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X Physiology 1A > Respiratory System > Flashcards

Respiratory System Flashcards

1
Q

Define external respiration

A

the exchange of CO2 and O2 between the external environment and the cells of the body

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2
Q

where does external respiration take place?

A

in the lungs

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3
Q

what is atmospheric pressure value at sea level?

A

760 mmHg

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4
Q

what is partial pressure?

A

the amount an individual gas contributes to overall air pressure

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5
Q

how can partial pressure of a gas be calculated?

A

fraction of air that the gas you are considering equates to x total air pressure

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6
Q

what do partial pressures define?

A

amount of o2 or other gas present in the lungs, blood or veins

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7
Q

What to PA, Pa and Pv stand for?

A

PA: Partial pressure in lungs/alveoli
Pa: Partial pressure in blood (arteries)
Pv: Partial pressure in veins

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8
Q

what factor must be considered when calculating partial pressures within the lungs?

A

water vapour is a gas so contributes to total atmospheric pressure

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9
Q

what is the partial pressure of water within the lungs?

A

47mmHg

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10
Q

what sort of muscle is the diaphragm formed from?

A

sheet of skeletal muscle

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11
Q

what two body cavities are separated by the diaphragm?

A

thoracic and abdominal

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12
Q

what nerve innervates the diaphragm?

A

phrenic nerve

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13
Q

when does the diaphragm contract (flatten)?

A

during inspiration

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14
Q

what is the chest wall formed from?

A

muscle and ribs

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15
Q

what do accessory muscles in the chest wall do?

A

lift ribs and sternum

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16
Q

name two accessory muscles in the chest wall

A

sternomastoid

scalene

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17
Q

what muscles contract during quiet inspiration?

A

diaphragm

external intercostals

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18
Q

what muscles contract during forceful inspiration?

A

diaphragm
external intercostals
accessory muscles

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19
Q

what muscles relax during quiet expiration?

A

diaphragm

external intercostals

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20
Q

what muscles are involved during forceful expiration?

A

diaphragm relaxes
internal intercoastals contract
abdominal muscles contract

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21
Q

what do change do chest movements lead to?

A

volume change

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22
Q

what happens to the chest volume during inspiration?

A

increases, leads to reduced pressure so air floods in

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23
Q

what happens to the chest volume during expiration?

A

reduced chest volume, increased pressure

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24
Q

what is the name of the membranes that covers the chest wall?

A

pleural membranes

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25
Q

what are the 2 types of pleural membranes?

A

parietal (chest wall)

visceral (lungs)

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26
Q

what fluid do membranes secrete?

A

intrapleural fluid to provide lubricaition

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27
Q

what are the 2 airway zones?

A

conducting zone

respiratory zone

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28
Q

what happens in the conducting zone?

A

movement of air into and out of lungs, no gas exchange

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29
Q

what happens in the respiratory zone?

A

gas exchange

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30
Q

what muscle is the airway made from?

A

smooth muscle

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31
Q

what changes resistance to airflow in the lungs?

A

changes in diameter of the conducting airways

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32
Q

what happens if the airway diameter dilates?

A

resistance to airflow will be reduced

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33
Q

what does contraction of airway smooth muscle cause?

A

narrowing (constriction) of airways

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34
Q

what body system is contraction and relaxation of airway smooth muscle influenced by?

A

autonomic nervous system

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35
Q

where within the lungs is most of the resistance to airflow?

A

upper airway (50-70%)

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36
Q

what are lungs held open by?

A

elasticity of lung tissue

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37
Q

what are the functional units of the lung?

A

alveoli

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38
Q

what are alveoli surrounded by?

A

sheet like capillaries

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39
Q

what type of cells is the alveolar wall formed of?

A

type 1 pneumocytes

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40
Q

what cells produce surfactant?

A

type 2 pneumocytes

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41
Q

what is the role of surfactant in lungs?

A

helps to stop the lung from collapsing and reduce the surface tension of fluid in the lungs

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42
Q

what is the driving force for the flow of air into and out of the lungs?

A

the difference between atmospheric pressure at the mouth and pressure within the alveoli

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43
Q

changes in which pressure determines the direction of airflow?

A

alveolar pressure

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44
Q

why does alveolar pressure determine the direction of airflow in and out of the lungs?

A

as atmospheric pressure is usually constant

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45
Q

in inspiration is the pressure greater in the lungs or the atmosphere?

A

greater in atmosphere

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46
Q

in expiration is the pressure greater in the lungs or the atmosphere?

A

greater in the lungs

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47
Q

what effect does movement of the ribs and diaphragm during inspiration have on the volume of the thoracic cavity?

A

increases

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48
Q

what effect does movement of the ribs and diaphragm during inspiration have on the intra-alveolar pressure?

A

decreases

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49
Q

why is inspiration phase active?

A

it requires muscles to achieve

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50
Q

what point must be reached to stop air flowing into the lungs

A

alveolar pressure reaches atmospheric pressure (PB)

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51
Q

what effect does movement of the ribs and diaphragm during expiration have on the volume of the thoracic cavity?

A

decreases

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52
Q

what effect does movement of the ribs and diaphragm during expiration have on the intra-alveolar pressure?

A

increases it

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53
Q

during quiet ventilation is the expiration phase passive or active?

A

passive

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54
Q

what does passive expiration depend on?

A

elastic recoil of lungs

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55
Q

when does air flowing out of lungs during expiration cease?

A

when alveolar pressure equals atmospheric pressure(PB)

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56
Q

is forceful ventilation active or passive?

A

active as it involves contraction of accessory expiratory muscles

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57
Q

what causes volume changes during respiration?

A

chest movements

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58
Q

what are the muscles of inspiration?

A

external intercostals

diaphragm

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59
Q

what is the diaphragm shaped like?

A

a parachute/dome

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60
Q

what shape does the diaphragm become on contraction?

A

flat

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61
Q

when the diaphragm flattens on inspiration what effect does this have on the thoracic and abdominal (visceral) cavity?

A

increases thoracic volume

displaces viscera caudally (downwards)

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62
Q

what are the 2 types of intercostal muscle?

A

external and internal

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63
Q

what are the two major accessory muscles of breathing?

A 
scalene (within the neck)
abdominal muscles (pressurize abdomen)
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64
Q

what are the 4 pressures that need to be considered during the breathing cycle?

A

atmospheric
intra-alveolar
intrapleural
transmural

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65
Q

what is intra-alveolar pressure?

A

pressure in lungs

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66
Q

what is intrapleural pressure?

A

pressure between lungs and chest wall

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67
Q

what is transmural pressure?

A

the difference between intra-alveolar and intrapleural pressure

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68
Q

when is lung tissue stretched?

A

at all times even after full expiration

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69
Q

is the chest wall compressed or stretched at resting lung volumes?

A

compressed

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70
Q

what are the opposing forces which contribute to intrapleural pressure?

A

outward recoil of chest

inward recoil of ‘elastic’ lungs

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71
Q

why do outward recoil of chest and inward recoil of ‘elastic’ lungs oppose each other?

A

because lungs and chest wall are attached

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72
Q

how is negative pressure in the pleural space produced?

A

force of elastic recoil of lung and chest wall oppose creating negative pressure in intrapleural spacethat exerts force on both.

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73
Q

define vital capacity

A

amount of air that can be expelled from lungs after full inhalation

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74
Q

what is functional residual capacity?

A

volume in lung remaining at the end of normal expiration

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75
Q

what are capacities the sum of?

A

two or more volumes

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76
Q

how is the work of breathing minimised?

A

when the lung volume at the end of expiration equals functional residual capacity

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77
Q

why is the lung volume at the end of expiration equal to functional residual capacity?

A

at FRC the inward force of lungs equals the outward force of chest

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78
Q

what quality aids the expansion of lungs during stretching?

A

high compliance (easy to distend)

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79
Q

what is the ‘collapse’ of lungs aided by when the stretching force is removed?

A

elasticity

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80
Q

for what 2 reasons does inspiration require energy?

A

stretch the lungs and chest wall

overcome the resistance of airways

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81
Q

what process recovers some of the energy stored as elastic recoil?

A

expiration

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82
Q

what can an increase in lung compliance be caused by?

A

emphysema (loss of elastic tissue so easier to stretch)

ageing

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83
Q

what can a decrease in lung compliance be caused by?

A

fibrosis (lung becomes stiffer)
pulmonary oedema
deficiency of surfactant

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84
Q

what does lung stretching (inspiration) increase within the lung?

A

tension

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85
Q

what does tension in the lung pull on and increase the size of?

A

airways and blood vessels

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86
Q

what effect does increasing the diameter of airways and blood vessels have?

A

reduces pulmonary vascular resistance

reduces airway resistance

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87
Q

what must breathing overcome within the fluid lining alveoli?

A

surface tension

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88
Q

what creates surface tension in the alveoli?

A

fluid lining

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89
Q

is pressure caused by surface tension greater in smaller or larger alveoli?

A

smaller

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90
Q

where do surfactent molecules sit in the lung?

A

between water molecules in alveoli

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91
Q

what effect does the presence of surfactant molecules in the alveoli have?

A

reduces surface tension

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92
Q

what is pressure in the small and large alveoli equalised by?

A

presence of surfactant

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93
Q

what effect does surfactant have on pulmonary compliance?

A

increases it and so reduces the work of inflating the lungs

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94
Q

what effect does surfactant have on the tendency of lungs to recoil?

A

reduces it so they do not collapse so readily

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95
Q

what is the name of the pulmonary surfactant?

A

dipalmitoyl phosphotidyl choline

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96
Q

what is the pulmonary surfactant formed from?

A

phospholipids

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97
Q

where does the pulmonary surfactant originate from?

A

type II alveolar cells (pneumocytes)

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98
Q

what is the function of pulmonary surfactant?

A

reduces surface tension

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99
Q

what is the release of pulmonary surfactant stimulated by?

A

during inspiration (stimulated by stretch)

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100
Q

what must airway resistance be overcome by?

A

the action of inspiratory muscles that create the air to alveolar pressure gradient

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101
Q

how can airflow be calculated?

A

pressure gradient (air -alveolar pressure) divided by resistance of airway

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102
Q

what diseases increase resistance of airways?

A

COPD (encompasses bronchitis and emphysema
oedema (fluid restricts airflow)
asthma (increased constriction of smooth muscle and increased mucus secretion and inflammation)

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103
Q

what is anatomical deadspace within the lungs?

A

volume in airways that does not support gas exchange

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104
Q

how many ml per kg is there of dead space within the average human?

A

2.2 ml per kg

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105
Q

where is anatomical deadspace found?

A

conducting zone (permits movement of air in and out of the lungs

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106
Q

what is alveolar dead space?

A

where the alveoli is ventilated but not perfused, so not involved in gas exchange

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107
Q

is there alveolar dead space in a healthy adult human?

A

no

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108
Q

what is physiological dead space?

A

anatomical dead space + alveolar dead space

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109
Q

in a healthy lung what is physiological dead space?

A

anatomical dead space only as there should not be any alveolar dead space

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110
Q

where is there most and least resistance to airflow in the lungs?

A

most: trachea and primary bronchi
least: terminal bronchiole and alveoli

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111
Q

what are the 3 influences on airway diameter and resistance?

A

physical factors affecting airflow
chemical influences on airways
autonomic control of airways

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112
Q

how are lung tissues connected to bronchioles?

A

by lung parenchyma

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113
Q

how does increased airway diameter affect resistance to airflow?

A

reduces resistance to airflow

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114
Q

what are the 4 types of chemical influences on airways?

A

nervous
hormonal
chemical
physical

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115
Q

give an example of a nervous bronchoconstrictor and bronchodilator

A

constrictor: cholinergenic
dilator: adregenic

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116
Q

what receptor to adrenogenic bronchodilators act on?

A

alpha and beta adrenoreceptors

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117
Q

give an example of a hormonal bronchoconstrictor and bronchodilator

A

constrictor: acetylcholine
dilator: norepinephrine

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118
Q

what receptor do norepinepherine bronchodilators act on?

A

alpha and beta adrenoreceptors

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119
Q

give an example of 3 chemical bronchoconstrictors and 2 bronchodilator

A

bronchoconstrictors: histemine, SRS-A, prostaglandin F-2alpha
bronchodilator: CO2

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120
Q

give an example of 3 physical bronchoconstrictors

A

smoke
dust
SO2

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121
Q

what does the diameter of the conducting airways determine?

A

resistance to airflow

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122
Q

how can ANS influence resistance and airflow?

A

constricting/dilating airways

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123
Q

what effect do beta-receptor agonists have on airways?

A

act to dilate airways

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124
Q

what system is airway resistance (bronchomotor tone) increased by?

A

parasympathetic nervous system

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125
Q

what nerve processes causes bronchoconstriction?

A

parasympathetic neurons release acetylcholine that activate muscarinic receptors which causes contraction of muscle and bronchoconstriction

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126
Q

How does the nervous system cause bronchodilation?

A

sympathetic nervous system release of adrenaline acts on beta 2 receptors and causes bronchodilation

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127
Q

describe the process of the cough reflex

A

irritant receptors - sensory receptors - vagal afferents - medulla oblongata respiratory centres - vagal efferent - effector/target organs (bronchioles leading to vasoconstriction)

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128
Q

describe the process of the hering-breuer reflex

A

lung stretch receptors - sensory receptors - vagal afferents - medulla oblongata respiratory centres - vagal efferent - effector/target organs (bronchioles leading to vasodilation also termination of inspiration)

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129
Q

what is the energy in respiration used to overcome?

A

to stretch the lung

overcome the resistance of the airways

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130
Q

how can disease alter compliance and resistance?

A

compliance increase: emphysema
compliance decrease: pulmonary fibrosis/oedema
resistance increase: asthma

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131
Q

what are the 3 ways the lung function can be measured?

A 
static volumes (breathing cycle)
dynamic volumes (change with time)
CO2 in expired air (over time)
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132
Q

what equipment is used to measure static volumes?

A

spirometry

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133
Q

what equipment is used to measure dynamic volumes?

A

vitalograph

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134
Q

what equipment is used to measure CO2 in expired air?

A

capnography

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135
Q

what are static volumes a measure of?

A

capacity and volume

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136
Q

what is forced vital capacity (FVC)?

A

total volume of air expired from lungs

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137
Q

what is FEV1?

A

forced expiratory volume in 1 second

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138
Q

how do lung volumes change with reduced compliance?

A

air leaves faster but less is expelled

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139
Q

how do lung volumes change with increased airway resistance?

A

it is harder to move air into and out of the lungs so volume is reduced

140
Q

what principle is capnography based on?

A

inspired air contains zero CO2 and expired air contains lots

141
Q

where is capnography often used?

A

anesthesia

142
Q

what is the usual mean BP in the pulmonary circulation?

A

15 mmHg

143
Q

what is the usual mean BP in the systemic circulation?

A

100 mmHg

144
Q

what are the two types of circulation in the lungs?

A

pulmonary and bronchial

145
Q

what does the bronchial circulation in the lungs provide?

A

arterial blood to the lung tissue

146
Q

what is the right to left anatomical shunt?

A

inclusion of some deoxygentated blood in the left atrium

147
Q

by how much does the venous blood from the bronchial and coronary systems reduce the partial pressure of oxygen in the aorta?

A

5-15 mmHg

148
Q

what can the measure of the A-a gradient be useful for?

A

in determining causes of hypoxaemia (low blood O2)

149
Q

what is the A-a gradient?

A

difference between partial pressure of O2 in the alveoli (PAO2) and the arteries (PaO2)

150
Q

what is the alveolar air equation?

A

PAO2 = PIO2 - (PaCO2/respiratory ratio)

151
Q

what is the respiratory ratio?

A

ratio of CO2 to O2

152
Q

what effect does hypoventilation have on PaO2?

A

reduces

153
Q

what effect does hyperventilation have on PaCO2?

A

reduces

154
Q

when does a physiological shunt occur in the lungs

A

when perfusion continues but alveoli is not ventilated

155
Q

what is an effect of a physiological shunt?

A

increased venous admixture (more deoxygenated/poorly oxygenated blood in the left atrium)

156
Q

what effect does a physiological shunt have on oxygenation?

A

reduced - similar to anatomical but larger

157
Q

what medical conditions can cause a physiological shunt to be observed?

A

pulmonary oedema
pneumonia
foreign body entry
obstructions

158
Q

what is the result of physiological shunt?

A

less oxygen in the blood

159
Q

what is PaO2 determined by?

A

average PO2 of all blood leaving the left side of the heart (including the venous blood from lungs and heart)

160
Q

what does pulmonary pressure prevent?

A

oedema

161
Q

what happens to pulmonary resistance at high arterial pressure?

A

distention of opened capillaries and recruitment of closed ones to reduce resistance

162
Q

what effect does the greater compression of alveolar capillaries at larger lung volumes have?

A

increases resistance

163
Q

what effect does greater tension in tissue at larger lung volumes have?

A

dilates extra-alveolar vessels and so reduces resistance

164
Q

does alveolar pressure rise or fall with increased lung volume?

A

rise

165
Q

does extra alveolar pressure rise or fall with increased lung volume?

A

fall

166
Q

what happens to pulmonary artery resistance while PAO2 falls?

A

rises which diverts blood away from the poorly ventilated regions of the lung

167
Q

what conditions in the body cause vasoconstriction?

A

hypoxia
hypercapnia
decreased pH
angiotensin II

168
Q

what substances can cause vasodilation?

A

adenosine
bradykinin
histamine
vasopressin

169
Q

what are vasodilators of the lung dependant on?

A

receptors in the endothelium and nitric oxide enzymes

170
Q

what is pulmonary hypertension caused by?

A

reduced perfusion, leading to less nitric oxide produced which leads to vasoconstriction

171
Q

what is the dominant effect of the sympathetic nervous system on the lungs?

A

vasoconstriction

172
Q

what receptor is sympathetic vasoconstriction in the lungs managed by?

A

alpha 1 adrenoreceptor (reduces pulmonary blood flow by 30%)

173
Q

what receptor is sympathetic vasodilation in the lungs managed by and stimulated by?

A

alpha 2 and beta 2 receptors on endothelium stimulated by adrenaline

174
Q

what effect does the PNS have on the lungs?

A

vasodilation

175
Q

what effect does VIP and CGRP have on the lungs?

A

dilate

176
Q

is pulmonary vascular resistance lower or higher than systemic?

A

lower

177
Q

what are the main deternimants of PVR?

A

capillaries

178
Q

what influences PVR (pulmonary vascular resistance)?

A

control by sympathetic and parasympathetic nervous systems
hypoxia
lung volume and alveolar pressure

179
Q

is the perfusion in lungs uniform and why?

A

no - increases down the lung due to the effect of gravity

180
Q

is the blood flow in lungs uniform and why?

A

no - blood vessels are more open lower down the lung and resistance is lower

181
Q

is ventilation of the lungs uniform and where does most take place?

A

no - in the base of the lung

182
Q

what ratio is PaO2 determined by?

A

ratio of ventilation to perfusion

183
Q

what must happen to ventilation and perfusion for optimal gas exchange?

A

must be matched (~5 litres/min at rest)

184
Q

what should VA/Q be equal to?

A

1

185
Q

what is happening in the lungs when V greater than 1?

A

ventilation is normal or elevated, perfusion is reduced

186
Q

what is happening in the lungs when V is equal to 1?

A

ventilation and perfusion are normal

187
Q

what happens when V is less than one?

A

ventilation is reduced, perfusion is reduced

188
Q

what are the consequences of V-Q mismatch?

A

hypoxia (low blood O2)

hypercapnia (high blood CO2)

189
Q

why may hypercapnia not be seen in mild to moderate V-Q mismatch?

A

hypoxia drives increased ventilation. so functioning alveoli are able to blow off more CO2 keeping PaCO2 normal

190
Q

what can areas with low VQ (shunt effect due to poor ventilation)|be caused by?

A

blocked airways

191
Q

what can areas with high VQ (poor perfusion dead space effect) be caused by?

A

loss of capillaries

192
Q

is the effect of gravity more pronounced in?

A

ventilation

193
Q

what is diffusion dependent on?

A

distance
surface area
permeability

194
Q

what Law is diffusion determined by?

A

Fick’s Law

195
Q

what is diffusion in alveoli driven by?

A

partial pressures

196
Q

how many alveoli are there approximately in the human?

A

~300 million

197
Q

what is the formula used to calculate the diffusion of volume of a gas?

A

lung area x diffusion constant x pressure gradient divided by thickness of alveolar membrane

198
Q

how thick are the alveolar membranes?

A

0.5 micrometres

199
Q

why is it so crucial that alveolar membranes are so thin?

A

to reduce the thickness and so distance gas must travel by diffusion

200
Q

what is the diffusion gradient in the lungs created by?

A

partial pressure of gases

201
Q

is the difference in partial pressure greater in oxygen or carbon dioxide?

A

oxygen

202
Q

what is the diffusion constant determined by?

A

solubility and molecular weight

203
Q

what does the diffusion constant measure?

A

how quickly gases diffuse

204
Q

how many more times more soluble in the blood is CO2 than O2?

A

up to 25 times

205
Q

What is transit time/

A

the time blood takes to move along capillary

206
Q

what is rate of gas uptake across the alveolar membrane limited by?

A

gas diffusion and blood perfusion

207
Q

which gases cross the alveolar membrane quickly?

A

nitrus oxide

208
Q

what is gas uptake limited by in gases which cross the alveolar membrane quickly?

A

perfusion - there is not enough blood in the capillaries to meet gas uptake

209
Q

why does CO appear to cross the membrane slowly even when it diffuses quickly?

A

is bound to haemoglobin so that partial pressure remains low

210
Q

what is diffusion limited gas exchange limited by?

A

rate of diffusion

211
Q

how is oxygen transfer normally limited?

A

by perfusion

212
Q

when can diffusion limited transfer happen in oxygen uptake?

A

if diffusion is impaired by thickening of alveolar wall

213
Q

what is the effect of diffusion limited transfer on A-a gradient?

A

increases it

214
Q

why does exercise in some species result in low PaO2 but high PAO2?

A

diffusion is limited as blood moves through the capillaries too quickly

215
Q

what is right to left shunt the result of?

A

blood passing through lungs without respiratory gas exchange and venous blood draining from bronchial circulation

216
Q

what level must PO2 in lungs remain at and why?

A

high to drive diffusion and match demand by tissues

217
Q

what are the 2 ways oxygen is transported in the blood?

A

dissolved in solution

bound to haemoglobin (Hb)

218
Q

what does the solubility coefficient determine?

A

how much oxygen dissolves in plasma

219
Q

how many ml of O2 per litre is present in the blood?

A

3ml/litre

220
Q

when saturated how much oxygen can 1g of haemoglobin transport?

A

1.39ml

221
Q

what is most of the O2 content of the blood bound to?

A

haemoglobin

222
Q

does gas that is bound (not in free solution) contribute to the partial pressure of that gas?

A

no

223
Q

what is blood PO2 a measure of?

A

the portion of O2 that is dissolved in the blood

224
Q

what is gas dissolved in a liquid determined by?

A

pressure and solubility of the gas

225
Q

what is the partial pressure of gas in liquid proportional to?

A

the partial pressure of the gas at the surface

226
Q

what does the partial pressure gradient determine?

A

movement between gas (air) and liquid (blood)

227
Q

does a bound gas exert partial pressure?

A

no

228
Q

what is the role of haemoglobin?

A

binds O2 to increase partial pressure gradient

229
Q

what does each alpha and beta polypeptide chain of haemoglobin contain?

A

a haem group

230
Q

how many haem groups are there in a single RBC?

A

4

231
Q

how is binding energy of oxygen to haem reduced?

A

allosteric effect of O2 binding

232
Q

In what sort of environment does Hb have low affinity for O2?

A

acidic environement

233
Q

why is oxygen released at tissues?

A

more CO2, lower pH, acidic

234
Q

why is oxygen taken up at lungs?

A

less CO2, higher pH, alkaline

235
Q

what is fully saturated oxygen known as?

A

oxyhaemoglobin

236
Q

how many oxygen molecules is oxyhaemoglobin carrying?

A

4

237
Q

what is haemoglobin with a single oxygen molecule known as?

A

deoxyhaemoglobin

238
Q

what does the high affinity for O2 and high pH at the lungs encourage?

A

uptake of O2

239
Q

what does the lower affinity for O2 and lower pH at the tissues encourage?

A

release of O2

240
Q

what is the oxygen dissociation curve relationship known as?

A

sigmoidal relationship

241
Q

what happens in anaemia?

A

Hb is reduced (can be up to by 50%)

242
Q

what is the Bohr shift?

A

for a given PO2 more oxygen is given up at the tissues. Affinity of Hb for O2 is lower

243
Q

how does increased temperature during skeletal muscle contractions affect oxygen dissociation?

A

causes reduced O2 affinity that aids unloading of oxygen

244
Q

what are the 5 reasons we need erythrocytes?

A

holds a high concentration of Hb which decreases blood viscosity
Provides an environment for DPG
Encapsulates and concentrates carbonic anhydrase (CO2 transport)
Prevents Hb loss via filtration in the kidneys
Concave shape aids passage through tight spaces

245
Q

how is carbon dioxide transported in the blood?

A

chemically in the form of HCO3-
combined with haemoglobin
dissolved in solution

246
Q

what percentage of CO2 is directly dissolved into the blood?

A

~5% of total

247
Q

what is the solubility coefficient of CO2?

A

0.3 mmol of CO2 per L blood per mmHg

248
Q

in what form is CO2 bound to haemoglobin?

A

carbaminohaemaglobin

249
Q

what percentage of CO2 is reversibly bound to Hb?

A

~30% of total

250
Q

what percentage of CO2 is bicarbonate?

A

~65% of total

251
Q

what is the chloride shift in red blood cells?

A

HCO3- is formed in RBC and diffuses into plasma via facilitated diffusion carrier in exchange for chloride (both negative, no charge difference)

252
Q

what enzyme is needed to form HCO3- in RBC?

A

carbonic anhydrase

253
Q

why is there no saturation of CO2 in blood as there is for oxygen?

A

Co2 is hugely soluble in plasma

254
Q

what is the Haldane effect?

A

difference between venous and arterial blood. It enhances the unloading of CO2 from tissues into the blood

255
Q

at low PO2 what does haemoglobin have a higher affinity for?

A

CO2

256
Q

why is the curve for venous blood (on CO2 dissociation curve) to the left and above that for arterial blood?

A

venous blood contains more CO2 at any given value of PCO2 than does arterial blood

257
Q

what does increased CO2 (due to ventilation) result in in terms of blood pH?

A

respiratory acidosis

258
Q

what does decreased CO2 (due to ventilation) result in in terms of blood pH?

A

respiratory alkalosis

259
Q

what is normal arterial blood pH?

A

~7.4

260
Q

what is ventilation normally closely matched to?

A

metabolic requirements

261
Q

what effect does increased ventilation have on PACO2?

A

reduced

262
Q

what relationship is there between PACO2 and alveolar ventilation?

A

inverse

263
Q

what effect can hyperventilation have on PaCO2?

A

<40mmHg

264
Q

what effect can hypoventilation have on PaCO2?

A

> 45mmHg

265
Q

what causes hyperventilation?

A

inducible: high anxiety and pain

altitude

266
Q

what does hyperventilation lead to?

A

hypocapnia

respiratory alkalosis

267
Q

what are the effects on the body of hyperventilation?

A 
cerebral vasoconstriction 
muscle cramps (low calcium in muscles)
268
Q

how can hyperventilation be compensated for?

A

hypoventilation or re breathing exhaled air

269
Q

what causes hypoventilation?

A

chest injury
obstruction (COPD)
impaired respiratory drive

270
Q

what does hypoventilation lead to?

A

hypercapnia
respiratory acidosis
hypoxia

271
Q

what are the effects of hypoventilation?

A

peripheral vasodilation
confusion
drowsiness
coma

272
Q

how can hypoventilation be compensated for?

A

hyperventilation

273
Q

what are the 2 types of respiratory chemoreceptors?

A

peripheral

central

274
Q

where are peripheral chemo receptors located?

A

carotid sinus and aortic arch

275
Q

where are central chemo receptors located?

A

within the medulla oblongata

276
Q

define hypoxia

A

low O2 levels

277
Q

define anoxia

A

no O2

278
Q

define asphyxia

A

low O2 and high CO2

279
Q

define hypercapnia

A

high CO2

280
Q

define hypocapnia

A

low CO2

281
Q

define hyperventilate

A

excessive breathing

282
Q

define hypoventilate

A

shallow/inadequate breathing

283
Q

define apnoea

A

no breathing

284
Q

define dyspnoea

A

sensation of breathlessness

285
Q

describe the reflex control system of breathing

A

CNS monitoring homeostasis of blood gases - motor efferent - effector/target organ: altered function of respiratory pump muscles (change in rate/depth of ventilation) - feedback - chemo (sensory) receptors - sensory afferent - CNS

286
Q

what nerve is innervated by the carotid peripheral chemoreceptors?

A

sinus nerve

287
Q

what nerve is innervated by the aortic peripheral chemoreceptors?

A

aortic nerve

288
Q

which nerve does the sinus nerve join?

A

glossopharyngeal nerve

289
Q

which nerve does the aortic nerve join?

A

vagus nerve

290
Q

where do both the glossopharyngeal and vagus nerves terminate?

A

nucleus tractus solitarii (NTS) in the medulla oblongata

291
Q

what is signalling from carotid body chemoreceptors stimulated by?

A

reduced PaO2

292
Q

what does the CNS equate repeat firing of carotid body chemoreceptors with?

A

hypoxia

293
Q

which cell releases the neurotransmitter to signal the chemoreceptor afferent ending

A

type 1 glomus cell

294
Q

what stimulates peripheral chemoreceptors?

A 
hypoxia
hypercapnia
haemmorrhage
acidosis
increased sympathetic activity
sodium cyanide (during experiments)
295
Q

what is the most effective stimulant of peripheral chemoreceptors?

A

combination of hypoxia and hypercapnia

296
Q

how quick is peripheral chemoreceptor response time?

A

fast! within 1 breath

297
Q

what surface of the medulla oblongata are the chemo-sensitive regions located?

A

ventral

298
Q

what is the CNS indirectly sensitive to?

A

PaCO2

299
Q

what is the effect of increased H+?

A

increases ventilation, reduces PaCO2

300
Q

what is the effect of reduced H+?

A

decreases ventilation

301
Q

can H+ cross the blood brain barrier?

A

not well

302
Q

does CO2 cross blood brain barrier?

A

yes

303
Q

once in the CSF what happens to CO2?

A

converted to H+ and bicarbonate by carbonic anhydrase

304
Q

why is the response of central chemoreceptors slow?

A

due to delay in creation of H+ and bicarb in CSF as H+ cannot pass blood brain barrier

305
Q

describe the ventilatory response to hypoxia

A

as PaO2 reduces respiration rate increases until it reaches peak respiratory response. there is then depression of nervous activity of the brain which eventually leads to apnoea due to no driving of ventilation by brain

306
Q

what percentage of the bodies receptors is the ventilatory response to hypercapnia mediated by?

A

80% central chemoreceptors

20% peripheral chemoreceptors

307
Q

what is the synergistic effect of response to hypercapnia?

A

sensitivity to PACO2 is high when PAO2 is low

308
Q

what effect do hypoxia and hypercapnia have on the nervous system?

A

increased sympathetic nerve activity

increase in release of adrenaline from adrenal medulla

309
Q

what is the hypocapnic braking response to hypoxia?

A

hypoxia drives ventilation increase less when PCO2 starts to fall. PaCO2 stimulates central chemoreceptors and a fall in PaCO2 will depress or ‘brake’ the response to low PO2

310
Q

what is hyperventilation driven by peripheral hypoxia reduced by?

A

subsequent central hypocapnia

311
Q

what is the advantage of a gas transport system based on haemoglobin?

A

blood O2 content can be relatively independent of the O2 content of inspired air due to the ability for saturation

312
Q

why is th eclose regulation of blood CO2 necessary?

A

to regulate blood pH

313
Q

why is the regulation of both blood CO2 and blood O2 not possible?

A

increased ventilation required to compensate for hypoxia would blow off blood CO2 and cause respiratory alkalosis

314
Q

what areas of the brain command the patterns of breathing?

A

brainstem and spinal cord

315
Q

what do afferent cranial nerves receive information from?

A

chemoreceptors and stretch receptors

316
Q

what do efferent cranial nerves send information to

A

bronchial muscles which control resistance

317
Q

where is the central control of ventilation located?

A

pons and medulla are only areas of the brain required to develop rhythm of ventilation (brainstem)

318
Q

where is the rhythm of breathing generated?

A

pons

319
Q

where is the pattern of breathing generated?

A

medulla

320
Q

what are PaCO2, PaO2 and pH levels monitored by?

A

central chemoreceptors
peripheral chemorecptors
pulmonal mechanoreceptors
mechanosensors in joints, tendons and muscles

321
Q

what are the types of sensory information which regulate breathing?

A

mechanoreceptors

chemoreceptors

322
Q

what nerve contains the afferent fibres of pulmonary mechanoreceptors?

A

vegus nerve

323
Q

what type of receptors are pulmonary mechanoreceptors?

A

slowly adapting stretch receptors

324
Q

wht are pulmonary mechanoreceptors stimulated by?

A

lung stretch and bronchoconstriction

325
Q

what effect does stimulation of pulmonary mechanoreceptors have?

A

terminates inspiration
prolongs expiration
activates expiritory muscles
bronchodilation

326
Q

what are 2 other vagal afferent receptors?

A

rapidly adapting stretch receptors (cough reflex)

juxtapulmonary capillary receptors (leads by oedema)

327
Q

what are 3 factors which drive breathing?

A

decrease in arterial PO2
increase in arterial PCO2
increase in H+ concentration

328
Q

what type of receptors are the factors which drive breathing monitored by?

A

peripheral and central chemoreceptors

329
Q

what is the venous partial pressure of oxygen?

A

40 mmHg

330
Q

what is the arterial partial pressure of CO2?

A

40 mmHg

331
Q

where are peripheral chemoreceptors located?

A

carotid bodies at carotid bifarcation

aortic bodies

332
Q

what are the carotid bodies activated by?

A

mainly decreased PaO2
increased PaCO2
decreased pH

333
Q

what are the integrated responses to breathing regulation?

A 
chemoreceptor feedback (interaction between CO2 and O2. Interaction between CO2 and H+)
feedforward regulation
334
Q

what is the central response to CO2 via/

A

pH

335
Q

what is CSF pH determined by?

A

arterial PCO2 and CSF concentration of H+

336
Q

what do central chemoreceptors not detect?

A

hypoxia/PO2

337
Q

in healthy breathing where does drive to breathe come from?

A

central chemoreceptors (PCO2 via H+), dependant on pH

338
Q

if PCO2 is constant at what point will PO2 produce drive to breathe in the brain?

A

<60 mmHg

339
Q

how can the pH set point change over time due to prolonged hypercapnia?

A

prolonged hypercapnia means CO2 removal is impaired leading to compensatory changes in HCO3- transport in CSF. The CSF pH is returned to normaleven though blood pH is still low due to elevated PCO2.

340
Q

when central drive via CO2 is reduced by prolonged hypercapnia where must the chemoreceptive drive come from?

A

O2- hypoxic drive in peripheral chemoreceptors

341
Q

what receptors does an increase in H+ stimulate?

A

peripheral chemo receptors

342
Q

why are central chemo receptors not stimulated by an increase in H+?

A

H+ does not cross blood brain barrier

343
Q

what is the effect of stimulation of peripheral chemo receptors but chemoreceptors not stimulated?

A

increase in ventilation reduced PaCO2 and reduces brain pH. This reduces the ability of both peripheral and central chemoreceptors

344
Q

describe the route to increased ventilation in the respiratory system

A

PCO2 increased stimulates peripheral and central chemo receptors. Peripheral chemo receptor afferents stimulate the respiratory centre via NTS. Central chemo receptor cell bodies in medulla which increase the output of pre-motor neurons. Leads to increased ventilation

345
Q

what factors can depress respiratory reflexes?

A 
sleep
opiates
GA
Alcohol
Bacterial toxins
Stress/pain/fever

X Physiology 1A (9 decks)

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