perfusion decreases airway resistance leading to increased airflow

64
Q

what is the increase in alveolar O2 a result of? what does it do?

A

a result of increased ventilation causes pulmonary vasodilation which increases blood flow to match larger airflow

65
Q

what happens when perfusion is greater than ventilation?

A
  • CO2 increases in area
  • dilatation of local airways
  • airflow increases
  • O2 decreases in area
  • constriction of local blood vessels
  • blood flow decreases
66
Q

what happens when ventilation is greater than perfusion?

A
  • CO2 decreases in area
  • constriction of local airways
  • airflow decrease
  • O2 increase in area
  • dilatation of local blood vessels
  • blood flow increases
67
Q

what is the effect of decreased O2 on pulmonary arterioles and systemic arterioles?

A

PA - vasoconstriction

SA - vasodilatation

68
Q

what is the effect of increased O2 on pulmonary arterioles and systemic arterioles?

A

SA - vasoconstriction

PA - vasodilatation

69
Q

which factors influence the rate of gas exchange across alveolar membrane?

A
  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
70
Q

what is Dalton’s law of partial pressures?

A

the total pressure exerted by a gaseous mixture = the sum of the partial pressures of each individual component in the gas mixture

71
Q

what is the partial pressure of gas in a mixture of gases that don’t react with each other?

A

the pressure that gas would exert if it occupied the total volume for the absence of other components

72
Q

what is the partial pressure of gas?

A

the pressure that one gas in a mixture of gases would exert if it were the only gas present in the whole volume occupied by the mixture at a given temperature

73
Q

what is the alveolar gas equation?

A

PAO2 = PiO2 - (PaCO2/0.8)

74
Q

what is the equation to work out the pressure of inspired air?

A

pressure of inspired air = atmospheric pressure - water vapour pressure

75
Q

what is the diffusion coefficient?

A

the solubility of gas in a membranes

76
Q

how much bigger is the diffusion coefficient for CO2 than O2?

A

20x

77
Q

what would a big gradient between PAO2 and PaO2 indicate?

A

problems with gas exchange in the lungs or a right to left shunt in the heart

78
Q

what is fick’s law of diffusion?

A

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

79
Q

what are alveoli?

A

thin-walled inflatable sacs, function in gas exchange, walls consist of a single layer of flattened type I alveolar cells

80
Q

what encircles each alveolus?

A

pulmonary capillaries

81
Q

what happens to gas transfer rate as the partial pressure gradient of O2 and CO2 increases?

A

increases

82
Q

what happens to gas transfer rate as the diffusion coefficient increases?

A

increases

83
Q

what happens to gas transfer rate as the surface area of alveolar membrane increases?

A

increases

84
Q

what happens to gas transfer rate as the thickness of alveolar membrane increases?

A

decreases

85
Q

what is Henry’s Law?

A

the amount of a given gas dissolve in a given type and volume of liquid (e.g. blood) at a constant temperature is proportional to the partial pressure of the gas in equilibrium with the liquid

86
Q

how is most oxygen in the blood transported?

A

bound to haemoglobin

87
Q

what are the two forms of oxygen present in the blood?

A
  1. bound to haemoglobin

2. physically dissolved (very little O2)

88
Q

how many haem groups does each haemoglobin have?

A

4

89
Q

what does each haem group do to one oxygen?

A

reversibly binds

90
Q

when is haemoglobin considered fully saturated?

A

when all the Hb present is carrying its maximum O2 load

91
Q

what is the primary factor which determines the percent saturation of haemoglobin with O2?

A

PO2

92
Q

how do you calculate oxygen delivery index (DO2I)?

A

= CaO2 (oxygen content in arterial blood) x Cl (cardiac index)

93
Q

what is O2 content of arterial blood determined by?

A

haemoglobin concentration and the saturation of Hb with O2

94
Q

How is oxygen content of arterial blood calculated (CaO2)?

A

= 1.34 x [Hb] x SaO2

95
Q

what can oxygen delivery to tissued be impaired by?

A

respiratory disease
decreased partial pressure of inspired oxygen (these can decrease arterial P02 and hence decrease Hb saturation with O2 and O2 content of the blood)

heart failure (decreases cardiac output)

aneamia (decreases Hb concentration and hence O2 Content of the blood)

96
Q

what is co-operatively of haemoglobin?

A

binding of one O2 increases the affinity of Hb for O2

97
Q

what is the Bohr effect?

A

a shift of the dissociation curve to the right

98
Q

which factors would shift the dissociation curve to the right?

A

increase PCO2
increase in [H+]
increase temperature
increase 2,3- biphsophoglycrate

99
Q

how does the structure of foetal haemoglobin differs from adult haemoglobin?

A

has 2 alpha and 2 gamma subunits

100
Q

why does O2 transfer from mother to foetus even if PO2 is low?

A

HbF has a higher affinity for O2

101
Q

where is myoglobin present?

A

skeletal and cardiac muscles

102
Q

how many haem groups per myoglobin?

A

one

103
Q

when does myoglobin release O2?

A

very low PO2

104
Q

what does presence of myoglobin in blood indicate?

A

muscle damage

105
Q

How is CO2 transported in the blood?

A 
as solution (10%)
As bicarbonate (60%)
as carbamino compounds (30%)
106
Q

which enzyme speeds up the formation of bicarbonate?

A

carbonic anhydrase

107
Q

where does the formation of bicarbonate occur?

A

red-blood cells

108
Q

how are carbamino compounds formed?

A

by combination of CO2 with terminal amine group in blood proteins

109
Q

what does globin of haemoglobin combine with carbon dioxide to form?

A

carboamino-haemoglobin

110
Q

what is the haldane effect?

A

removing O2 from Hb increases the ability of Hb to pick up CO2 and CO2 generated H+

111
Q

what does the bohr effect and the haldane effect work in synchrony to facilitate?

A

O2 liberation and uptake of CO2 and CO2 generated H+ at tissue

112
Q

which part of the brain is a major rhythm generator?

A

medulla

113
Q

what is the breathing rhythm generated by?

A

a network of neurones called the pre-botzinger complex

114
Q

what gives rise to inspiration?

A

rhythm generated by pre-botzinger complx
excites dorsal respiratory group neurones
fire in bursts
firing leads to contraction of inspiratory muscles - inspiration
when firing stops, passive expiration

115
Q

what is the ‘bucket handle’ mechanism?

A

external intercostal muscle contraction lifts the ribs and moves out the sternum

116
Q

what happens during hyperventilation?

A

inreased firing of dorsal neurones excites second group, ventral respiratory group neurones, excites internal intercostals, abdominals ect. this is forceful expiration

117
Q

what happens when the pneumotaxic centre (TC) is stimulated?

A

terminated inspiration

118
Q

when is the PC stimulated?

A

when dorsal respiratory neurones fire

119
Q

what is apneusis?

A

without PC, breathing is prolonged inspiratory gasps with brief expiration

120
Q

what does stimulation of the apneustic centre do?

A

impulses from these neuronws excite inspiratory area of medulla, prolong inspiration

121
Q

what can rhythm be modified by?

A

inputs from pons

122
Q

the respiratory centres are influenced by stimuli received from where?

A
  • higher brain centres
  • stretch receptors - the inflation of hering-breur reflex - guard against hyperinflation
  • juxtapulmonary receptors - stimulated by pulmonary capillary congestion and pulmonary oedema and pulmonary emboli
  • joint receptors
  • baroreceptors
123
Q

how is respiration chemically controlled?

A

central chemoreceptors

peripheral chemoreceptors

124
Q

what are joint receptor reflexes?

A

moving limbs reflexly increase breathing

125
Q

which factors increase ventilation during exercise?

A
  • reflexes originating from body movement
  • adrenaline release
  • impulses from the cerebral cortex
  • increase in body temperature
  • later: accumulation of CO2 and H+ generated by active muscles
126
Q

how is the cough reflex activated?

A

irritation of airways or tight airways

127
Q

what does the cough reflex do?

A

clears airways of dust, dirt or excessive secretions

128
Q

what happens during coughing?

A

short intake of breath
closure of larynx
contraction of abdominal muscles
opening of larynx and expulsion of air

129
Q

what are the controlled variables of chemical control of respiration?

A

blood gas tensions, especially CO2

130
Q

what do peripheral chemoreceptors do?

A

sense tension of oxygen and carbon dioxide and [H+] in the blood

131
Q

where are central chemoreceptors situated?

A

near the surface of the medulla of the brainstem

132
Q

what do central chemoreceptors respond to?

A

[H+] of the cerebrospinal fluid (CSF)

133
Q

what is hypoxia at high altitudes caused by?

A

decreased partial pressure of inspired oxygen (PiO2)

134
Q

what is the acute response to hypoxia at high altitudes?

A

hyperventilation and increased cardiac output

135
Q

what are the symptoms of acute mountain sickness?

A 
headache
fatigue
nausea
tachycardia
dizziness
sleep disturbance
exhaustion 
shortness of breath
unconsciousness
136
Q

what are the chronic adaptations to high altitude hypoxia?

A 
increase RBC production
increase 2,3 BPG produced within RBC
increase number of capillaries
increase number of mitochondria
kidneys conserve acid
137
Q

what is the arterial PCO2 effect on peripheral and central chemoreceptors?

A

weak stimulation of peripheral chemoreceptors, strong stimulation of central chemoreceptors

138
Q

what is the arterial PO2 effect on peripheral and central chemoreceptors?

A

effect on peripheral chemoreceptors only important if PO2 falls to <8kPa and effect on central chemoreceptors is severe hypoxia depresses respiratory centre

139
Q

what is the arterial [H+] effect on peripheral and central chemoreceptors?

A

peripheral chemoreceptors are stimulated and central chemoreceptors are not as H+ cannot cross the BBB

140
Q

what are type 1 pneumocytes?

A

very thin squamous cells which cover around 97% of the alveolar surface

141
Q

what are type 2 pneumocytes?

A

cuboidal cells
secrete sufactant
can differentiate into type 1 pneumocytes during lung damage

142
Q

what are club cells?

A

non-ciliated dome-shaped cells found in the bronchioles. they have varied roles including protecting against the deleterious effects of inhaled toxins and the secretion of glycosaminoglycans and lysozymes

143
Q

where are cell bodies of the preganglionic fibres located?

A

brainstem

144
Q

where are cell bodies of postganglionic fibres located?

A

in walls of the bronchi and bronchioles

145
Q

what does stimulation of parasympathetic postganglionic cholinergic fibres cause?

A
  • bronchial smooth muscle contraction mediated by M3 muscurinic ACh receptors on ASM cells
  • increased mucus secretion mediated by M3 muscarinic ACh receptors on gland (goblet) cells
146
Q

what does simulation of parasympathetic postganglionic noncholinergic fibres cause?

A

bronchial smooth muscle relaxation mediated by nitric oxide (NO) and vasoactive intestinal peptide (VIP)

147
Q

what does stimulation of sympathetic post-ganglionic fibres cause?

A
  • bronchial smooth muscle relaxation via beta2-adrenoceptors on ASM cells activated by adrenaline released from the adrenal gland
  • decreased mucus secretion mediated by beta2-adrenoceptors on goblet cells
  • increased mucociliary clearance mediated by beta2-adrenoceptors on epithelial cells
  • vascular smooth muscle contraction, mediated by alpha1-adrenoceptors on vascular smooth muscle

Respiratory (12 decks)

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